Carcinoma, Pancreatic Ductal: Carcinoma that arises from the PANCREATIC DUCTS. It accounts for the majority of cancers derived from the PANCREAS.Pancreatic Neoplasms: Tumors or cancer of the PANCREAS. Depending on the types of ISLET CELLS present in the tumors, various hormones can be secreted: GLUCAGON from PANCREATIC ALPHA CELLS; INSULIN from PANCREATIC BETA CELLS; and SOMATOSTATIN from the SOMATOSTATIN-SECRETING CELLS. Most are malignant except the insulin-producing tumors (INSULINOMA).Pancreatic Ducts: Ducts that collect PANCREATIC JUICE from the PANCREAS and supply it to the DUODENUM.Carcinoma: A malignant neoplasm made up of epithelial cells tending to infiltrate the surrounding tissues and give rise to metastases. It is a histological type of neoplasm but is often wrongly used as a synonym for "cancer." (From Dorland, 27th ed)Carcinoma, Ductal, Breast: An invasive (infiltrating) CARCINOMA of the mammary ductal system (MAMMARY GLANDS) in the human BREAST.Carcinoma in Situ: A lesion with cytological characteristics associated with invasive carcinoma but the tumor cells are confined to the epithelium of origin, without invasion of the basement membrane.Carcinoma, Squamous Cell: A carcinoma derived from stratified SQUAMOUS EPITHELIAL CELLS. It may also occur in sites where glandular or columnar epithelium is normally present. (From Stedman, 25th ed)Carcinoma, Hepatocellular: A primary malignant neoplasm of epithelial liver cells. It ranges from a well-differentiated tumor with EPITHELIAL CELLS indistinguishable from normal HEPATOCYTES to a poorly differentiated neoplasm. The cells may be uniform or markedly pleomorphic, or form GIANT CELLS. Several classification schemes have been suggested.Adenocarcinoma: A malignant epithelial tumor with a glandular organization.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Carcinoma, Intraductal, Noninfiltrating: A noninvasive (noninfiltrating) carcinoma of the breast characterized by a proliferation of malignant epithelial cells confined to the mammary ducts or lobules, without light-microscopy evidence of invasion through the basement membrane into the surrounding stroma.Carcinoma, Ductal: Malignant neoplasms involving the ductal systems of any of a number of organs, such as the MAMMARY GLANDS, the PANCREAS, the PROSTATE, or the LACRIMAL GLAND.Pancreas: A nodular organ in the ABDOMEN that contains a mixture of ENDOCRINE GLANDS and EXOCRINE GLANDS. The small endocrine portion consists of the ISLETS OF LANGERHANS secreting a number of hormones into the blood stream. The large exocrine portion (EXOCRINE PANCREAS) is a compound acinar gland that secretes several digestive enzymes into the pancreatic ductal system that empties into the DUODENUM.Tumor Markers, Biological: Molecular products metabolized and secreted by neoplastic tissue and characterized biochemically in cells or body fluids. They are indicators of tumor stage and grade as well as useful for monitoring responses to treatment and predicting recurrence. Many chemical groups are represented including hormones, antigens, amino and nucleic acids, enzymes, polyamines, and specific cell membrane proteins and lipids.Carcinoma, Papillary: A malignant neoplasm characterized by the formation of numerous, irregular, finger-like projections of fibrous stroma that is covered with a surface layer of neoplastic epithelial cells. (Stedman, 25th ed)Cell Line, Tumor: A cell line derived from cultured tumor cells.Pancreatitis, Chronic: INFLAMMATION of the PANCREAS that is characterized by recurring or persistent ABDOMINAL PAIN with or without STEATORRHEA or DIABETES MELLITUS. It is characterized by the irregular destruction of the pancreatic parenchyma which may be focal, segmental, or diffuse.Neoplasm Invasiveness: Ability of neoplasms to infiltrate and actively destroy surrounding tissue.Adenocarcinoma, Mucinous: An adenocarcinoma producing mucin in significant amounts. (From Dorland, 27th ed)Gene Expression Regulation, Neoplastic: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.Pancreatectomy: Surgical removal of the pancreas. (Dorland, 28th ed)Prognosis: A prediction of the probable outcome of a disease based on a individual's condition and the usual course of the disease as seen in similar situations.Carcinoma, Acinar Cell: A malignant tumor arising from secreting cells of a racemose gland, particularly the salivary glands. Racemose (Latin racemosus, full of clusters) refers, as does acinar (Latin acinus, grape), to small saclike dilatations in various glands. Acinar cell carcinomas are usually well differentiated and account for about 13% of the cancers arising in the parotid gland. Lymph node metastasis occurs in about 16% of cases. Local recurrences and distant metastases many years after treatment are common. This tumor appears in all age groups and is most common in women. (Stedman, 25th ed; Holland et al., Cancer Medicine, 3d ed, p1240; from DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p575)Breast Neoplasms: Tumors or cancer of the human BREAST.Pancreatitis: INFLAMMATION of the PANCREAS. Pancreatitis is classified as acute unless there are computed tomographic or endoscopic retrograde cholangiopancreatographic findings of CHRONIC PANCREATITIS (International Symposium on Acute Pancreatitis, Atlanta, 1992). The two most common forms of acute pancreatitis are ALCOHOLIC PANCREATITIS and gallstone pancreatitis.Liver Neoplasms: Tumors or cancer of the LIVER.Pancreaticoduodenectomy: The excision of the head of the pancreas and the encircling loop of the duodenum to which it is connected.Neoplasm Staging: Methods which attempt to express in replicable terms the extent of the neoplasm in the patient.Pancreatic Juice: The fluid containing digestive enzymes secreted by the pancreas in response to food in the duodenum.Tissue Array Analysis: The simultaneous analysis of multiple samples of TISSUES or CELLS from BIOPSY or in vitro culture that have been arranged in an array format on slides or microchips.Carcinoma, Basal Cell: A malignant skin neoplasm that seldom metastasizes but has potentialities for local invasion and destruction. Clinically it is divided into types: nodular, cicatricial, morphaic, and erythematoid (pagetoid). They develop on hair-bearing skin, most commonly on sun-exposed areas. Approximately 85% are found on the head and neck area and the remaining 15% on the trunk and limbs. (From DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1471)Genes, ras: Family of retrovirus-associated DNA sequences (ras) originally isolated from Harvey (H-ras, Ha-ras, rasH) and Kirsten (K-ras, Ki-ras, rasK) murine sarcoma viruses. Ras genes are widely conserved among animal species and sequences corresponding to both H-ras and K-ras genes have been detected in human, avian, murine, and non-vertebrate genomes. The closely related N-ras gene has been detected in human neuroblastoma and sarcoma cell lines. All genes of the family have a similar exon-intron structure and each encodes a p21 protein.Precancerous Conditions: Pathological processes that tend eventually to become malignant. (From Dorland, 27th ed)Reverse Transcriptase Polymerase Chain Reaction: A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.Tumor Cells, Cultured: Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.Adenocarcinoma, Papillary: An adenocarcinoma containing finger-like processes of vascular connective tissue covered by neoplastic epithelium, projecting into cysts or the cavity of glands or follicles. It occurs most frequently in the ovary and thyroid gland. (Stedman, 25th ed)Mice, Nude: Mutant mice homozygous for the recessive gene "nude" which fail to develop a thymus. They are useful in tumor studies and studies on immune responses.Cell Proliferation: All of the processes involved in increasing CELL NUMBER including CELL DIVISION.Lymphatic Metastasis: Transfer of a neoplasm from its primary site to lymph nodes or to distant parts of the body by way of the lymphatic system.Acinar Cells: Cells lining the saclike dilatations known as acini of various glands or the lungs.Proto-Oncogene Proteins p21(ras): Cellular proteins encoded by the H-ras, K-ras and N-ras genes. The proteins have GTPase activity and are involved in signal transduction as monomeric GTP-binding proteins. Elevated levels of p21 c-ras have been associated with neoplasia. This enzyme was formerly listed as EC 3.6.1.47.Neoplasm Proteins: Proteins whose abnormal expression (gain or loss) are associated with the development, growth, or progression of NEOPLASMS. Some neoplasm proteins are tumor antigens (ANTIGENS, NEOPLASM), i.e. they induce an immune reaction to their tumor. Many neoplasm proteins have been characterized and are used as tumor markers (BIOMARKERS, TUMOR) when they are detectable in cells and body fluids as monitors for the presence or growth of tumors. Abnormal expression of ONCOGENE PROTEINS is involved in neoplastic transformation, whereas the loss of expression of TUMOR SUPPRESSOR PROTEINS is involved with the loss of growth control and progression of the neoplasm.Smad4 Protein: A signal transducing adaptor protein and tumor suppressor protein. It forms a complex with activated RECEPTOR-REGULATED SMAD PROTEINS. The complex then translocates to the CELL NUCLEUS and regulates GENETIC TRANSCRIPTION of target GENES.Neoplasm Metastasis: The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.Disease Progression: The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.Carcinoma, Transitional Cell: A malignant neoplasm derived from TRANSITIONAL EPITHELIAL CELLS, occurring chiefly in the URINARY BLADDER; URETERS; or RENAL PELVIS.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Cell Transformation, Neoplastic: Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.Carcinoma, Bronchogenic: Malignant neoplasm arising from the epithelium of the BRONCHI. It represents a large group of epithelial lung malignancies which can be divided into two clinical groups: SMALL CELL LUNG CANCER and NON-SMALL-CELL LUNG CARCINOMA.Neoplasms, Multiple Primary: Two or more abnormal growths of tissue occurring simultaneously and presumed to be of separate origin. The neoplasms may be histologically the same or different, and may be found in the same or different sites.Carcinoma, Medullary: A carcinoma composed mainly of epithelial elements with little or no stroma. Medullary carcinomas of the breast constitute 5%-7% of all mammary carcinomas; medullary carcinomas of the thyroid comprise 3%-10% of all thyroid malignancies. (From Dorland, 27th ed; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1141; Segen, Dictionary of Modern Medicine, 1992)Kaplan-Meier Estimate: A nonparametric method of compiling LIFE TABLES or survival tables. It combines calculated probabilities of survival and estimates to allow for observations occurring beyond a measurement threshold, which are assumed to occur randomly. Time intervals are defined as ending each time an event occurs and are therefore unequal. (From Last, A Dictionary of Epidemiology, 1995)Carcinoma, Adenoid Cystic: Carcinoma characterized by bands or cylinders of hyalinized or mucinous stroma separating or surrounded by nests or cords of small epithelial cells. When the cylinders occur within masses of epithelial cells, they give the tissue a perforated, sievelike, or cribriform appearance. Such tumors occur in the mammary glands, the mucous glands of the upper and lower respiratory tract, and the salivary glands. They are malignant but slow-growing, and tend to spread locally via the nerves. (Dorland, 27th ed)Ampulla of Vater: A dilation of the duodenal papilla that is the opening of the juncture of the COMMON BILE DUCT and the MAIN PANCREATIC DUCT, also known as the hepatopancreatic ampulla.Carcinoma, Small Cell: An anaplastic, highly malignant, and usually bronchogenic carcinoma composed of small ovoid cells with scanty neoplasm. It is characterized by a dominant, deeply basophilic nucleus, and absent or indistinct nucleoli. (From Stedman, 25th ed; Holland et al., Cancer Medicine, 3d ed, p1286-7)Gene Expression Profiling: The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.Metaplasia: A condition in which there is a change of one adult cell type to another similar adult cell type.Survival Analysis: A class of statistical procedures for estimating the survival function (function of time, starting with a population 100% well at a given time and providing the percentage of the population still well at later times). The survival analysis is then used for making inferences about the effects of treatments, prognostic factors, exposures, and other covariates on the function.Neoplasm Recurrence, Local: The local recurrence of a neoplasm following treatment. It arises from microscopic cells of the original neoplasm that have escaped therapeutic intervention and later become clinically visible at the original site.Carcinoma, Lobular: A infiltrating (invasive) breast cancer, relatively uncommon, accounting for only 5%-10% of breast tumors in most series. It is often an area of ill-defined thickening in the breast, in contrast to the dominant lump characteristic of ductal carcinoma. It is typically composed of small cells in a linear arrangement with a tendency to grow around ducts and lobules. There is likelihood of axillary nodal involvement with metastasis to meningeal and serosal surfaces. (DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1205)Neoplasm Transplantation: Experimental transplantation of neoplasms in laboratory animals for research purposes.Survival Rate: The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods.Carcinoma, Neuroendocrine: A group of carcinomas which share a characteristic morphology, often being composed of clusters and trabecular sheets of round "blue cells", granular chromatin, and an attenuated rim of poorly demarcated cytoplasm. Neuroendocrine tumors include carcinoids, small ("oat") cell carcinomas, medullary carcinoma of the thyroid, Merkel cell tumor, cutaneous neuroendocrine carcinoma, pancreatic islet cell tumors, and pheochromocytoma. Neurosecretory granules are found within the tumor cells. (Segen, Dictionary of Modern Medicine, 1992)Immunoenzyme Techniques: Immunologic techniques based on the use of: (1) enzyme-antibody conjugates; (2) enzyme-antigen conjugates; (3) antienzyme antibody followed by its homologous enzyme; or (4) enzyme-antienzyme complexes. These are used histologically for visualizing or labeling tissue specimens.DeoxycytidineRetrospective Studies: Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.CA-19-9 Antigen: Sialylated Lewis blood group carbohydrate antigen found in many adenocarcinomas of the digestive tract, especially pancreatic tumors.Epithelial Cells: Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.Tumor Suppressor Protein p53: Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. A mutant or absent p53 protein has been found in LEUKEMIA; OSTEOSARCOMA; LUNG CANCER; and COLORECTAL CANCER.Nasopharyngeal Neoplasms: Tumors or cancer of the NASOPHARYNX.DNA, Neoplasm: DNA present in neoplastic tissue.Cyclic S-OxidesSignal Transduction: The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.Antineoplastic Agents: Substances that inhibit or prevent the proliferation of NEOPLASMS.Thyroid Neoplasms: Tumors or cancer of the THYROID GLAND.Breast: In humans, one of the paired regions in the anterior portion of the THORAX. The breasts consist of the MAMMARY GLANDS, the SKIN, the MUSCLES, the ADIPOSE TISSUE, and the CONNECTIVE TISSUES.Treatment Outcome: Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.Mutation: Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.ras Proteins: Small, monomeric GTP-binding proteins encoded by ras genes (GENES, RAS). The protooncogene-derived protein, PROTO-ONCOGENE PROTEIN P21(RAS), plays a role in normal cellular growth, differentiation and development. The oncogene-derived protein (ONCOGENE PROTEIN P21(RAS)) can play a role in aberrant cellular regulation during neoplastic cell transformation (CELL TRANSFORMATION, NEOPLASTIC). This enzyme was formerly listed as EC 3.6.1.47.Apoptosis: One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.Carcinoma, Adenosquamous: A mixed adenocarcinoma and squamous cell or epidermoid carcinoma.Mucin-1: Carbohydrate antigen elevated in patients with tumors of the breast, ovary, lung, and prostate as well as other disorders. The mucin is expressed normally by most glandular epithelia but shows particularly increased expression in the breast at lactation and in malignancy. It is thus an established serum marker for breast cancer.Lung Neoplasms: Tumors or cancer of the LUNG.Keratins: A class of fibrous proteins or scleroproteins that represents the principal constituent of EPIDERMIS; HAIR; NAILS; horny tissues, and the organic matrix of tooth ENAMEL. Two major conformational groups have been characterized, alpha-keratin, whose peptide backbone forms a coiled-coil alpha helical structure consisting of TYPE I KERATIN and a TYPE II KERATIN, and beta-keratin, whose backbone forms a zigzag or pleated sheet structure. alpha-Keratins have been classified into at least 20 subtypes. In addition multiple isoforms of subtypes have been found which may be due to GENE DUPLICATION.Cadherins: Calcium-dependent cell adhesion proteins. They are important in the formation of ADHERENS JUNCTIONS between cells. Cadherins are classified by their distinct immunological and tissue specificities, either by letters (E- for epithelial, N- for neural, and P- for placental cadherins) or by numbers (cadherin-12 or N-cadherin 2 for brain-cadherin). Cadherins promote cell adhesion via a homophilic mechanism as in the construction of tissues and of the whole animal body.Carcinoma, Mucoepidermoid: A tumor of both low- and high-grade malignancy. The low-grade grow slowly, appear in any age group, and are readily cured by excision. The high-grade behave aggressively, widely infiltrate the salivary gland and produce lymph node and distant metastases. Mucoepidermoid carcinomas account for about 21% of the malignant tumors of the parotid gland and 10% of the sublingual gland. They are the most common malignant tumor of the parotid. (From DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p575; Holland et al., Cancer Medicine, 3d ed, p1240)Genes, Tumor Suppressor: Genes that inhibit expression of the tumorigenic phenotype. They are normally involved in holding cellular growth in check. When tumor suppressor genes are inactivated or lost, a barrier to normal proliferation is removed and unregulated growth is possible.RNA, Neoplasm: RNA present in neoplastic tissue.Tumor Burden: The total amount (cell number, weight, size or volume) of tumor cells or tissue in the body.Pancreatic Stellate Cells: Star-shaped, myofibroblast-like cells located in the periacinar, perivascular, and periductal regions of the EXOCRINE PANCREAS. They play a key role in the pathobiology of FIBROSIS; PANCREATITIS; and PANCREATIC CANCER.Common Bile Duct Neoplasms: Tumor or cancer of the COMMON BILE DUCT including the AMPULLA OF VATER and the SPHINCTER OF ODDI.Neoplasm Grading: Methods which attempt to express in replicable terms the level of CELL DIFFERENTIATION in neoplasms as increasing ANAPLASIA correlates with the aggressiveness of the neoplasm.Nitrosamines: A class of compounds that contain a -NH2 and a -NO radical. Many members of this group have carcinogenic and mutagenic properties.Antigens, Neoplasm: Proteins, glycoprotein, or lipoprotein moieties on surfaces of tumor cells that are usually identified by monoclonal antibodies. Many of these are of either embryonic or viral origin.Cystadenoma, Papillary: A benign neoplasm of the ovary.Oligonucleotide Array Sequence Analysis: Hybridization of a nucleic acid sample to a very large set of OLIGONUCLEOTIDE PROBES, which have been attached individually in columns and rows to a solid support, to determine a BASE SEQUENCE, or to detect variations in a gene sequence, GENE EXPRESSION, or for GENE MAPPING.Cystadenocarcinoma, Mucinous: A malignant cystic or semisolid tumor most often occurring in the ovary. Rarely, one is solid. This tumor may develop from a mucinous cystadenoma, or it may be malignant at the onset. The cysts are lined with tall columnar epithelial cells; in others, the epithelium consists of many layers of cells that have lost normal structure entirely. In the more undifferentiated tumors, one may see sheets and nests of tumor cells that have very little resemblance to the parent structure. (Hughes, Obstetric-Gynecologic Terminology, 1972, p184)HSP47 Heat-Shock Proteins: Basic glycoprotein members of the SERPIN SUPERFAMILY that function as COLLAGEN-specific MOLECULAR CHAPERONES in the ENDOPLASMIC RETICULUM.Epithelium: One or more layers of EPITHELIAL CELLS, supported by the basal lamina, which covers the inner or outer surfaces of the body.Carcinoma, Endometrioid: An adenocarcinoma characterized by the presence of cells resembling the glandular cells of the ENDOMETRIUM. It is a common histological type of ovarian CARCINOMA and ENDOMETRIAL CARCINOMA. There is a high frequency of co-occurrence of this form of adenocarcinoma in both tissues.Head and Neck Neoplasms: Soft tissue tumors or cancer arising from the mucosal surfaces of the LIP; oral cavity; PHARYNX; LARYNX; and cervical esophagus. Other sites included are the NOSE and PARANASAL SINUSES; SALIVARY GLANDS; THYROID GLAND and PARATHYROID GLANDS; and MELANOMA and non-melanoma skin cancers of the head and neck. (from Holland et al., Cancer Medicine, 4th ed, p1651)Xenograft Model Antitumor Assays: In vivo methods of screening investigative anticancer drugs, biologic response modifiers or radiotherapies. Human tumor tissue or cells are transplanted into mice or rats followed by tumor treatment regimens. A variety of outcomes are monitored to assess antitumor effectiveness.Nipples: The conic organs which usually give outlet to milk from the mammary glands.Blotting, Western: Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.Keratin-19: A type I keratin found associated with KERATIN-7 in ductal epithelia and gastrointestinal epithelia.Pancreatic Diseases: Pathological processes of the PANCREAS.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Carcinoma, Embryonal: A highly malignant, primitive form of carcinoma, probably of germinal cell or teratomatous derivation, usually arising in a gonad and rarely in other sites. It is rare in the female ovary, but in the male it accounts for 20% of all testicular tumors. (From Dorland, 27th ed & Holland et al., Cancer Medicine, 3d ed, p1595)Esophageal Neoplasms: Tumors or cancer of the ESOPHAGUS.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Mouth Neoplasms: Tumors or cancer of the MOUTH.Cyclin-Dependent Kinase Inhibitor p16: A product of the p16 tumor suppressor gene (GENES, P16). It is also called INK4 or INK4A because it is the prototype member of the INK4 CYCLIN-DEPENDENT KINASE INHIBITORS. This protein is produced from the alpha mRNA transcript of the p16 gene. The other gene product, produced from the alternatively spliced beta transcript, is TUMOR SUPPRESSOR PROTEIN P14ARF. Both p16 gene products have tumor suppressor functions.Carcinoma, Merkel Cell: A carcinoma arising from MERKEL CELLS located in the basal layer of the epidermis and occurring most commonly as a primary neuroendocrine carcinoma of the skin. Merkel cells are tactile cells of neuroectodermal origin and histologically show neurosecretory granules. The skin of the head and neck are a common site of Merkel cell carcinoma, occurring generally in elderly patients. (Holland et al., Cancer Medicine, 3d ed, p1245)Cholangiopancreatography, Endoscopic Retrograde: Fiberoptic endoscopy designed for duodenal observation and cannulation of VATER'S AMPULLA, in order to visualize the pancreatic and biliary duct system by retrograde injection of contrast media. Endoscopic (Vater) papillotomy (SPHINCTEROTOMY, ENDOSCOPIC) may be performed during this procedure.Transplantation, Heterologous: Transplantation between animals of different species.Tumor Microenvironment: The milieu surrounding neoplasms consisting of cells, vessels, soluble factors, and molecules, that can influence and be influenced by, the neoplasm's growth.Cell Division: The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.Cell Growth Processes: Processes required for CELL ENLARGEMENT and CELL PROLIFERATION.RNA, Small Interfering: Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.Ovarian Neoplasms: Tumors or cancer of the OVARY. These neoplasms can be benign or malignant. They are classified according to the tissue of origin, such as the surface EPITHELIUM, the stromal endocrine cells, and the totipotent GERM CELLS.Mice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.Hyperplasia: An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells.Up-Regulation: A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.Mucins: High molecular weight mucoproteins that protect the surface of EPITHELIAL CELLS by providing a barrier to particulate matter and microorganisms. Membrane-anchored mucins may have additional roles concerned with protein interactions at the cell surface.Mucin-2: A gel-forming mucin found predominantly in SMALL INTESTINE and variety of mucous membrane-containing organs. It provides a protective, lubricating barrier against particles and infectious agents.Down-Regulation: A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.gamma-Synuclein: A homolog of ALPHA-SYNUCLEIN that plays a role in neurofilament network integrity. It is overexpressed in a variety of human NEOPLASMS and may be involved in modulating AXON architecture during EMBRYONIC DEVELOPMENT and in the adult. Gamma-Synuclein may also activate SIGNAL TRANSDUCTION PATHWAYS associated with ETS-DOMAIN PROTEIN ELK-1.Colonic Neoplasms: Tumors or cancer of the COLON.Adrenocortical Carcinoma: A malignant neoplasm of the ADRENAL CORTEX. Adrenocortical carcinomas are unencapsulated anaplastic (ANAPLASIA) masses sometimes exceeding 20 cm or 200 g. They are more likely to be functional than nonfunctional, and produce ADRENAL CORTEX HORMONES that may result in hypercortisolism (CUSHING SYNDROME); HYPERALDOSTERONISM; and/or VIRILISM.Fatal Outcome: Death resulting from the presence of a disease in an individual, as shown by a single case report or a limited number of patients. This should be differentiated from DEATH, the physiological cessation of life and from MORTALITY, an epidemiological or statistical concept.Proto-Oncogene Proteins: Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity.Stromal Cells: Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the hematopoietic system and elsewhere.Carcinoma, Verrucous: A variant of well-differentiated epidermoid carcinoma that is most common in the oral cavity, but also occurs in the larynx, nasal cavity, esophagus, penis, anorectal region, vulva, vagina, uterine cervix, and skin, especially on the sole of the foot. Most intraoral cases occur in elderly male abusers of smokeless tobacco. The treatment is surgical resection. Radiotherapy is not indicated, as up to 30% treated with radiation become highly aggressive within six months. (Segen, Dictionary of Modern Medicine, 1992)Follow-Up Studies: Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.Carcinoma, Signet Ring Cell: A poorly differentiated adenocarcinoma in which the nucleus is pressed to one side by a cytoplasmic droplet of mucus. It usually arises in the gastrointestinal system.Trans-Activators: Diffusible gene products that act on homologous or heterologous molecules of viral or cellular DNA to regulate the expression of proteins.Urinary Bladder Neoplasms: Tumors or cancer of the URINARY BLADDER.Stomach Neoplasms: Tumors or cancer of the STOMACH.Disease Models, Animal: Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.Tomography, X-Ray Computed: Tomography using x-ray transmission and a computer algorithm to reconstruct the image.MicroRNAs: Small double-stranded, non-protein coding RNAs, 21-25 nucleotides in length generated from single-stranded microRNA gene transcripts by the same RIBONUCLEASE III, Dicer, that produces small interfering RNAs (RNA, SMALL INTERFERING). They become part of the RNA-INDUCED SILENCING COMPLEX and repress the translation (TRANSLATION, GENETIC) of target RNA by binding to homologous 3'UTR region as an imperfect match. The small temporal RNAs (stRNAs), let-7 and lin-4, from C. elegans, are the first 2 miRNAs discovered, and are from a class of miRNAs involved in developmental timing.Skin Neoplasms: Tumors or cancer of the SKIN.Cell Movement: The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.Disease-Free Survival: Period after successful treatment in which there is no appearance of the symptoms or effects of the disease.Calculi: An abnormal concretion occurring mostly in the urinary and biliary tracts, usually composed of mineral salts. Also called stones.Pancreatic Pseudocyst: Cyst-like space not lined by EPITHELIUM and contained within the PANCREAS. Pancreatic pseudocysts account for most of the cystic collections in the pancreas and are often associated with chronic PANCREATITIS.Receptor, Epidermal Growth Factor: A cell surface receptor involved in regulation of cell growth and differentiation. It is specific for EPIDERMAL GROWTH FACTOR and EGF-related peptides including TRANSFORMING GROWTH FACTOR ALPHA; AMPHIREGULIN; and HEPARIN-BINDING EGF-LIKE GROWTH FACTOR. The binding of ligand to the receptor causes activation of its intrinsic tyrosine kinase activity and rapid internalization of the receptor-ligand complex into the cell.Mammary Glands, Animal: MAMMARY GLANDS in the non-human MAMMALS.Receptor, erbB-2: A cell surface protein-tyrosine kinase receptor that is overexpressed in a variety of ADENOCARCINOMAS. It has extensive homology to and heterodimerizes with the EGF RECEPTOR, the ERBB-3 RECEPTOR, and the ERBB-4 RECEPTOR. Activation of the erbB-2 receptor occurs through heterodimer formation with a ligand-bound erbB receptor family member.Gene Silencing: Interruption or suppression of the expression of a gene at transcriptional or translational levels.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Serpins: A family of serine proteinase inhibitors which are similar in amino acid sequence and mechanism of inhibition, but differ in their specificity toward proteolytic enzymes. This family includes alpha 1-antitrypsin, angiotensinogen, ovalbumin, antiplasmin, alpha 1-antichymotrypsin, thyroxine-binding protein, complement 1 inactivators, antithrombin III, heparin cofactor II, plasminogen inactivators, gene Y protein, placental plasminogen activator inhibitor, and barley Z protein. Some members of the serpin family may be substrates rather than inhibitors of SERINE ENDOPEPTIDASES, and some serpins occur in plants where their function is not known.Cystadenoma, Serous: A cystic tumor of the ovary, containing thin, clear, yellow serous fluid and varying amounts of solid tissue, with a malignant potential several times greater than that of mucinous cystadenoma (CYSTADENOMA, MUCINOUS). It can be unilocular, parvilocular, or multilocular. It is often bilateral and papillary. The cysts may vary greatly in size. (Dorland, 27th ed; from Hughes, Obstetric-Gynecologic Terminology, 1972)Ki-67 Antigen: A CELL CYCLE and tumor growth marker which can be readily detected using IMMUNOCYTOCHEMISTRY methods. Ki-67 is a nuclear antigen present only in the nuclei of cycling cells.Carcinoma, Large Cell: A tumor of undifferentiated (anaplastic) cells of large size. It is usually bronchogenic. (From Dorland, 27th ed)Antibodies, Monoclonal: Antibodies produced by a single clone of cells.Mice, SCID: Mice homozygous for the mutant autosomal recessive gene "scid" which is located on the centromeric end of chromosome 16. These mice lack mature, functional lymphocytes and are thus highly susceptible to lethal opportunistic infections if not chronically treated with antibiotics. The lack of B- and T-cell immunity resembles severe combined immunodeficiency (SCID) syndrome in human infants. SCID mice are useful as animal models since they are receptive to implantation of a human immune system producing SCID-human (SCID-hu) hematochimeric mice.Transfection: The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.Multivariate Analysis: A set of techniques used when variation in several variables has to be studied simultaneously. In statistics, multivariate analysis is interpreted as any analytic method that allows simultaneous study of two or more dependent variables.Receptors, Estrogen: Cytoplasmic proteins that bind estrogens and migrate to the nucleus where they regulate DNA transcription. Evaluation of the state of estrogen receptors in breast cancer patients has become clinically important.Salivary Ducts: Any of the ducts which transport saliva. Salivary ducts include the parotid duct, the major and minor sublingual ducts, and the submandibular duct.Neovascularization, Pathologic: A pathologic process consisting of the proliferation of blood vessels in abnormal tissues or in abnormal positions.Carcinoembryonic Antigen: A glycoprotein that is secreted into the luminal surface of the epithelia in the gastrointestinal tract. It is found in the feces and pancreaticobiliary secretions and is used to monitor the response to colon cancer treatment.Drug Resistance, Neoplasm: Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.Sensitivity and Specificity: Binary classification measures to assess test results. Sensitivity or recall rate is the proportion of true positives. Specificity is the probability of correctly determining the absence of a condition. (From Last, Dictionary of Epidemiology, 2d ed)beta Catenin: A multi-functional catenin that participates in CELL ADHESION and nuclear signaling. Beta catenin binds CADHERINS and helps link their cytoplasmic tails to the ACTIN in the CYTOSKELETON via ALPHA CATENIN. It also serves as a transcriptional co-activator and downstream component of WNT PROTEIN-mediated SIGNAL TRANSDUCTION PATHWAYS.Preoperative Period: The period before a surgical operation.Endoscopy: Procedures of applying ENDOSCOPES for disease diagnosis and treatment. Endoscopy involves passing an optical instrument through a small incision in the skin i.e., percutaneous; or through a natural orifice and along natural body pathways such as the digestive tract; and/or through an incision in the wall of a tubular structure or organ, i.e. transluminal, to examine or perform surgery on the interior parts of the body.Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.Lymph Nodes: They are oval or bean shaped bodies (1 - 30 mm in diameter) located along the lymphatic system.Laryngeal Neoplasms: Cancers or tumors of the LARYNX or any of its parts: the GLOTTIS; EPIGLOTTIS; LARYNGEAL CARTILAGES; LARYNGEAL MUSCLES; and VOCAL CORDS.Uterine Cervical Neoplasms: Tumors or cancer of the UTERINE CERVIX.Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.Real-Time Polymerase Chain Reaction: Methods used for detecting the amplified DNA products from the polymerase chain reaction as they accumulate instead of at the end of the reaction.Ductus Arteriosus: A fetal blood vessel connecting the pulmonary artery with the descending aorta.Secretin: A peptide hormone of about 27 amino acids from the duodenal mucosa that activates pancreatic secretion and lowers the blood sugar level. (USAN and the USP Dictionary of Drug Names, 1994, p597)Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.Neoplasms, Experimental: Experimentally induced new abnormal growth of TISSUES in animals to provide models for studying human neoplasms.In Situ Hybridization: A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes.Mesocricetus: A genus of the family Muridae having three species. The present domesticated strains were developed from individuals brought from Syria. They are widely used in biomedical research.Matrix Metalloproteinase 7: The smallest member of the MATRIX METALLOPROTEINASES. It plays a role in tumor progression.Tumor Suppressor Proteins: Proteins that are normally involved in holding cellular growth in check. Deficiencies or abnormalities in these proteins may lead to unregulated cell growth and tumor development.Promoter Regions, Genetic: DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.Proportional Hazards Models: Statistical models used in survival analysis that assert that the effect of the study factors on the hazard rate in the study population is multiplicative and does not change over time.Adenocarcinoma, Follicular: An adenocarcinoma of the thyroid gland, in which the cells are arranged in the form of follicles. (From Dorland, 27th ed)Epithelial-Mesenchymal Transition: Phenotypic changes of EPITHELIAL CELLS to MESENCHYME type, which increase cell mobility critical in many developmental processes such as NEURAL TUBE development. NEOPLASM METASTASIS and DISEASE PROGRESSION may also induce this transition.Antimetabolites, Antineoplastic: Antimetabolites that are useful in cancer chemotherapy.Mammary Neoplasms, Experimental: Experimentally induced mammary neoplasms in animals to provide a model for studying human BREAST NEOPLASMS.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Homeodomain Proteins: Proteins encoded by homeobox genes (GENES, HOMEOBOX) that exhibit structural similarity to certain prokaryotic and eukaryotic DNA-binding proteins. Homeodomain proteins are involved in the control of gene expression during morphogenesis and development (GENE EXPRESSION REGULATION, DEVELOPMENTAL).Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.DNA Mutational Analysis: Biochemical identification of mutational changes in a nucleotide sequence.Predictive Value of Tests: In screening and diagnostic tests, the probability that a person with a positive test is a true positive (i.e., has the disease), is referred to as the predictive value of a positive test; whereas, the predictive value of a negative test is the probability that the person with a negative test does not have the disease. Predictive value is related to the sensitivity and specificity of the test.Gallbladder Neoplasms: Tumors or cancer of the gallbladder.Gene Knockdown Techniques: The artificial induction of GENE SILENCING by the use of RNA INTERFERENCE to reduce the expression of a specific gene. It includes the use of DOUBLE-STRANDED RNA, such as SMALL INTERFERING RNA and RNA containing HAIRPIN LOOP SEQUENCE, and ANTI-SENSE OLIGONUCLEOTIDES.Breast Diseases: Pathological processes of the BREAST.Hedgehog Proteins: A family of intercellular signaling proteins that play and important role in regulating the development of many TISSUES and organs. Their name derives from the observation of a hedgehog-like appearance in DROSOPHILA embryos with genetic mutations that block their action.Combined Modality Therapy: The treatment of a disease or condition by several different means simultaneously or sequentially. Chemoimmunotherapy, RADIOIMMUNOTHERAPY, chemoradiotherapy, cryochemotherapy, and SALVAGE THERAPY are seen most frequently, but their combinations with each other and surgery are also used.Embryonal Carcinoma Stem Cells: The malignant stem cells of TERATOCARCINOMAS, which resemble pluripotent stem cells of the BLASTOCYST INNER CELL MASS. The EC cells can be grown in vitro, and experimentally induced to differentiate. They are used as a model system for studying early embryonic cell differentiation.Nuclear Proteins: Proteins found in the nucleus of a cell. Do not confuse with NUCLEOPROTEINS which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus.

Dpc-4 protein is expressed in virtually all human intraductal papillary mucinous neoplasms of the pancreas: comparison with conventional ductal adenocarcinomas. (1/1051)

DPC4 (MADH4, SMAD4) encodes a nuclear transcription factor shown to be genetically inactivated in over one-half of conventional infiltrating ductal adenocarcinomas of the pancreas. Intraductal papillary mucinous neoplasms (IPMNs) of the pancreas have been suggested to be distinct neoplasms with a significantly less aggressive course than conventional ductal adenocarcinomas of the pancreas, but molecular comparisons of these tumor types have previously been impaired by technical difficulties. Recently, immunohistochemical labeling for the DPC4 gene product has been shown to be an extremely sensitive and specific marker for DPC4 gene alterations in pancreatic adenocarcinomas. Therefore, we analyzed the immunohistochemical expression of Dpc4 protein in 79 IPMNs using a previously characterized monoclonal antibody. Twenty-nine of the IPMNs also had an associated infiltrating adenocarcinoma available for analysis. The labeling patterns observed were compared to those we have previously reported for conventional ductal carcinomas. All 79 of the intraductal components of the IPMNs strongly expressed Dpc4 protein. In 77 of the 79 cases (97%), the labeling was diffusely positive, and in 2 of the 79 (3%) the labeling was focally positive. Dpc4 expression was seen in 28 (97%) of the associated 29 invasive cancers. The one infiltrating carcinoma that showed loss of Dpc4 expression was associated with an intraductal component which showed focal loss of Dpc4 expression. The strong and almost universal expression of Dpc4 in IPMNs contrasts sharply with the loss of Dpc4 expression seen in approximately 30% of in situ adenocarcinomas of the pancreas (so-called pancreatic intraepithelial neoplasms, grade 3; P: < 0.001) and in 55% of pancreatic duct carcinomas (P: < 0.0001). Differences in Dpc4 expression between IPMNs and ductal carcinomas suggest a fundamental genetic difference in tumorigenesis, which may relate to the significantly better clinical outcomes observed for IPMNs.  (+info)

Phase III evaluation of octreotide versus chemotherapy with 5-fluorouracil or 5-fluorouracil plus leucovorin in advanced exocrine pancreatic cancer: a North Central Cancer Treatment Group study. (2/1051)

There continues to be a need for new systemic approaches for the treatment of advanced pancreatic cancer. The purpose of this study was to compare the antitumor activity of the somatostatin analogue octreotide to 5-fluorouracil chemotherapy in a Phase III setting. Eighty-four patients with an Eastern Cooperative Oncology Group performance status of 0 or 1 and limited tumor volume were randomized to receive octreotide 200 microg three times daily or 5-fluorouracil with or without leucovorin. After the first 12 patients had been randomized to octreotide, we increased the dose in the remaining patients to 500 microg three times daily. This change was based on early reports in other studies, suggesting that our original dose may not have been effective and that higher doses of octreotide were well tolerated. A planned interim analysis performed after 84 patients were enrolled demonstrated inferior time to progression and survival for the patients randomized to octreotide. Further accrual to the octreotide arm of this protocol was therefore terminated. Octreotide in doses of 200-500 microg three times daily does not delay progression or extend survival in patients with advanced pancreatic cancer compared with treatment with 5-fluorouracil with or without leucovorin.  (+info)

Expression of stromal cell-derived factor 1 and CXCR4 ligand receptor system in pancreatic cancer: a possible role for tumor progression. (3/1051)

To examine the expression of the stromal cell-derived factor 1 (SDF-1)/CXCR4 receptor ligand system in pancreatic cancer cells and endothelial cells, we performed immunohistochemical analysis for 52 pancreatic cancer tissue samples with anti-CXCR4 antibody and reverse transcription-PCR analysis for CXCR4 and SDF-1 in five pancreatic cancer cell lines (AsPC-1, BxPC-3, CFPAC-1, HPAC, and PANC-1), an endothelial cell line (HUVEC), and eight pancreatic cancer tissues. We then performed cell migration assay on AsPC-1 cells, HUVECs, and CFPAC-1 cells in the presence of SDF-1 or MRC-9 fibroblast cells. Immunoreactive CXCR4 was found mainly in pancreatic cancer cells and endothelial cells of relatively large vessels around a tumorous lesion. The immunopositive ratio in the pancreatic cancer was 71.2%. There was no statistically significant correlation with clinicopathological features. SDF-1 mRNA expressions were detected in all pancreatic cancer tissues but not in pancreatic cancer cell lines and HUVECs; meanwhile, CXCR4 mRNA was detected in all pancreatic cancer tissues, cancer cell lines, and HUVECs. The results indicate that the paracrine mechanism is involved in the SDF-1/CXCR4 receptor ligand system in pancreatic cancer. In vitro studies demonstrated that SDF-1 significantly increased the migration ability of AsPC-1 and HUVECs, and these effects were inhibited by CXCR4 antagonist T22, and that the coculture system with MRC-9 also increased the migration ability of CFPAC-1 cells, and this effect was significantly inhibited by T22. Our results suggested that the SDF-1/CXCR4 receptor ligand system may have a possible role in the pancreatic cancer progression through tumor cell migration and angiogenesis.  (+info)

Multiple primaries in pancreatic cancer patients: indicator of a genetic predisposition? (4/1051)

BACKGROUND: The genetic basis of several familial cancers including breast and colon cancers has been identified recently. The occurrence of multiple cancers in one individual is also suggestive of a genetic predisposition. To evaluate inherited predisposition in pancreatic cancer we compared the clinical data of pancreatic cancer patients with and without multiple primaries as well as the frequency of malignancies among their relatives. METHODS: Detailed data on 69 pancreatic cancer patients included survival time and TNM-classification. Index case data were separated into two groups. The first group (group 1) developed only pancreatic cancer during their lifetime, whereas the second group (group 2) developed additional primary tumours. A systematic family history was taken from 59 of these pancreatic cancer patients using a standardized questionnaire. The pancreatic cancers and the multiple primaries of the 59 patients were histologically proven. RESULTS: Of the 69 pancreatic cancer patients, 13 (18.8%) had multiple primaries. Neither the clinical data nor the survival data of the index cases revealed differences between the two groups (all nominal P-values >0.05). In the family history study blood relatives developed a malignancy in 51% (24 of 47) of the families in group 1 compared to 75% (9 of 12) in group 2. The risk of relatives in group 2 of developing a malignant tumour was significantly higher (P = 0.034) than in group 1 after adjustments for family size and age of disease onset of the index case. The cancer spectrum of the 59 families mainly included tumours of the digestive tract and the reproductive organs. CONCLUSIONS: A multiple primary cancer history is a common condition among pancreatic cancer patients. Relatives of these patients seem to have an increased risk for the development of distinct malignant solid tumours, which might be caused by an inherited predisposition. Clinical and genetic investigation of pancreatic cancer patients with multiple primaries and their families might lead to the identification of predisposing gene defects providing a new goal for the understanding of a shared genetic basis of different solid tumours.  (+info)

PGP9.5 as a prognostic factor in pancreatic cancer. (5/1051)

The expression of PGP9.5 was evaluated using immunohistochemistry in 69 resected ductal carcinomas of the pancreas and in normal pancreatic tissue. Overexpression did not seem to differ with histological type or pathological stage. A significant negative correlation was found between overexpression of PGP9.5 and postoperative survival. Multivariate analysis also suggested PGP9.5 along with tumor stage and extrapancreatic plexus invasion as strong predictors of the outcome. This study suggests that PGP9.5 expression may be used as a marker for predicting the outcome of resection-treated pancreatic cancer patients.  (+info)

Pancreatic tumours: molecular pathways implicated in ductal cancer are involved in ampullary but not in exocrine nonductal or endocrine tumorigenesis. (6/1051)

Alterations of K- ras, p53, p16 and DPC4/Smad4 characterize pancreatic ductal cancer (PDC). Reports of inactivation of these latter two genes in pancreatic endocrine tumours (PET) suggest that common molecular pathways are involved in the tumorigenesis of pancreatic exocrine and endocrine epithelia. We characterized 112 primary pancreatic tumours for alterations in p16 and DPC4 and immunohistochemical expression of DPC4. The cases included 34 PDC, 10 intraductal papillary-mucinous tumours (IPMT), 6 acinar carcinomas (PAC), 5 solid-pseudopapillary tumours (SPT), 16 ampulla of Vater cancers (AVC) and 41 PET. All tumours were also presently or previously analysed for K- ras and p53 mutations and allelic loss at 9p, 17p and 18q. Alterations in K- ras, p53, p16 and DPC4 were found in 82%, 53%, 38% and 9% of PDC, respectively and in 47%, 60%, 25% and 6% of AVC. Alterations in these genes were virtually absent in PET, PAC or SPT, while in IPMT only K- ras mutations were present (30%). Positive immunostaining confirmed the absence of DPC4 alterations in all IPMT, SPT, PAC and PET, while 47% of PDC and 38% of AVC were immunonegative. These data suggest that pancreatic exocrine and endocrine tumourigenesis involves different genetic targets and that among exocrine pancreatic neoplasms, only ductal and ampullary cancers share common molecular events.  (+info)

Expression of p8 in human pancreatic cancer. (7/1051)

The p8 gene is a recently identified gene with mitogenic activity. p8 expression is induced in acute pancreatitis, pancreatic development, and regeneration. However, the expression of p8 in pancreatic cancer is not reported. We investigated p8 expression in 72 human pancreatic tissues, including 38 pancreatic cancers (PCs), by immunohistochemistry. p8 was overexpressed (positive cells >25% in 1,000 cells) in 71% (27 of 38) of PCs, but in only 17% (3 of 18) of chronic pancreatitis cases. There was no overexpression in mucinous cystadenoma or in normal pancreas. The p8 overexpression rate in PC was significantly higher than that in other conditions (P < 0.05). Reverse transcription-PCR analysis confirmed p8 mRNA overexpression (tumor/nontumor ratio >2) in 75% (3 of 4) of PCs. p8 was overexpressed also in human pancreatic cancer cell lines (MIA PaCa-2 and PANC-1). These results suggest that p8 is involved in the development of pancreatic cancer, reflecting its mitogenic activity.  (+info)

Genetic and clinical features of human pancreatic ductal adenocarcinomas with widespread microsatellite instability. (8/1051)

The incidences of microsatellite instability (MSI) and underlying DNA mismatch repair (MMR) defects in pancreatic carcinogenesis have not been well established. We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high-frequency MSI (MSI-H) and low-frequency MSI (MSI-L) tumors were further analyzed for frameshift mutations of possible target genes and for promoter methylation and mutation of DNA MMR genes, including hMLH1, hMSH2, hMSH3, and hMSH6 genes. Among the 100 sporadic tumors, 13 (13%) were MSI-H, 13 (13%) were MSI-L, and 74 (74%) were microsatellite stable (MSS) tumors. All of the three hereditary tumors from hereditary nonpolyposis colorectal cancer (HNPCC) patients were MSI-H. MSI-H tumors were significantly associated with poor differentiation and the presence of wild-type K-RAS and p53 genes. Patients with MSI-H tumors had a significantly longer overall survival time than did those with MSI-L or MSS tumors (P = 0.0057). Frameshift mutations of hMSH3, hMLH3, BRCA-2, TGF-beta type II receptor, and BAX genes were detected in MSI-H tumors. Hypermethylation of the hMLH1 promoter was observed in 6 (46%) of the 13 sporadic MSI-H tumors but not in any of the 3 hereditary MSI-H tumors or 13 MSI-L tumors. All of the 3 HNPCC cases had germ-line hMLH1 mutation accompanied by loss of heterogeneity or other mutation in the tumor. Our results suggest that pancreatic carcinomas with MSI-H represent a distinctive oncogenic pathway because they exhibit peculiar clinical, pathological, and molecular characteristics. Our results also suggest the principal involvement of epigenetic or genetic inactivation of the hMLH1 gene in the pathogenesis of pancreatic carcinoma with MSI-H.  (+info)

Pancreatic ductal adenocarcinoma has a poor prognosis due to late diagnosis and a lack of effective therapeutic options. Thus, it is important to better understand its molecular mechanisms and to develop more effective treatments for the disease. The ternary complex factor Net, which exerts its strong inhibitory function on transcription of proto-oncogene gene c-fos by forming ternary complexes with a second transcription factor, has been suspected of being involved in pancreatic cancer and other tumors biology. In this study, we found that the majority of pancreatic ductal adenocarcinoma tissues and cell lines had weak or no expression of Net, whereas significantly high level of Net expression occurred in paired adjacent normal tissues we studied. Furthermore, using in vitro and in vivo model systems, we found that overexpression of Net inhibited cell growth and survival and induced cell apoptosis in human pancreatic ductal adenocarcinoma cell PL45; the mechanisms by which Net inhibited the cell cycle
TY - JOUR. T1 - Ex vivo organotypic culture system of precision-cut slices of human pancreatic ductal adenocarcinoma. AU - Misra, Sougat. AU - Moro, Carlos F.. AU - Del Chiaro, Marco. AU - Pouso, Soledad. AU - Sebestyén, A.. AU - Löhr, Matthias. AU - Björnstedt, Mikael. AU - Verbeke, Caroline S.. PY - 2019/12/1. Y1 - 2019/12/1. N2 - Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis, which is mainly due to late diagnosis and profound resistance to treatment. The latter is to a large extent attributed to the tumor stroma that is exceedingly prominent in PDAC and engages in complex interactions with the cancer cells. Hence, relevant preclinical models of PDAC should also include the tumor stroma. We herein describe the establishment and functional validation of an ex vivo organotypic culture of human PDAC that is based on precision-cut tissue slices from surgical specimens and reproducibly recapitulates the complex cellular and acellular composition of PDAC, including its ...
In the present study, we found that the centrosomes in nearly all pancreatic ductal carcinomas displayed structural abnormalities, such as an increase in their number and size, and an irregular distribution. Quantitative analysis demonstrated a significant difference in centrosome number between normal and cancer cells. In addition, double-labeled immunofluorescence analysis of MIA PaCa-2 pancreatic cancer cells suggest that these aberrant centrosomes contribute to the assembly of multipolar spindles, which may result in the improper segregation of chromosomes during mitosis. These results are consistent with previous studies describing centrosome abnormalities in human malignant tumors of the breast, prostate, brain, lung, and colon (10 , 11) . To our knowledge, however, this is the first report to demonstrate centrosome abnormalities in pancreatic carcinoma.. The centrosome plays a key role in the organization of cytoplasmic microtubules, in the determination of cell polarity, and in the ...
Osteopontin (OPN) is a secreted phospho-protein that confers on cancer cells a migratory phenotype. We have recently shown that nicotine, a risk factor in pancreatic ductal adenocarcinoma (PDA), induces an alpha7-nicotine acetylcholine receptor (α7-nAChR)-mediated increase of OPN in PDA cells. In this study, we tested nicotines effect on the expression of OPN splice variants (OPNa, b, c) in PDA cells. We also analyzed the correlation between patients smoking history with OPN and α7-nAChR levels. RT-PCR and UV-light-illumination of ethidium-bromide staining were used to examine the mRNA expression in tissue and PDA cells treated with or without nicotine (3-300 nM). Localization of total OPN, OPNc and α7-nAChR was analyzed by immunohistochemistry, and their mRNA tissue expression levels were correlated with the patients smoking history. PDA cells expressed varying levels of OPNa, OPNb, and α7-nAChR. Nicotine treatment selectively induced denovo expression of OPNc and increased α7-nAChR expression
Avarol is a sesquiterpenoid hydroquinone with potent cytotoxicity. Although resolving endoplasmic reticulum (ER) stress is essential for intracellular homeostasis, erratic or excessive ER stress can lead to apoptosis. Here, we reported that avarol selectively induces cell death in pancreatic ductal adenocarcinomas (PDAC), which are difficult to treat owing to the availability of few chemotherapeutic agents. Analyses of the molecular mechanisms of avarol-induced apoptosis indicated upregulation of ER stress marker BiP and ER stress-dependent apoptosis inducer CHOP in PDAC cells but not in normal cells, suggesting that avarol selectively induces ER stress responses. We also showed that avarol activated the PERK-eIF2α pathway but did not affect the IRE1 and ATF6 pathways. Moreover, CHOP downregulation was significantly suppressed by avarol-induced apoptosis. Thus, the PERK-eIF2α-CHOP signaling pathway may be a novel molecular mechanism of avarol-induced apoptosis. The present data indicate that avarol
Glycolytic cancer cells produce large quantities of lactate that must be removed to sustain metabolism in the absence of oxidative phosphorylation. The only venting mechanism described to do this at an adequate rate is H+-coupled lactate efflux on monocarboxylate transporters (MCTs). Outward MCT activity is, however, thermodynamically inhibited by extracellular acidity, a hallmark of solid tumours. This inhibition would feedback unfavourably on metabolism and growth, raising the possibility that other venting mechanisms become important in under-perfused tumours. We investigated connexin-assembled gap junctions as an alternative route for discharging lactate from pancreatic ductal adenocarcinoma (PDAC) cells. Diffusive coupling (calcein transmission) in vitro was strong between Colo357 cells, weaker yet hypoxia-inducible between BxPC3 cells, and very low between MiaPaCa2 cells. Coupling correlated with levels of connexin-43 (Cx43), a protein previously linked to late-stage disease. Evoked lactate
In February of this year the U.S. National Cancer Institute published an important overview of the state of the science and medicine of pancreatic cancer. We will comment on aspects of it from time to time in the future, but as it so comprehensive and precise, in a departure from our usual practice, we will show a copy it here (sans bibliography and figures) in our pancreatic cancer blog. The term "Pancreatic Ductal Carcinoma" is accurate and abbreviated PDAC in the original paper; here in the interests of a potential lay reader we will add in parentheses the term: pancreatic cancer.. Scientific Framework for Pancreatic Ductal Carcinoma Executive Summary Significant scientific progress has been made in the last decade in understanding the biology and natural history of pancreatic ductal adenocarcinoma (PDAC, pancreatic cancer); major clinical advances, however, have not occurred. Although PDAC (pancreatic cancer) shares some of the characteristics of other solid malignancies, such as mutations ...
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive disease with limited and, very often, ineffective medical and surgical therapeutic options. The treatment of patients with advanced unresectable PDAC is restricted to systemic chemotherapy, a therapeutic intervention to which most eventually develop resistance. Recently, nab-paclitaxel (n-PTX) has been added to the arsenal of first-line therapies, and the combination of gemcitabine and n-PTX has modestly prolonged median overall survival. However, patients almost invariably succumb to the disease, and little is known about the mechanisms underlying n-PTX resistance. Using the conditionally reprogrammed (CR) cell approach, we established and verified continuously growing cell cultures from treatment-naïve patients with PDAC. To study the mechanisms of primary drug resistance, nab-paclitaxel-resistant (n-PTX-R) cells were generated from primary cultures and drug resistance was verified in vivo, both in zebrafish and in athymic nude ...
Telomerase activity was measured in surgically resected tissues of 20 human pancreatic ductal carcinomas, 12 adenomas, 5 pancreatitis tissues, 14 normal pancreatic ducts, and 13 normal pancreatic tissues (primarily made up of acinar cells) using a PCR-based telomerase assay. Relative telomerase activity was expressed as the equivalent telomerase intensity of the number of cells of a human pancreatic cancer cell line, MIA PaCa-2, per microgram of protein in the tissue samples. The median value (25th percentile, 75th percentile) of relative telomerase activity in pancreatic carcinomas was 13.2 (3.58, 244), which was significantly higher relative to normal tissues, normal ducts, pancreatitis tissues, and adenomas (P , 0.0001). When the cutoff value of relative telomerase activity was set at 1.00 and 3.00, the positivity rates of telomerase activity in pancreatic ductal carcinomas were 100 and 80%, respectively. Some of the adenoma samples displayed a weak telomerase ladder. However, when ...
Growing tumors are hypoxic and respond to microenvironmental stress through increased expression of the hypoxia inducible factor-1α (HIF-1α) transcription factor, resulting in an adaptive switch to glycolytic metabolism, angiogenic signaling, survival, and metastasis. HIF-1α expression is associated with tumor resistance to cytotoxic therapy and inferior patient outcomes. Pancreatic cancer is the most hypoxic of all solid tumors and remains refractory to current chemoradiotherapy. We have seen nuclear HIF-1α in 88% of human pancreatic ductal carcinoma but in only 16% of normal pancreas. Stroma adjacent to the pancreatic ductal carcinoma also showed HIF-1α in 43% of cases. We investigated the novel selective HIF-1α inhibitor PX-478 on in vitro and in vivo radiation response of human pancreatic cancer models. Inhibition of HIF-1α by PX-478 increased cell killing by radiation. In mice with Panc-1, CF-PAC-1, or SU.86.86 pancreatic xenografts, concurrent administration of PX-478 potentiated ...
The Wnt/β-catenin pathway has a key role in regulating cellular processes and its aberrant signaling can lead to cancer development. The role of β-catenin expression in pancreatic ductal adenocarcinoma is somewhat controversial. Transcription factor PROX1 is a target of Wnt/β-catenin signaling and it is involved in carcinogenesis through alterations in its expression. The actions can be either oncogenic or tumor suppressive depending on the tissue. The aim of this study was to investigate PROX1 and β-catenin expression in pancreatic ductal adenocarcinoma (PDAC). Expression of PROX1 and β-catenin were evaluated in 156 patients by immunohistochemistry of tissue microarrays. Associations between tumor marker expression and clinicopathological parameters were assessed by the Fischers exact-test or the linear-by-linear association test. The Kaplan-Meier method and log-rank test were used for survival analysis. Uni- and multivariate survival analyses were carried out by the Cox regression proportional
TY - JOUR. T1 - Pancreatic ductal adenocarcinoma radiology reporting template. T2 - Consensus statement of the society of abdominal radiology and the american pancreatic association. AU - Al-Hawary, Mahmoud M.. AU - Francis, Isaac R.. AU - Chari, Suresh T. AU - Fishman, Elliot K.. AU - Hough, David M.. AU - Lu, David S.. AU - Macari, Michael. AU - Megibow, Alec J.. AU - Miller, Frank H.. AU - Mortele, Koenraad J.. AU - Merchant, Nipun B.. AU - Minter, Rebecca M.. AU - Tamm, Eric P.. AU - Sahani, Dushyant V.. AU - Simeone, Diane M.. PY - 2014/1. Y1 - 2014/1. N2 - Pancreatic ductal adenocarcinoma is an aggressive malignancy with a high mortality rate. Proper determination of the extent of disease on imaging studies at the time of staging is one of the most important steps in optimal patient management. Given the variability in expertise and definition of disease extent among different practitioners as well as frequent lack of complete reporting of pertinent imaging findings at radiologic ...
Pancreatic cancer is among the most lethal malignancies worldwide. This study aimed to identify a novel prognostic biomarker, facilitating treatment selection, using mass spectrometry (MS)-based proteomic analysis with formalin-fixed paraffin-embedded (FFPE) tissue. The two groups with poor prognosis (n = 4) and with better prognosis (n = 4) had been carefully chosen among 96 resected cases of pancreatic cancer during 1998 to 2007 in Tohoku University Hospital. Although those 2 groups had adjusted background (UICC-Stage IIB, Grade2, R0, gemcitabine adjuvant), there was a significant difference in postoperative mean survival time (poor 21.0 months, better 58.1 months, P = 0.0067). Cancerous epithelial cells collected from FFPE tissue sections by laser micro-dissection (LMD) were processed for liquid chromatography-tandem mass spectrometry (LC-MS/MS). In total, 1099 unique proteins were identified and 6 proteins showed different expressions in the 2 groups by semi-quantitative comparison. Among these 6
A pancreatic adenocarcinoma cell line (Paca44) was treated with trichostatin-A (TSA), a potent inhibitor of histone deacetylases, in order to evaluate the effect of this drug on protein expression. Master maps of control and treated Paca44 cells were generated by analysis with the PDQuest software. The comparison between such maps showed up- and downregulation of 51 polypeptide chains, out of a total of 700 spots detected by a medium-sensitivity stain, micellar Coomassie Brilliant Blue. Fingerprinting by matrix-assisted laser desorption/ionization-time of flight (MALDI-TOF)-mass spectrometry analysis enabled the identification of 22 of these spots. Among these proteins, of particular interest are the two downregulated proteins nucleophosmin and translationally controlled tumor protein, as well as the upregulated proteins programmed cell death protein 5 (also designated as TFAR19) and stathmin (oncoprotein 18). The modulation of these four proteins is consistent with our observation that TSA is ...
Pancreatic ductal adenocarcinoma (PDAC) remains amongst the most lethal human cancers. PDAC is characterized by the tumor mass containing a paucity of malignant cells in association with a large desmoplastic reaction comprised of a variety of stromal components. Sporadic PDAC oncogenesis occurs as a result of the sequential acquisition of genetic aberrations occurring in core genetic pathways. Unfortunately, the average PDAC contains a large number of genetic aberrations that are not uniform between individual cancers. The interplay between the complex genetics and stromal component may represent a significant barrier to the development of effective therapy for this disease and ultimately be an important factor in PDAC lethality. The Wnt pathway has been identified as a one of the common pathways undergoing genetic alterations in PDAC. Wnt is a complex signal transduction pathway utilizing both a b-catenin dependent (canonical) and b-catenin independent (noncanonical) signals to affect a wide array of
Importance: The patterns of disease recurrence after resection of pancreatic ductal adenocarcinoma with adjuvant chemotherapy remain unclear. Objective: To define patterns of recurrence after adjuvant chemotherapy and the association with survival. Design, Setting, and Participants: Prospectively collected data from the phase 3 European Study Group for Pancreatic Cancer 4 adjuvant clinical trial, an international multicenter study. The study included 730 patients who had resection and adjuvant chemotherapy for pancreatic cancer. Data were analyzed between July 2017 and May 2019. Interventions: Randomization to adjuvant gemcitabine or gemcitabine plus capecitabine. Main Outcomes and Measures: Overall survival, recurrence, and sites of recurrence. Results: Of the 730 patients, median age was 65 years (range 37-81 years), 414 were men (57%), and 316 were women (43%). The median follow-up time from randomization was 43.2 months (95% CI, 39.7-45.5 months), with overall survival from time of surgery of 27.9
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers with an overall five-year survival rate of 8%. Due to subtle texture changes of PDAC, pancreatic dual-phase imaging is...
TY - JOUR. T1 - The personalized medicine for pancreatic ductal adenocarcinoma patients: The oncologist perspective. AU - Peretti, U. AU - Zanon, Silvia. AU - Reni, M. PY - 2017. Y1 - 2017. N2 - No abstract available. AB - No abstract available. U2 - 10.4103/eus.eus_62_17. DO - 10.4103/eus.eus_62_17. M3 - Article. VL - 6. SP - S66-S68. JO - Endoscopic Ultrasound. JF - Endoscopic Ultrasound. SN - 2303-9027. IS - Suppl.3. ER - ...
Background Pancreatic ductal adenocarcinoma frequently recurs despite curative surgical resection. This study aims to investigate the patterns of recu..
... , Sia Kim, Malinda Itchins, Jennifer Arena, Chris Nahm, Nick
Chronic pancreatitis increases by 16 fold the risk of developing pancreatic ductal adenocarcinoma (PDAC), one of the deadliest human cancers. Activating Kras mutations have been detected in 30% of early pancreatic intraepithelial neoplasias (PanINs), increasing to 100% in advanced pancreatic ductal adenocarcinoma (PDAC).. We hypothesize that inflammatory cells recruited to the pancreas in response to chronic injury can interact with epithelial cells harboring activated KrasG12D and affect the progression of PanIN lesions. To test this hypothesis, we have used the inducible transgenic Mist1:CreERT2; LSL-KrasG12D (KCiMist1) adult mice in which the LSL KrasG12D allele is activated specifically in the acinar compartment. This model leads to rapid formation of PanINs with a classic "ductal" phenotype and the progression of lesions is further accelerated with the induction of chronic pancreatitis (CP) generated by recurrent injections of cerulein.. We have found that TH17 cells, a subtype of CD4+ ...
TY - JOUR. T1 - Phase 2 study of erlotinib combined with adjuvant chemoradiation and chemotherapy in patients with resectable pancreatic cancer. AU - Herman, Joseph M.. AU - Fan, Katherine Y.. AU - Wild, Aaron T.. AU - Hacker-Prietz, Amy. AU - Wood, Laura D.. AU - Blackford, Amanda L.. AU - Ellsworth, Susannah. AU - Zheng, Lei. AU - Le, Dung T.. AU - De Jesus-Acosta, Ana. AU - Hidalgo, Manuel. AU - Donehower, Ross C.. AU - Schulick, Richard D.. AU - Edil, Barish H.. AU - Choti, Michael A.. AU - Hruban, Ralph H.. AU - Pawlik, Timothy M.. AU - Cameron, John L.. AU - Laheru, Daniel A.. AU - Wolfgang, Christopher L.. PY - 2013/7/15. Y1 - 2013/7/15. N2 - Purpose: Long-term survival rates for patients with resected pancreatic ductal adenocarcinoma (PDAC) have stagnated at 20% for more than a decade, demonstrating the need to develop novel adjuvant therapies. Gemcitabine- erlotinib therapy has demonstrated a survival benefit for patients with metastatic PDAC. Here we report the first phase 2 study of ...
Pancreatic cancer is lethal, as it is often detected late. Thus, novel biomarkers of precursor lesions are needed to devise timely therapies. Pancreatic intraepithelial neoplasia (PanIN) and intraductal papillary mucinous neoplasm (IPMN) are major precursors of pancreatic cancer. In normal gastric mucosa, gastric gland mucin-specific O-glycans are unique in having α1,4-linked N-acetylglucosamine (αGlcNAc) residues attached to MUC6. Recently we reported that αGlcNAc functions as a tumor suppressor for differentiated-type gastric adenocarcinoma (Karasawa et al., J Clin Invest 122, 923, 2012). MUC6 is also expressed in pancreatic neoplasms, including PanIN and IPMN, but the role of αGlcNAc expression in pancreatic neoplasms remains unknown. Here, we analyze expression patterns of αGlcNAc, MUC6 and MUC5AC in pancreatic neoplasms and compare them with progression from PanIN to invasive ductal adenocarcinoma (IDAC) (the PanIN-IDAC sequence; 20 cases) and from IPMN to IPMN with associated invasive
Introduction IPMN is characterized by a predominantly noninvasive growth pattern with mucin production and cystic duct dilatation. The distinction between IPMN and pancreatic intraepithelial neoplasia (PanIN) ,which is the common precursor of invasive carcinomas
There is a lack of well-established clinical tools for predicting dendritic cell (DC) vaccination response of pancreatic ductal adenocarcinoma (PDAC). DC vaccine treatment efficiency was demonstrated using histological analysis in pre-clinical studies; however, its usage was limited due to invasiveness. In this study, we aimed to investigate the potential of MRI texture features for detection of early immunotherapeutic response as well as overall survival (OS) of PDAC subjects following dendritic cell (DC) vaccine treatment in LSL-KrasG12D;LSL-Trp53R172H;Pdx-1-Cre (KPC) transgenic mouse model of pancreatic ductal adenocarcinoma (PDAC). KPC mice were treated with DC vaccines, and tumor growth was dynamically monitored. A total of a hundred and fifty-two image features of T2-weighted MRI images were analyzed using a kernel-based support vector machine model to detect treatment effects following the first and third weeks of the treatment. Moreover, univariate analysis was performed to describe the
There will be two phases to this study. The lead-in phase will evaluate the safety, pharmacokinetics, and define the maximum tolerated dose (MTD) of momelotinib (MMB) combined with nab-paclitaxel and gemcitabine (nab-P + G) in adults with previously untreated metastatic pancreatic ductal adenocarcinoma. The randomized treatment phase will evaluate the efficacy, safety, and tolerability of nab-P + G with either MMB administered at the MTD or placebo in adults with previously untreated metastatic pancreatic ductal adenocarcinoma. Participants will continue study treatment until disease progression, unacceptable toxicity, consent withdrawal, or participants refusal of treatment. Following treatment, participants will be followed for safety for 30 days and for survival approximately every 3 months for up to 3 years ...
BACKGROUND & AIMS: Small nucleolar noncoding RNAs (snoRNAs) regulate function of ribosomes, and specific snoRNAs are dysregulated in some cancer cells. We investigated dysregulation of snoRNAs in pancreatic ductal adenocarcinoma (PDAC) cells. METHODS: We investigated snoRNA expression in PDAC cell lines by complementary DNA microarray and quantitative reverse transcription polymerase chain reaction. In PDAC (n = 133), intraductal papillary mucinous neoplasm (n = 16), mucinous cystic neoplasm-associated PDAC (n = 1), and non-tumor pancreas (n = 8) and liver (n = 3) tissues from subjects who underwent surgical resection, levels of snoRNA were measured by quantitative reverse transcription polymerase chain reaction and compared with clinicopathologic parameters and survival times determined by Kaplan-Meier analysis ...
Depending on the cellular context, transforming growth factor β (TGFβ) has been observed to exert protumorigenic functions, such as inducing an epithelial-mesenchymal transition (EMT), or inhibit tumorigenesis by activating apoptosis. The proapoptotic functions of TGFβ have been linked with the transcription factor SMAD4, which acts downstream of TGFβ and is frequently deleted in pancreatic ductal carcinoma (PDAC). To elucidate the mechanism by which TGFβ promotes apoptosis, David and colleagues used a Kras-mutant/Smad4-deleted PDAC murine model and found that reintroduction of SMAD4 sensitized cells to TGFβ treatment and promoted changes in cell morphology and loss of E-cadherin consistent with EMT. Moreover, SNAIL was shown to be upregulated following TGFβ treatment, and genetic depletion of SNAIL inhibited TGFβ-induced EMT, apoptosis, and accelerated pancreatic carcinogenesis in SMAD4-wild-type cells, raising the unexpected possibility that EMT precedes apoptosis and is required for ...
One of the hallmarks of human pancreatic ductal adenocarcinoma (PDAC) is its pronounced type I collagen-rich fibrotic reaction. Although recent reports have shown that the fibrotic reaction can limit the efficacy of gemcitabine chemotherapy, the underlying mechanisms remain poorly understood. In this article, we show that the type I collagen allows PDAC cells to override checkpoint arrest induced by gemcitabine. Relative to cells grown on tissue culture plastic, PDAC cells grown in 3-dimensional collagen microenvironment have minimal Chk1 phosphorylation and continue to proliferate in the presence of gemcitabine. Collagen increases membrane type 1 matrix metalloproteinase (MT1-MMP)-dependent ERK1/2 phosphorylation to limit the effect of gemcitabine. Collagen also increases MT1-MMP-dependent high mobility group A2 (HMGA2) expression, a nonhistone DNA-binding nuclear protein involved in chromatin remodeling and gene transcription, to attenuate the effect of gemcitabine. Overexpression of MT1-MMP ...
BAG3 Directly Stabilizes Hexokinase 2 mRNA and Promotes Aerobic Glycolysis in Pancreatic Cancer Cells Scientists showed that aberrant expression of BAG3 significantly contributes to the reprogramming of glucose metabolism in pancreatic ductal adenocarcinoma cells. [J Cell Biol] Abstract Long Noncoding RNA NORAD, a Novel Competing Endogenous RNA, Enhances the Hypoxia-Induced Epithelial-Mesenchymal Transition to Promote Metastasis in Pancreatic Cancer NORAD expression was measured in 33 paired cancerous and noncancerous tissue samples by real-time PCR. The effects of NORAD on pancreatic cancer cells were studied by overexpression and knockdown in vitro. [Mol Cancer] Full Article A New Panel of Pancreatic Cancer Biomarkers Discovered Using a Mass Spectrometry-Based Pipeline Scientists developed a coherent, high-throughput and non-discriminatory pipeline for the novel clinical biomarker discovery of pancreatic carcinoma. [Br J Cancer] Abstract Alternative Polyadenylation of ZEB1 Promotes Its ...
HuR (Hu protein antigen R) is an mRNA binding protein previously described as a predictive biomarker for selecting pancreatic ductal adenocarcinoma patients for gemcitabine-based therapy. In an independent, validating sample set, high HuR cytoplasmic expression strongly correlated with patients response to gemcitabine, and cytoplasmic HuR status correlated with adverse pathologic characteristics of pancreatic ductal adenocarcinoma better than vascular endothelial growth factor and cyclooxygenase-2. This study supports the notion that cytoplasmic HuR status can help guide the treatment of pancreatic ductal adenocarcinoma ...
Epigenetic alterations have been recognized as important contributors to the pathogenesis of PDAC. However, the role of histone variants in pancreatic tumor progression is still not completely understood. The aim of this study was to explore the expression and prognostic significance of histone protein variants in PDAC patients. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was employed for qualitative analysis of histone variants and histone related post-translational modifications (PTMs) in PDAC and normal pancreatic tissues. Survival analysis was conducted using the Kaplan-Meier method and Cox proportional hazards regression. Histone variant H1.3 was found to be differentially expressed (p = 0.005) and was selected as a PDAC specific histone variant candidate. The prognostic role of H1.3 was evaluated in an external cohort of patients with resected PDAC using immunohistochemistry. Intratumor expression of H1.3 was found to be an important risk factor for overall survival in PDAC, with an
Qian ZR, Rubinson DA, Nowak JA, Morales-Oyarvide V, Dunne RF, Kozak MM, Welch MW, Brais LK, Da Silva A, Li T, Li W, Masuda A, Yang J, Shi Y, Gu M, Masugi Y, Bui J, Zellers CL, Yuan C, Babic A, Khalaf N, Aguirre A, Ng K, Miksad RA, Bullock AJ, Chang DT, Tseng JF, Clancy TE, Linehan DC, Findeis-Hosey JJ, Doyle LA, Thorner AR, Ducar M, Wollison B, Laing A, Hahn WC, Meyerson M, Fuchs CS, Ogino S, Hornick JL, Hezel AF, Koong AC, Wolpin BM. Association of Alterations in Main Driver Genes With Outcomes of Patients With Resected Pancreatic Ductal Adenocarcinoma. JAMA Oncol. 2017 Nov 02. PMID: 29098284. ...
Pancreatic ductal adenocarcinoma (PDAC) ranks as the fourth leading cause of cancer mortality in the United States and causes ,200,000 deaths worldwide annually (1, 2). Histopathological analyses have identified precursor lesions, pancreatic intraepithelial neoplasias (PanIN), which appear to progress through increasingly severe stages of cellular atypia leading to invasive PDAC (3). These lesions show multistep molecular progression that includes early activating KRAS mutations and telomere attrition, and subsequent inactivation of p16Ink4a , p14ARF , p53, and/or SMAD4 tumor suppressors in a high percentage of cases (4-6).. The Ink4a/Arf locus (hereafter denoted p16Ink4a /p19Arf ) encodes tumor suppressors p16INK4A and p14ARF (p19Arf in the mouse). p16INK4A is a G1 cyclin-dependent kinase (CDK) inhibitor that binds to CDK4 and CDK6 and prevents their association with D-type cyclins (7), thereby facilitating CDK4/6-cyclin D-mediated phosphorylation and inactivation of retinoblastoma protein (RB) ...
Rushika M. Perera, PhD, University of California, San Francisco. Dr. Perera has characterized cancer-specific lysosomal proteins and showed that these proteins confer upon pancreatic ductal adenocarcinoma cells two key properties: the ability to rapidly repair cell membranes in the face of sustained mechanical and chemical insults and to alter cell membrane composition to evade recognition by the host immune system. Collectively, these results suggest largely unexplored roles for the lysosome and highlight novel vulnerabilities ...
Pancreatic ductal adenocarcinoma (PDAC) is one of the most fatal cancers worldwide, partly because methods are lacking to detect disease at an early, operable stage. Noninvasive PDAC precursors called intraductal papillary mucinous neoplasms (IPMN) exist, and strategies are needed to aid in their proper diagnosis and management. Data support the importance of miRNAs in the progression of IPMNs to malignancy, and we hypothesized that miRNAs may be shed from IPMN tissues and detected in blood. Our primary goals were to measure the abundance of miRNAs in archived preoperative plasma from individuals with pathologically confirmed IPMNs and healthy controls and discover plasma miRNAs that distinguish between IPMN patients and controls and between "malignant" and "benign" IPMNs. Using novel nCounter technology to evaluate 800 miRNAs, we showed that a 30-miRNA signature distinguished 42 IPMN cases from 24 controls [area underneath the curve (AUC) = 74.4; 95% confidence interval (CI), 62.3-86.5, P = ...
Although my undergraduate research explored language perception in human subjects, my training has been largely in the fields of basic neuroscience and pain neurobiology. My graduate training focused on channel-channel and channel-receptor interactions involved in the development of masseter hypersensitivity as well as analgesia. My current interests involve exploring how communication between neurons, immune cells, and their target organs not only regulate homeostasis but also how these interactions drive the development of pathophysiological states. My main research program employs a mouse model of human pancreatic ductal adenocarcinoma (PDAC) to study the role of the nervous system in cancer, both with respect to pain and neurogenic inflammation as well as tumorigenesis itself. Our most recent studies focus on how denervation of the pancreas can slow or halt development of tumors. We are currently interested in elucidating the mechanisms underlying the efficacy of denervation. Toward this ...
Background : Carcinoma of the pancreas is a fatal malignant disease with limited therapeutic options. Cyclooxygenase-2 (COX-2) and c-erbB-2 are known to be involved in the carcinogenesis, differentiation and invasiveness of various neoplasms. We studied the immunohistochemical expressions of c-erbB-2 and COX-2 and the correlation between these expressions and the clinicopathologic parameters and the relation between the expressions. Methods : Immunohistochemical staining for c-erbB-2 and COX-2 were performed on the paraffin embedded sections of 36 cases of surgically resected ductal adenocarcinoma of the pancreas and 10 cases of non-neoplastic pancreas tissue. Results : The non-neoplastic control group showed a c-erbB-2 expression in the acini (8/10) and ducts (2/10), and a COX-2 expression in the acini (6/10) and ducts (3/10). The overexpression of c-erbB-2 was observed in 58% (21/36) of the carcinoma specimens. No significant correlation was found between c-erbB-2 and age, gender, tumor size, ...
Inflammation is paramount in pancreatic oncogenesis. We identified a uniquely activated γδT cell population, which constituted ∼40% of tumor-infiltrating T cells in human pancreatic ductal adenocarcinoma (PDA). Recruitment and activation of γδT cells was contingent on diverse chemokine signals. Deletion, depletion, or blockade of γδT cell recruitment was protective against PDA and resulted in increased infiltration, activation, and Th1 polarization of αβT cells. Although αβT cells were dispensable to outcome in PDA, they became indispensable mediators of tumor protection upon γδT cell ablation. PDA-infiltrating γδT cells expressed high levels of exhaustion ligands and thereby negated adaptive anti-tumor immunity. Blockade of PD-L1 in γδT cells enhanced CD4(+) and CD8(+) T cell infiltration and immunogenicity and induced tumor protection suggesting that γδT cells are critical sources of immune-suppressive checkpoint ligands in PDA. We describe γδT cells as central regulators of
Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of death with a mere 9% survival rate. PDACs harbor KRAS (92-95%) and CDKN2A (90%) mutations, overexpress tyrosine kinase receptors, their ligands, and transforming growth factor-? (TGF-β) isoforms. Canonical TGF-β signaling is mediated via Smad2, Smad3 and Smad4, whereas inhibitory Smad6 and Smad7 attenuate TGF-β signaling. Smad7 is overexpressed in PDAC and blocks TGF-β-mediated growth inhibition in vitro. However, the exact role of Smad7 in PDAC is not known. We have established a genetically engineered mouse model of PDAC in which conditional expression of Smad7 and oncogenic KrasG12D are driven in the pancreas by Pdx1-Cre. These LSL-KrasG12D;SMAD7;Pdx1-Cre(KS7C) mice exhibit accelerated progression of pancreatic intraepithelial neoplasia (PanIN) to PDAC by comparison with LSL-KrasG12D;Pdx1-Cre (KC) mice harboring the KrasG12D mutation alone, whereas in the absence of oncogenic Kras, pancreatic histology remains normal ...
Inflammation is paramount in pancreatic oncogenesis. We identified a uniquely activated γδT cell population, which constituted ∼40% of tumor-infiltrating T cells in human pancreatic ductal adenocarcinoma (PDA). Recruitment and activation of γδT cells was contingent on diverse chemokine signals. Dele …
In the present study, it was determined that the ISOC1 mRNA level is significantly increased in PDAC tissues, compared with normal pancreatic tissues, and the same trend was observed in PDAC cell lines, compared with normal pancreatic cells. Furthermore, the shISOC1-infected PDAC cell lines, SW 1990 and PANC-1, were demonstrated to have a reduced level of ISOC1 expression, compared with the respective control cell lines. Cell growth and proliferation was indicated to be significantly inhibited following ISOC1 knockdown. Furthermore, this inhibition of the cell growth and proliferation was determined to be associated with cell apoptosis. Finally, ISOC1 inhibition also resulted in an impairment of cell migration and invasion. To the best of our knowledge, this is the first study to have revealed how ISOC1 is involved in pancreatic cancer growth and migration.. Pancreatic cancer is notoriously difficult to detect early and to cure. Current therapeutic options for patients are limited and ...
Background: Pancreatic ductal adenocarcinomas (PDACs) are highly resistant to treatment due to changes in various signalling pathways. CK1 isoforms play important regulatory roles in these pathways.. Aims: We analysed the expression levels of CK1 delta and epsilon (CK1δ/∊) in pancreatic tumour cells in order to validate the effects of CK1 inhibition by 3-[2,4,6-(trimethoxyphenyl)methylidenyl]-indolin-2-one (IC261) on their proliferation and sensitivity to anti-CD95 and gemcitabine.. Methods: CK1δ/∊ expression levels were investigated by using western blotting and immunohistochemistry. Cell death was analysed by FACS analysis. Gene expression was assessed by real-time PCR and western blotting. The putative anti-tumoral effects of IC261 were tested in vivo in a subcutaneous mouse xenotransplantation model for pancreatic cancer.. Results: We found that CK1δ/∊ are highly expressed in pancreatic tumour cell lines and in higher graded PDACs. Inhibition of CK1δ/∊ by IC261 reduced pancreatic ...
Results Both mouse models developed PDAC, but Duct:KPcKO mice developed PDAC earlier than Acinar:KPcKO mice. Tumour development was more rapid and associated with high-grade murine PanIN (mPanIN) lesions in Duct:KPcKO mice. In contrast, Acinar:KPcKO mice exhibited widespread metaplasia and low-grade as well as high-grade mPanINs with delayed progression to PDAC. Acinar-cell-derived tumours also had a higher prevalence of mucinous glandular features reminiscent of early mPanIN lesions. ...
Authors: Amin S, Mhango G, Lin J, Aronson A, Wisnivesky J, Boffetta P, Lucas AL. Title: Metformin Improves Survival in Patients with Pancreatic Ductal Adenocarcinoma and Pre-Existing Diabetes: A Propensity Score Analysis.. Journal: Am J Gastroenterol 111(9):1350-7. Date: 2016 Sep. Abstract: OBJECTIVES: Pancreatic ductal adenocarcinoma (PDAC) remains a highly lethal disease. Diabetes mellitus (DM) is both a risk factor for and a sequela of PDAC. Metformin is a commonly prescribed biguanide oral hypoglycemic used for the treatment of type II DM. We investigated whether metformin use before PDAC diagnosis affected survival of patients with DM, controlling confounders such as diabetic severity. METHODS: We used the Surveillance, Epidemiology, and End Results registry (SEER)-Medicare linked database to identify patients with PDAC diagnosed between 2007 and 2011. The diabetic TO comorbidity severity index (DCSI) controlled for DM severity. Inverse propensity weighted Cox Proportional-Hazard Models ...
Pancreatic ductal adenocarcinoma is the most common pancreatic neoplasm. There are approximately 33,000 new cases of pancreatic ductal adenocarcinoma annually in the United States with approximately the same number of deaths. Surgery represents the only opportunity for cure, but this is restricted t …
Pancreatic cancer poses a particular challenge for The Cancer Genome Atlas (TCGA). All cancerous tumors are made up of a combination of normal and cancerous cells - and pancreatic cancer tumors have a relatively low percentage of cancerous cells. TCGA has strict requirements on only accepting samples of tumors with a high percentage of cancerous cells, as this allows for more accurate mutation detection. Because of the challenging nature of this disease, TCGA has relaxed its criteria regarding the percentage of cancerous cells to ensure samples received are representative of the disease. View additional information on pancreatic cancer.. TCGA researchers have:. ...
This clinical trial is looking at the effect of a new drug called GDC-0449 in patients with cancer of the pancreas. Laboratory studies have shown that this drug blocks a process in pancreatic cells thought to be involved in cancer development and spread. This process is called the Hedgehog signalling pathway. As yet, it is unclear whether blocking hedgehog signalling will directly affect the tumour cells themselves or the surrounding normal tissue. Understanding this distinction will help improve treatment strategies for pancreatic cancer. Patients will be offered to participate in this research study if they have localised pancreatic cancer that can be removed by surgery. In the period between diagnosis and surgery the investigators do not normally treat patients, however in this trial the investigators will ask patients to take GDC-0449 during the approximately two weeks until the day of surgery. All patients that enter this study will have undergone a diagnostic biopsy of the pancreatic ...
OBJECTIVE: The aim of this study was to improve the 8th edition (8th) of the American Joint Committee on Cancer (AJCC) staging system for pancreatic ductal adenocarcinoma (PDAC). BACKGROUND: The new 8th AJCC staging system for PDAC was released in October, 2016, and will be applied in clinical practice in 2018. METHODS: Two large cohorts were included in this analysis. One consisted of 45,856 PDAC patients in the Surveillance, Epidemiology, and End Results (SEER) database (2004-2014), and the other consisted of 3166 PDAC patients in the Fudan University Shanghai Cancer Center (FUSCC) database (2005-2015 ...
Context Most pancreatic ductal adenocarcinoma (PDAC) patients present with advanced disease (i.e., locally-advanced or metastatic) at diagnosis, and identification of prognostic biomarkers is essential to improve their clinical management. Enhancer of Zeste Homolog-2 (EZH2) plays an essential role in cancer-stem-cell self-renewal through methylation of histone-H3. In radically-resected patients, nuclear accumulation of EZH2 was associated with increased invasiveness [1] and poor prognosis. Still, no data are available on the prognostic role of EZH2 in the subset of advanced PDACs. Objective This is the first study aimed at evaluating EZH2 mRNA and protein expression in locally-advanced or metastatic PDACs, that we enriched for tumor cell content by laser-microdissection. Furthermore, since (1) recent studies suggested a role for candidate polymorphisms of EZH2 in lung cancer risk and colorectal cancer prognosis, and (2) polymorphisms can be assessed with a simple test in blood samples, we ...
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Aim of the study To determine the correlation of protein serum levels of two cytokines and their polymorphisms, which have an influence on their expression. Material and methods The study group consisted of 65 patients (33 men, 31 women) who met the criteria for inclusion and exclusion of...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
췌장 덕트 선암의 환자 유래 오르가노이드 배양은 높은 충실도를 가진 상피 종양 세포 구획을 나타내는 급속하게 확립된 3차원 모형, 이 치명적인 악성에 번역 연구를 가능하게 합니다. 여기에서, 우리는 이 모형을 사용하여 관련 생물학 생물학...
https://doi.org/10.18632/oncotarget.17519 Yan Sun, Weiwei He, Man Luo, Yuhong Zhou, Guilin Chang, Weiying Ren, Kefen Wu, Xi Li, Jiping Shen, Xiaoping Zhao, Yu Hu
The PTEN tumor suppressor is a lipid phosphatase that dephosphorylates phosphatidylinositol-3, 4, 5-trisphosphate and negatively regulates the PI3K/AKT pathway. Although PTEN aberrations are present in many cancer types, it is thought to play little role in pancreatic ductal adenocarcinoma (PDAC), a disease with very low 5-year survival rates. Now, Ying and colleagues show loss of PTEN expression and deletion of the PTEN locus in a significant percentage of human PDAC tumor samples. The authors turn to a mouse model in which activated Kras is expressed in the pancreas and one allele of Pten is deleted. Interestingly, these mice present with invasive pancreatic tumors that exhibited infiltration of inflammatory cells. Gene expression analysis of primary cells derived from the tumors showed activation of NF-κB transcription that was dependent on PI3K signaling. Further, inhibition of NF-κB activity reduced tumor growth when such cells were implanted into nude mice. Finally, the authors showed ...
BACKGROUND & AIMS: Obesity is a risk factor for pancreatic cancer. In mice, a high-fat diet (HFD) and expression of oncogenic KRAS lead to development of invasive pancreatic ductal adenocarcinoma (PDAC) by unknown mechanisms. We investigated how oncogenic KRAS regulates the expression of fibroblast growth factor 21, FGF21, a metabolic regulator that prevents obesity, and the effects of recombinant human FGF21 (rhFGF21) on pancreatic tumorigenesis. METHODS: We performed immunohistochemical analyses of FGF21 levels in human pancreatic tissue arrays, comprising 59 PDAC specimens and 45 nontumor tissues. We also studied mice with tamoxifen-inducible expression of oncogenic KRAS in acinar cells (KrasG12D/+ mice) and fElasCreERT mice (controls). KrasG12D/+ mice were placed on an HFD or regular chow diet (control) and given injections of rhFGF21 or vehicle; pancreata were collected and analyzed by histology, immunoblots, quantitative polymerase chain reaction, and immunohistochemistry. We measured ...
Whereas genomic aberrations in the SLIT-ROBO pathway are frequent in pancreatic ductal adenocarcinoma (PDAC), their function in the pancreas is unclear. Here we report that in pancreatitis and PDAC mouse models, epithelial Robo2 expression is lost while Robo1 expression becomes most prominent in the stroma. Cell cultures of mice with loss of epithelial Robo2 (Pdx1Cre;Robo2F/F) show increased activation of Robo1+ myofibroblasts and induction of TGF-β and Wnt pathways. During pancreatitis, Pdx1Cre;Robo2F/F mice present enhanced myofibroblast activation, collagen crosslinking, T-cell infiltration and tumorigenic immune markers. The TGF-β inhibitor galunisertib suppresses these effects. In PDAC patients, ROBO2 expression is overall low while ROBO1 is variably expressed in epithelium and high in stroma. ROBO2low;ROBO1high patients present the poorest survival. In conclusion, Robo2 acts non-autonomously as a stroma suppressor gene by restraining myofibroblast activation and T-cell infiltration. ...
Abstract. Pancreatic cancer (pancreatic ductal adenocarcinoma, PDA) is infamously moving to the top of the list as one of the most lethal cancers with an overall 5 year survival rate of 7%. Multiple genomic-based and molecular characterization studies of PDA specimens and established animal models have provided the field with multiple targets and a progression model of this disease. Still, to date, the best therapeutic options are surgery and combination cytotoxic therapies. In general, even in the best case scenario (i.e., an early stage diagnosis and a response to a specific therapy), most of these fortunate patients PDA cells acquire or exert resistance mechanisms and eventually kill the patient. Herein, we touch on a growing field of investigation that focuses on PDA cell therapeutic resistance mechanisms. We examine extrinsic elements (i.e., the tumor microenvironment, hypoxia) to the intrinsic processes within the cell (i.e., post-transcriptional gene regulation and somatic mutations) ...
Pancreatic Ductal Adenocarcinoma (PDA) is a very aggressive tumor for which effective therapeutical strategies are still lacking. The global five-years survival is of 5% and surgery is the only potentially curative treatment. The PDA-associated antigen α-enolase (ENO1), beside its glycolytic function, acts as a plasminogen receptor, promoting activation into plasmin, involved in extracellular matrix degradation. Antibodies against ENO1 are detected in more than 60% of PDA patients and correlate with a better prognosis. Furthermore, anti-ENO1 antibodies are induced in mice after ENO1-DNA vaccination. We observed an increased ENO1 expression on the cell surface of both PDA and myeloid cells (MDSC), suggesting a role in tumor progression and spreading. The immunotherapy represents a chance to selectively target PDA cells and MDSC. Mouse anti-human ENO1 monoclonal antibody (mAb) inhibits plasminogen-dependent invasion of human PDA cells and metastatic spreading in immunosuppressed mice, as well as ...
10th September, 2019. Dr Chee L Khoo. Lets face it. We all dread the diagnosis of pancreatic cancer in any of our patients. There arent too many red flags that we can rely on to warn us that something is not right with this deep seated abdominal organ. Many of the symptoms are either subtle or non-specific like nausea, intermittent epigastric pain, nausea, weight loss, loss of appetite or back pain. Pancreatic cancer is pretty much a universally fatal disease where the number diagnosed equal the number of deaths. Would it make sense then to screen for pancreatic cancer?. The US Preventative Services Task Force (UKPSTF) recently recommends against screening for pancreatic ductal adenocarcinoma (PDAC) in asymptomatic adults (1). PDAC is relatively rare with an incidence of ~12 per 100,000 in the average risk population. PDAC unfortunately progress rapidly, leaving us with only a small window of opportunity for early detection (2). Nonetheless, there are a few things we need to do if we were to ...
As the most common and most important cancer of the pancreas, with rapid mortality and now also as the third leading cause of cancer-related deaths in the United States, pancreatic ductal adenocarcinoma (PDAC) has become synonymous with "pancreas cancer". PDAC is also the prototype of the "pancreatobiliary-type" adenocarcinomas, along the biliary tract, ampullary and gallbladder cancers with the similar morphology and behavior. Recent molecular profiling studies have identified distinct subsets of PDAC, potentially with different behaviors and targetability. Moreover, while PDAC is by far the most common cancer of the pancreas, there are various other types that occur in this organ and are erroneously classified together with PDAC. Many of these have different molecular and biologic characteristics that warrant their management separately although they are also technically "pancreatic cancers". While some are closely related to PDAC and have as aggressive behavior (such as adenosquamous ...
PHILADELPHIA - Pancreatic ductal adenocarcinomas (PDAC) do not typically respond to immunotherapy, which limits treatment options for this cancer. By priming with a therapeutic vaccine and a low-dose chemotherapy combination prior to surgery, researchers converted PDACs into immunogenic cancers that may respond to immunotherapy, according to a study published in Cancer Immunology Research, a journal…
TY - JOUR. T1 - Diabetes Mellitus and Obesity as Risk Factors for Pancreatic Cancer. AU - Consortium for the Study of Chronic Pancreatitis, Diabetes, and Pancreatic Cancer. AU - Eibl, Guido. AU - Cruz-Monserrate, Zobeida. AU - Korc, Murray. AU - Petrov, Maxim S.. AU - Goodarzi, Mark O.. AU - Fisher, William E.. AU - Habtezion, Aida. AU - Lugea, Aurelia. AU - Pandol, Stephen J.. AU - Hart, Phil A.. AU - Andersen, Dana K.. PY - 2018/4. Y1 - 2018/4. N2 - Pancreatic ductal adenocarcinoma (PDAC) is among the deadliest types of cancer. The worldwide estimates of its incidence and mortality in the general population are eight cases per 100,000 person-years and seven deaths per 100,000 person-years, and they are significantly higher in the United States than in the rest of the world. The incidence of this disease in the United States is more than 50,000 new cases in 2017. Indeed, total deaths due to PDAC are projected to increase dramatically to become the second leading cause of cancer-related deaths ...
Nucleolin (NCL) is a nucleolar protein regulating ribogenesis and cell cycle progression, and is overexpressed in tumor cells. Shuttling to the cell surface of tumor cells and tumor vessels NCL is a marker of tumor tissues and a target for cancer therapy. Recently, we developed a family of nucleolin antagonist pseudopeptides (NucANT). The N6L peptide, strongly inhibits human tumor growth by inducing apoptosis of tumor cells (1), and is currently in clinical trial for cancer. Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal human malignancies, and an explanation of the failure of treatments is that chemotherapies are poorly delivered to the tumor because of a deficient and pathologic vasculature. We investigated the possibility that N6L could dually target tumor cells and tumor vasculature and be a promising new option for the treatment of PDAC.. NCL targeting by N6L inhibited pancreatic tumor cell proliferation and pancreatic tumor cell motility similarly to other tumor cell ...
TY - JOUR. T1 - Genetic events that limit the efficacy of MEK and RTK inhibitor therapies in a mouse model of KRAS-driven pancreatic cancer. AU - Pettazzoni, Piergiorgio. AU - Viale, Andrea. AU - Shah, Parantu. AU - Carugo, Alessandro. AU - Ying, Haoqiang. AU - Wang, Huamin. AU - Genovese, Giannicola. AU - Seth, Sahil. AU - Minelli, Rosalba. AU - Green, Tessa. AU - Huang-Hobbs, Emmet. AU - Corti, Denise. AU - Sanchez, Nora. AU - Nezi, Luigi. AU - Marchesini, Matteo. AU - Kapoor, Avnish. AU - Yao, Wantong. AU - Di Francesco, Maria E.. AU - Petrocchi, Alessia. AU - Deem, Angela K.. AU - Scott, Kenneth. AU - Colla, Simona. AU - Mills, Gordon. AU - Fleming, Jason B.. AU - Heffernan, Timothy P.. AU - Jones, Philip. AU - Toniatti, Carlo. AU - Depinho, Ronald A.. AU - Draetta, Giulio F.. PY - 2015/3/15. Y1 - 2015/3/15. N2 - Mutated KRAS (KRAS∗) is a fundamental driver in the majority of pancreatic ductal adenocarcinomas (PDAC). Using an inducible mouse model of KRAS∗-driven PDAC, we compared ...
Pancreatic ductal adenocarcinoma has a dire prognosis with 85% of patients presenting with tumors that are unresectable. The current standard of care therapy for these patients only prolongs survival to a median of 6 months. Even patients that undergo potentially curative resection almost inevitably develop metastatic disease. Thus, new treatment options are required both for patients with resectable disease and for patients with advanced disease.. In this study, we show that a functional axis can define survival in patients that undergo pancreaticoduodenectomy and that a "hypoxia/LOX" signature and high levels of fibrillar collagen are associated with poor prognosis. This suggests that fibrillar collagen (potentially quantifiable by elastography using endoscope‐guided ultrasound in the clinic) and LOX expression have potential as prognostic markers in pancreatic cancer. We also show that manipulation of a key element of this hypoxia/LOX signature can reverse most of the features of the axis ...
Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer death in North America. The highest risk factor for PDAC is recurrent pancreatitis. While the link between PDAC and pancreatitis is unknown, de-differentiation of acinar cells is common to both diseases. Our lab has shown that Activating Transcription Factor 3 (ATF3), a factor upregulated during pancreatic injury, contributes to the development of acinar-to-ductal cell metaplasia (ADM), a precursor phenotype of PDAC. The goal of this study was to identify how ATF3 contributes to ADM. I hypothesize that ATF3 regulates acinar gene expression promoting ADM. We observed decreased ADM development in Atf3-/- acinar cultures, along with expression changes in differentiation genes and ADM promoting pathways (EGFR) in vivo. Assessment following chronic injury indicated absence of ATF3 resulted in decreased tissue damage. These results suggest a novel mechanism where ATF3 promotes ADM through loss of the mature acinar cell phenotype.
Pancreatic ductal adenocarcinoma remains one of the deadliest cancers and is projected to become the second leading cause of cancer death by 2020. More alarming, is the projection of death in minority populations for this cancer. Although several risk factors have been associated with the etiology of this cancer, such as smoking, diet, obesity and recently nicotine, it continues to steadily increase. Numerous studies have shown the importance of cancer stem cells in cancer resistance and self-renewal. Dedifferentiation of cancer cells requires key factors to be present in the tumor environment. These factors are regulated by key transcription factors that are known to control cancer stem cells and dedifferentiation. Using a human embryonic stem cell RT2 Profiler gene array, numerous stem cell genes expressed in pancreatic cancer cell lines (MIAPaca2, Panc1) can be identified. However, this study focused on those involved in dedifferentiation of cancer cells. Although both cell lines, Panc-1 and ...
Pancreatic ductal adenocarcinoma (PDA) accounts for 95% of all pancreatic cancers. About 230,000 PDA cases are diagnosed worldwide each year. PDA has the lowest five-year survival rate as compared to others cancers. PDA in Poland is the fifth leading cause of death after lung, stomach, colon and...
DESCRIPTION (provided by applicant): Understanding human health problems requires a detailed functional understanding of the various organs and tissues within the body. These organs and tissues comprise mixtures of different cell types, and obtaining a functional understanding of these cell types at the molecular level is impeded by their complex pattern of interspersion. In this project, our main biomedical goal is to derive information about the global transcriptional and epigenetic states within the different cells of the pancreas, and to particularly identify changes as these cells enter into neoplasia resulting in pancreatic ductal adenocarcinoma (PDAC). The main technical goal of this project is to solve the problem of identifying the neoplastic cells, and characterizing their transcriptional and epigenomic states, within a background of normal cells of various types. A general solution to this problem is proposed based on the following observations: (a) that global profiling of nuclear ...
Genetic association studies have identified more than a dozen genes associated with risk of pancreatic cancer. Given this genetic heterogeneity, family history can be useful for identifying individuals at high-risk for this disease. The goal of this analysis was to evaluate associations of family history of diabetes and family history of pancreatic cancer with risk of pancreatic cancer. PACIFIC is a case-control study based in two large health plans. Cases were diagnosed with pancreatic ductal adenocarcinoma (PDA) and controls were selected from the health plan enrollment databases and frequency-matched to cases. Family history data were collected using an interviewer-administered questionnaire and were available on 654 cases and 697 controls. Logistic regression was used for the association analyses. First-degree relative history of diabetes was statistically significantly associated with increased risk of PDA (odds ratio (OR): 1.37, 95% confidence interval (CI): 1.10-1.71). The highest risk of ...
The 5-year survival rate for Pancreatic ductal adenocarcinoma (PDAC) patients is about 5% and has remained largely unchanged over the past 25 years. It is imper...
Several types of aggressive cancers, including pancreatic ductal adenocarcinoma PDAC, may become invasive when a recently discovered cell process called extrusion is defective. Researchers at Huntsman Cancer Institute discovered cell extrusion and now have
Pancreatic ductal adenocarcinoma (PDAC) is an extremely lethal cancer characterized by a high frequency of activating mutations in the KRAS oncogene (95%), which is a well-validated driver of PDAC growth. With limited treatment options for this disease, there is an urgent need to better understand the aberrant signaling that occurs in order to better design therapeutic strategies. However, to date, no successful anti-K-Ras therapies have been developed. Current efforts have focused on inhibition of effectors of K-Ras signaling, in particular the Raf and PI3K effector signaling pathways. However, inhibitors targeting components of these pathways, when used as monotherapy or in combination, have been ineffectual for long-term treatment of KRAS mutant cancers. The lack of success of these inhibitors is due, in part, to the importance of other effectors in K-Ras-dependent cancer growth and the upregulation of compensatory signaling programs that overcome inhibitor activity. Consequently, in order to ...
We searched for genes that are potentially important for the maintenance of Pancreatic Ductal Adenocarcinoma (PDAC). PDAC is the 4th leading cause for cancer-related deaths and exhibits a 5-year survival rate of less than ...
Virtual microdissection identifies distinct tumor- and stroma-specific subtypes of pancreatic ductal adenocarcinoma, which may be highly prognostic.
Ductal adenocarcinoma (DAC) of the prostate is an uncommon histologic subtype whose prognostic factors and immunoprofile have not been fully defined.To define its prognostic factors and immunoprofile, the clinicopathological features, including biochemical recurrence (BCR), of 61 cases of DAC were analyzed.
Pancreatic ductal adenocarcinoma (PDAC) is the ninth most common cancer in the United States, but due to symptoms - such as back pain, jaundice and unexpla
Overview of the recently described KRAS function in pancreatic ductal adenocarcinoma and findings in screening cohorts(a) Mutant KRAS increases redox-equivalent
celebrates its 5th birthday this year! Since 2012 we have been bringing you the latest breakthroughs in biomedical materials science with a strong focus on improving human health, and we will continue to do so in 2017. Read more about this in our latest editorial.. No access to our published content yet? Make sure to recommend Advanced Healthcare Materials to your librarian. More information can be found here.. In this monthly feature, we highlight some of the most read Advanced Healthcare Materials publications over the last month. These top-downloaded articles are therefore currently freely accessible! Click on the titles below to get to the corresponding papers. Also check out our cover art feature here.. Desmoplastic Reaction in 3D-Pancreatic Cancer Tissues Suppresses Molecular Permeability. by Michiya Matsusaki, Misaki Komeda, Simona Mura, Hiroyoshi Y. Tanaka, Mitsunobu R. Kano, Patrick Couvreur, and Mitsuru Akashi. The survival rate for pancreatic ductal adenocarcinoma is still the lowest ...
Your healthcare professional is the single best source of information regarding your health. Diabetes Self Management Education Uk Ketotic Non Hyperglycemia by planning ahead & ordering wisely you can have an enjoyable dining experience with diabetes. Although this syndrome is more common in type 1 diabetics it can also occur with type 2 diabetes. Journal of Living Food and Healing. Diabetic Fruits Prediabetes Food ::The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days.. Finding mouthwatering diabetic-friendly recipes can be a here are 32 diabetic-friendly holiday recipes from appetizers to Holiday Sugar Cookies; If you have diabetes and are fasting Beim Typ-2-Diabetes gibt ein Getting Back Together After Breakup Or Divorce. Pancreatic Ductal Adenocarcinoma Cancer Stem Cell. pasta compared with traditional pasta. Banana Oatmeal Raisin Cookies. diabetic oil and vinegar dressing postprandial hour gestational one Estimates of the incidence of type 1 diabetes mellitus (DM) ...
Chen, Y., Zheng*, B., Robbins, DH., Lewin, DN., Mikhitarian, K, Graham, A., Rumpp, L, Glenn, T, Gillanders, WE, Cole, DJ, Lu, X, Hoffman, BJ. and Michael Mitas (2007) Accurate discrimination of pancreatic ductal adenocarcinoma and chronic focal pancreatitis using multi-marker expression data and samples obtained by minimally invasive fine needle aspiration. International Journal of Cancer, 120(7):1511. PMID: 17192896 ...
Classification of CD133-positive expression in the invasive ductal adenocarcinoma of the pancreas head samples from 80 patients. Tumour samples were classified
TY - JOUR. T1 - Regulation of endothelial Fas expression as a mechanism of promotion of vascular integrity by mural cells in tumors. AU - Kamei, Ryosuke. AU - Tanaka, Hiroyoshi Y.. AU - Kawano, Takao. AU - Morii, Chiharu. AU - Tanaka, Sayaka. AU - Nishihara, Hiroshi. AU - Iwata, Caname. AU - Kano, Mitsunobu R.. PY - 2017/5/1. Y1 - 2017/5/1. N2 - Angiogenesis is a multi-step process that culminates in vascular maturation whereby nascent vessels stabilize to become functional, and mural cells play an essential role in this process. Recent studies have shown that mural cells in tumors also promote and maintain vascular integrity, with wide-reaching clinical implications including the regulation of tumor growth, metastases, and drug delivery. Various regulatory signaling pathways have been hitherto implicated, but whether regulation of Fas-dependent apoptotic mechanisms is involved has not yet been fully investigated. We first compared endothelial FAS staining in human pancreatic ductal ...
https://doi.org/10.18632/oncotarget.8994 Erin L. Wuebben, Phillip J. Wilder, Jesse L. Cox, James A. Grunkemeyer, Thomas Caffrey, Michael A. Hollingsworth, Angie Rizzino
Pancreatic cancer, most commonly in the form of a solid ductal adenocarcinoma, accounts for 3% of all cancers but ranks in the top five leading causes of cancer deaths in most developed countries, reflecting the fact that it has a very poor prognosis (median survival 6 to 9 months). It is a disease of old age (85% of patients >65 years), and commoner in smokers....
The duration of DM at the time of IPMN diagnosis was 9.3±10.3 years. 14 patients were complicated with main-duct IPMN and 20 patients were complicated with ...
Learn more about Incorporating Genetic Testing into the Care of a PDAC Patient. Discover more CME courses from our experts at UPMC.
Intraductal papillary mucinous neoplasm (IPMN) is a type of tumor that can occur within the cells of the pancreatic duct. IPMN tumors produce mucus, and this mucus can form pancreatic cysts. Although intraductal papillary mucinous neoplasms are benign tumors, they can progress to pancreatic cancer. As such IPMN is viewed as a precancerous condition. Once an intraductal papillary mucinous neoplasm has been found, the management options include close monitoring and pre-emptive surgery.[medical citation needed] Pathologists classify intraductal papillary mucinous neoplasms (IPMNs) into two broad groups - those that are associated with an invasive cancer and those that are not associated with an invasive cancer. This separation has critical prognostic significance. Patients with a surgically resected intraductal papillary mucinous neoplasm without an associated invasive cancer have an excellent prognosis (>95% will be cured), while patients with a surgically resected intraductal papillary mucinous ...
TY - JOUR. T1 - Invasive carcinoma derived from intestinal-type intraductal papillary mucinous neoplasm is associated with minimal invasion, colloid carcinoma, and less invasive behavior, leading to a better prognosis. AU - Nakata, Kohei. AU - Ohuchida, Kenoki. AU - Aishima, Shinichi. AU - Sadakari, Yoshihiko. AU - Kayashima, Tadashi. AU - Miyasaka, Yoshihiro. AU - Nagai, Eishi. AU - Mizumoto, Kazuhiro. AU - Tanaka, Masao. AU - Tsuneyoshi, Masazumi. AU - Oda, Yoshinao. PY - 2011/5/1. Y1 - 2011/5/1. N2 - Objectives: Although intestinal-type intraductal papillary mucinous carcinoma (IPMC) is reported to have a better prognosis, few studies have addressed its invasive pattern. The meaning of "minimal invasion" (MI) in IPMC also remains unclear. We investigated the prognosis of intraductal papillary mucinous neoplasm (IPMN) focusing on MI and subtypes. Methods: We evaluated 71 patients with IPMC among a total of 179 patients with resected IPMN. Results: Although 2 of 10 MI-IPMC patients had lymph ...
Intraductal papillary mucinous neoplasms of the pancreas: an increasingly recognized clinicopathologic entity.: Intraductal papillary mucinous neoplasms represe
Expression of MUC4 Mucin Is Observed Mainly in the Intestinal Type of Intraductal Papillary Mucinous Neoplasm of the PancreasExpression of MUC4 Mucin Is Observed Mainly in the Intestinal Type of Intraductal Papillary Mucinous Neoplasm of the Pancreas ...
We have previously shown that WW domain-containing oxidoreductase (WWOX) has tumour-suppressing effects and that its expression is frequently reduced in pancreatic carcinoma. In this study, we examined WWOX expression in intraductal papillary mucinous neoplasm of the pancreas (IPMN) to assess the function of WWOX in pancreatic duct tumourigenesis using immunohistochemistry and methylation-specific polymerase chain reaction analysis. Among 41 IPMNs including intraductal papillary mucinous adenomas (IPMAs) and intraductal papillary mucinous carcinomas (IPMCs), loss or reduced WWOX immunoreactivity was detected in 3 (15%) of 20 IPMAs and 17 (81%) of 21 IPMCs. In addition, hypermethylation of the WWOX regulatory site was detected in 1 (33%) of 3 WWOX(−) IPMAs and 9 (53%) of 17 WWOX(−) IPMCs, suggesting that hypermethylation may possibly be important in the suppression of WWOX expression. Reduction of WWOX expression was significantly correlated with a higher Ki-67 labelling index but was not correlated
Hruban RH, Takaori K, Klimstra DS, Adsay NV, Albores-Saavedra J, Biankin AV, Biankin SA, Compton C, Fukushima N, Furukawa T, Goggins M, Kato Y, Kloppel G, Longnecker DS, Luttges J, Maitra A, Offerhaus GJ, Shimizu M, Yonezawa S. An illustrated consensus on the classification of pancreatic intraepithelial neoplasia and intraductal papillary mucinous neoplasms. Am J Surg Pathol. 2004 Aug;28(8):977-87 ...
ASA 2018 Abstracts: Does Surgical Margin Impact Recurrence in Non-Invasive Intraductal Papillary Mucinous Neoplasms? A Multi-Institutional Study
article{41680afa-1eab-45c3-aa76-62b426b1b7aa, author = {Ansari, Daniel and Aronsson, Linus and Andersson, Roland}, issn = {1479-6694}, keyword = {biomarkers,gastrointestinal,molecular oncology,oncogenes,pancreatic biliary,surgery}, language = {eng}, month = {08}, number = {20}, pages = {1751--1753}, publisher = {Future Medicine Ltd.}, series = {Future Oncology}, title = {Biomarkers, imaging and multifocality in intraductal papillary mucinous neoplasms : Relevant for decision making?}, url = {http://dx.doi.org/10.2217/fon-2017-0244}, volume = {13}, year = {2017 ...
TY - JOUR. T1 - Invasive carcinoma derived from intraductal papillary-mucinous carcinoma of the pancreas. T2 - Clinicopathologic and immunohistochemical study of eight cases. AU - Fukushima, Noriyoshi. AU - Mukai, Kiyoshi. AU - Sakamoto, Michiie. AU - Hasebe, Takahiro. AU - Shimada, Kazuaki. AU - Kosuge, Tomoo. AU - Kinoshita, Taira. AU - Hirohashi, Setsuo. PY - 2001/7/30. Y1 - 2001/7/30. N2 - Most intraductal papillary-mucinous carcinomas (IPMCs) of the pancreas are resectable and curable, but some develop into frankly invasive carcinomas. We studied the clinicopathologic features of eight cases of invasive carcinoma derived from IPMC (IC-IPMC) of the pancreas. The patients were aged 54-75 years (mean, 66.6 years); six were male and two were female. The mean tumor size was 7.7 cm (range 5.5-10.5 cm). Two patients without lymph node metastasis had no peripancreatic invasion, and survived longer (115 and 20 months). Three out of four patients with extrapancreatic invasion died of their tumors or ...
"Secretion of N-ERC/mesothelin and expression of C-ERC/mesothelin in human pancreatic ductal carcinoma". Oncol. Rep. 20 (6): ... Hellstrom I, Hellstrom KE (2008). "SMRP and HE4 as biomarkers for ovarian carcinoma when used alone and in combination with ... Bharadwaj U, Li M, Chen C, Yao Q (2008). "Mesothelin-Induced Pancreatic Cancer Cell Proliferation Involves Alteration of Cyclin ... Mesothelin is over expressed in several human tumors, including mesothelioma and ovarian and pancreatic adenocarcinoma. The ...
... expression analysis in human pancreatic ductal carcinomas". Genomics. 46 (2): 284-6. doi:10.1006/geno.1997.5018. PMID 9417916. ... Cattaneo M, Fontanella E, Canton C, Delia D, Biunno I (2006). "SEL1L affects human pancreatic cancer cell cycle and ...
... miR-224 has also been linked with pancreatic ductal carcinoma, where it is thought to repress CD40 expression in cancer cells. ... "Involvement of CD40 targeting miR-224 and miR-486 on the progression of pancreatic ductal adenocarcinomas". Annals of Surgical ... miR-224 has been noted as the most upregulated microRNA in hepatocellular carcinoma. The same study identified a target of mir- ... "Profiling microRNA expression in hepatocellular carcinoma reveals microRNA-224 up-regulation and apoptosis inhibitor-5 as a ...
... esophageal adenocarcinoma and esophageal squamous-cell carcinoma, gastric cancer, bile duct cancer, pancreatic cancer, small ... "Characterization of extensive genetic alterations in ductal carcinoma in situ by fluorescence in situ hybridization and ... January 1983). "Unstable methotrexate resistance in human small-cell carcinoma associated with double minute chromosomes". N. ... to field defects include head and neck squamous cell carcinoma (HNSCC), oropharyngeal/laryngeal cancer, ...
... ductal carcinoma of the pancreas and colorectal cancer. Several germline KRAS mutations have been found to be associated with ... Somatic KRAS mutations are found at high rates in leukemias, colorectal cancer, pancreatic cancer and lung cancer. The impact ... Almoguera C, Shibata D, Forrester K, Martin J, Arnheim N, Perucho M (May 1988). "Most human carcinomas of the exocrine pancreas ... Burmer GC, Loeb LA (April 1989). "Mutations in the KRAS2 oncogene during progressive stages of human colon carcinoma". ...
Overexpression contributes to the malignant phenotype of a subset of human ductal pancreatic cancers. Mice lacking Akt2 have a ... The gene was shown to be amplified and overexpressed in 2 of 8 ovarian carcinoma cell lines and 2 of 15 primary ovarian tumors ... Cheng JQ, Ruggeri B, Klein WM, Sonoda G, Altomare DA, Watson DK, Testa JR (1996). "Amplification of AKT2 in human pancreatic ... is amplified in human ovarian carcinomas". Proc Natl Acad Sci U S A. 89 (19): 9267-71. doi:10.1073/pnas.89.19.9267. PMC 50107 ...
Poor prognosis and clinical progression of hepatocellular carcinoma, pancreatic adenocarcinoma, and colorectal cancer are all ... "Expression of MAP4K4 is associated with worse prognosis in patients with stage II pancreatic ductal adenocarcinoma". Clinical ... Additionally, miRNA silencing of MAP4K4 in pancreatic beta-cells conferred protection against TNF-α repression of insulin ... pancreatic and ovarian cancer where such up-regulation is associated with increased cell migration, adhesion and invasiveness. ...
Pancreatic ductal carcinoma. *cystic neoplasms: Serous microcystic adenoma. *Intraductal papillary mucinous neoplasm ... Micrographs of normal pancreas, pancreatic intraepithelial neoplasia (precursors to pancreatic carcinoma) and pancreatic ... Other exocrine cancers include adenosquamous carcinomas, signet ring cell carcinomas, hepatoid carcinomas, colloid carcinomas, ... List of people diagnosed with pancreatic cancer. References[edit]. *^ a b c d e f g "Pancreatic Cancer Treatment (PDQ®) Patient ...
... thyroid carcinoma, bladder urothelial carcinoma - nonpapillary, uterine corpus (endometrial carcinoma), pancreatic ductal ... lung squamous cell carcinoma, kidney papillary carcinoma, clear cell kidney carcinoma, breast ductal carcinoma, renal cell ... Pancreatic Cancer - Ductal adenocarcinoma and Ovarian Cancer - Serous cystadenocarcinoma Canada: Pancreatic Cancer - Ductal ... esophageal carcinoma, ovarian serous cystadenocarcinoma, lung squamous cell carcinoma, adrenocortical carcinoma, Diffuse Large ...
Ductal, lobular,. and medullary (8500-8549). Ductal carcinoma. *Mammary ductal carcinoma. *Pancreatic ductal carcinoma ... In some types of carcinomas, Stage 0 carcinoma has been used to describe carcinoma in situ, and occult carcinomas detectable ... Breast: Nearly all breast cancers are ductal carcinoma.. *Prostate: The most common form of carcinoma of the prostate is ... Some carcinomas are named for their or the putative cell of origin, (e.g.hepatocellular carcinoma, renal cell carcinoma). ...
A recent study investigated the use of miRNA as a biomarker in pancreatic ductal adenocarcinoma, a form of pancreatic cancer. ... Included in the findings was an association between hepatocellular carcinoma and the upregulation of miR-92a, a member of ... The study analyzed RNA from biopsied pancreatic cysts to identify deviations in expression of miRNAs. The study found that 228 ... "Towards a clinical use of miRNAs in pancreatic cancer biopsies". Expert Rev Mol Diagn. 13 (1): 31-4. doi:10.1586/erm.12.136. ...
Invasive ductal carcinoma: 55% of breast cancers Ductal carcinoma in situ: 13% Invasive lobular carcinoma: 5% The vast majority ... pancreas; over 80% of pancreatic cancers are ductal adenocarcinomas. prostate cancer is nearly always adenocarcinoma cervical ... Thus invasive ductal carcinoma, the most common form of breast cancer, is adenocarcinoma but does not use the term in its name- ... "The changing incidence of in situ and invasive ductal and lobular breast carcinomas: United States, 1999-2004". Cancer ...
... ductal MeSH C04.557.470.615.132.500 --- carcinoma, ductal, breast MeSH C04.557.470.615.132.750 --- carcinoma, pancreatic ductal ... carcinoma, ductal, breast MeSH C04.557.470.200.025.232.750 --- carcinoma, pancreatic ductal MeSH C04.557.470.200.025.240 --- ... carcinoma, pancreatic ductal MeSH C04.588.322.455 --- ovarian neoplasms MeSH C04.588.322.455.398 --- granulosa cell tumor MeSH ... carcinoma, pancreatic ductal MeSH C04.588.274.780 --- peritoneal neoplasms MeSH C04.588.322.078 --- adrenal gland neoplasms ...
... carcinoma, pancreatic ductal MeSH C19.344.609.145 --- acth-secreting pituitary adenoma MeSH C19.344.609.145.500 --- nelson ... carcinoma, islet cell MeSH C19.344.421.500.124 --- gastrinoma MeSH C19.344.421.500.249 --- glucagonoma MeSH C19.344.421.500.500 ... carcinoma, endometrioid MeSH C19.391.630.705.398 --- granulosa cell tumor MeSH C19.391.630.705.464 --- luteoma MeSH C19.391. ... adrenocortical carcinoma MeSH C19.053.347.500 --- adrenal cortex neoplasms MeSH C19.053.347.500.500 --- adrenocortical adenoma ...
... carcinoma, pancreatic ductal MeSH C06.405.117.102 --- barrett esophagus MeSH C06.405.117.119 --- deglutition disorders MeSH ... carcinoma, pancreatic ductal MeSH C06.689.750.650 --- pancreatitis, acute necrotizing MeSH C06.689.750.660 --- pancreatitis, ... carcinoma, islet cell MeSH C06.301.761.500.124 --- gastrinoma MeSH C06.301.761.500.249 --- glucagonoma MeSH C06.301.761.500.500 ... pancreatic pseudocyst MeSH C06.689.667.249 --- adenoma, islet cell MeSH C06.689.667.249.500 --- insulinoma MeSH C06.689.667.500 ...
... for metastatic small cell lung cancer Treatment of advanced or metastatic pancreatic ductal adenocarcinoma Comparison of ... aldoxorubicin and doxorubicin for patients with metastatic or locally advanced carcinoma A phase III trial for patients with ... therapy schedules of doxorubicin and an acid-sensitive albumin-binding prodrug of doxorubicin in the MIA PaCa-2 pancreatic ...
Cancer Prostate Cancer Pancreatic ductal carcinoma Cosmetic applications Facial rejuvenation Breast Augmentation Alopecia or ...
... thyroid carcinoma, bladder urothelial carcinoma - nonpapillary, uterine corpus (endometrial carcinoma), pancreatic ductal ... kidney papillary carcinoma, clear cell kidney carcinoma, breast ductal carcinoma, renal cell carcinoma, cervical cancer ( ... esophageal carcinoma, ovarian serous cystadenocarcinoma, lung squamous cell carcinoma, adrenocortical carcinoma, Diffuse Large ... "Integrated Genomic Characterization of Pancreatic Ductal Adenocarcinoma". Cancer Cell. 32 (2): 185-203.e13. doi:10.1016/j.ccell ...
"Prognostic significance of growth factors and the urokinase-type plasminogen activator system in pancreatic ductal ... "Altered expression of members of the IGF-axis in clear cell renal cell carcinoma". Int. J. Oncol. 26: 923-31. doi:10.3892/ijo. ... pancreatic cancer, and clear cell renal cell cancer in which high tissue IGFBP-3 expression has been linked to poor prognostic ... expression of insulin-like growth factor binding protein-3 and its promoter hypermethylation in human hepatocellular carcinoma ...
Pancreatic ductal carcinoma is a common form of pancreatic cancer. ERCP image showing the pancreatic duct and biliary tree. ... The pancreatic duct, or duct of Wirsung (also, the major pancreatic duct due to the existence of an accessory pancreatic duct ... However, some have an additional accessory pancreatic duct, called the Duct of Santorini. An accessory pancreatic duct can be ... Bile backing up into the pancreatic duct may initiate pancreatitis. The pancreatic duct is generally regarded as abnormally ...
Types include: Mammary Ductal carcinoma in situ Invasive ductal carcinoma Pancreatic ductal carcinoma. ... Ductal carcinoma is a type of tumor that primarily presents in the ducts of a gland. ...
The most common is ductal adenocarcinoma. The most significant risk factors for pancreatic cancer are advanced age (over 60) ... Moss, AC; Morris, E; Mac Mathuna, P (Apr 19, 2006). "Palliative biliary stents for obstructing pancreatic carcinoma". The ... are more likely to be carcinomas, whilst those located below (towards the feet) are more likely to be squamous cell carcinomas ... Pancreatic cancer has a poor prognosis, with a five-year survival rate of less than 5%. By the time the cancer is diagnosed, it ...
"Expression of the hypoxia-inducible and tumor-associated carbonic anhydrases in ductal carcinoma in situ of the breast". Am. J ... Lee, MG; Ohana, E; Park, HW; Yang, D; Muallem, S (January 2012). "Molecular mechanism of pancreatic and salivary gland fluid ... of clear cell renal carcinomas. Two transcript variants encoding different isoforms have been identified for this gene. Loss of ... "Down-regulation of transmembrane carbonic anhydrases in renal cell carcinoma cell lines by wild-type von Hippel-Lindau ...
"FXYD3 is overexpressed in pancreatic ductal adenocarcinoma and influences pancreatic cancer cell growth". International Journal ... prostate cancer and its siRNA-mediated inhibition of expression induces a decrease in proliferation of human prostate carcinoma ...
Carzelesin also proved to be more efficacious than U-76074 or adozelesin against mouse pancreatic ductal 02 adenocarcinoma, a ... implanted Lewis lung carcinoma, i.p. or s.c. implanted B16 melanoma, s.c. implanted colon 38 carcinoma, and five s.c. implanted ... ovarian 2780 carcinoma, and prostatic DU-145 carcinoma. Carzelesin treatment produced 100% complete remissions (no palpable ... and adozelesin caused marked tumor shrinkage in mice bearing human lung LX-1 or advanced-stage human ovarian 2780 carcinoma; ...
Pancreatic cancer. Over-expression. 74%. Immunohistochemistry. [18]. Pancreatic cancer. Over-expression. 66%. ... Breast cancer (invasive ductal). Over-expression. -. Immunohistochemistry. [12]. Breast cancer (BRCA1 deficient). Over- ... Renal cell carcinoma. Under-expression. 100%. Western (protein) blotting and mRNA. [25]. ... Klopfleisch R, Schütze M, Gruber AD (Jan 2010). "RAD51 protein expression is increased in canine mammary carcinomas". ...
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Immunofluorescence staining of normal pancreatic tissue and pancreatic ductal carcinoma. Formalin-fixed, paraffin-embedded ... Centrosome Abnormalities in Pancreatic Ductal Carcinoma. Norihiro Sato, Kazuhiro Mizumoto, Masafumi Nakamura, Kenjiro Nakamura ... Centrosome Abnormalities in Pancreatic Ductal Carcinoma. Norihiro Sato, Kazuhiro Mizumoto, Masafumi Nakamura, Kenjiro Nakamura ... Centrosome Abnormalities in Pancreatic Ductal Carcinoma. Norihiro Sato, Kazuhiro Mizumoto, Masafumi Nakamura, Kenjiro Nakamura ...
Abstract 1543: Clinical significance of ZNF185 intracellular localization in pancreatic ductal carcinoma. Daisuke Furukawa, ... Clinical significance of ZNF185 intracellular localization in pancreatic ductal carcinoma. [abstract]. In: Proceedings of the ... Abstract 1543: Clinical significance of ZNF185 intracellular localization in pancreatic ductal carcinoma ... Abstract 1543: Clinical significance of ZNF185 intracellular localization in pancreatic ductal carcinoma ...
... and less pancreatic ductal and common biliary dilation. Keywords: acinar cell carcinoma, computed tomography, pancreatic ductal ... The percentage of common bile duct and pancreatic ductal dilation was 14.3% (2/14) and 7.1% (1/14), respectively. The mean size ... Pancreatic acinar cell carcinoma (ACC) is a rare tumor that is difficult to diagnose preoperatively. The aim of this study was ... features of ACC and compare the results with pancreatic ductal adenocarcinoma (DAC) for improving preoperative diagnosis. The ...
Identification and validation of differential expressed apoptotic genes in microdissected pancreatic ductal carcinomas. ... Identification and validation of differential expressed apoptotic genes in microdissected pancreatic ductal carcinomas ... Identification and validation of differential expressed apoptotic genes in microdissected pancreatic ductal carcinomas ... Identification and validation of differential expressed apoptotic genes in microdissected pancreatic ductal carcinomas ...
Telomerase elevation in pancreatic ductal carcinoma compared to nonmalignant pathological states.. N Suehara, K Mizumoto, T ... Telomerase elevation in pancreatic ductal carcinoma compared to nonmalignant pathological states.. N Suehara, K Mizumoto, T ... Telomerase elevation in pancreatic ductal carcinoma compared to nonmalignant pathological states.. N Suehara, K Mizumoto, T ... Telomerase elevation in pancreatic ductal carcinoma compared to nonmalignant pathological states. Message Subject (Your Name) ...
Carcinoma, Pancreatic ductal M384. Predesigned 384-well panel for use with SYBR® Green ...
... have been implicated in the development and progression of human prostatic carcinoma and pancreatic ductal adenocarcinoma. We ... The human prostate carcinoma cell line PC-3, the human prostatic/bladder carcinoma TSU-Pr1, and the human ovarian carcinoma ... pancreatic, lung, and medullary thyroid carcinoma (5, 6, 7, 8, 9, 10) . Specifically, human prostatic carcinoma cells have been ... RT-PCR detection of trkA expression in PC-3 prostatic, CFPAC pancreatic, and SK-OV-3 ovarian carcinoma tumor cell lines but not ...
The Sustained Induction of c-MYC Drives Nab-paclitaxel Resistance in Primary Pancreatic Ductal Carcinoma Cells. Erika Parasido ... The Sustained Induction of c-MYC Drives Nab-paclitaxel Resistance in Primary Pancreatic Ductal Carcinoma Cells ... The Sustained Induction of c-MYC Drives Nab-paclitaxel Resistance in Primary Pancreatic Ductal Carcinoma Cells ... The Sustained Induction of c-MYC Drives Nab-paclitaxel Resistance in Primary Pancreatic Ductal Carcinoma Cells ...
Build: Fri Jul 27 09:23:34 EDT 2018 (commit: a5c8d99). National Center for Advancing Translational Sciences (NCATS), 6701 Democracy Boulevard, Bethesda MD 20892-4874 • 301-435-0888. ...
... puede explicar cómo una forma común del cáncer de pecho del temprano-escenario conocido como in situ de carcinoma ductal (DCIS ... Screening for pancreatic cancer using artificial intelligence. Dr. Ananya Malhotra. Dr. Ananya Malhotra speaks to News-Medical ... El estudio ofrece discernimiento en cómo el cáncer de pecho del temprano-escenario progresa al carcinoma ductal invasor. * ... El estudio ofrece nuevo discernimiento en cómo DCIS lleva al carcinoma ductal invasor (IDC), y ofrece una comprensión más sin ...
Carcinoma that arises from the PANCREATIC DUCTS. It accounts for the majority of cancers derived from the PANCREAS. ...
Pancreatic. adenocarcinoma. cancer. Additional relevant MeSH terms: Adenocarcinoma. Carcinoma. Neoplasms, Glandular and ... Hedgehog Inhibition for Pancreatic Ductal Adenocarcinoma (PDAC) in the Preoperative Setting (HIPPoS) (HIPPoS). The safety and ... Proof of Mechanism Study of an Oral Hedgehog Inhibitor (GDC-0449) in Patients With Resectable Pancreatic Ductal Adenocarcinoma ... Documented tissue diagnosis of pancreatic ductal adenocarcinoma with a sufficient amount of tissue for Laser Capture Micro- ...
History of malignancy other than pancreatic carcinoma within 2 years prior to screening, with the exception of those with a ... Histologically or cytologically confirmed metastatic pancreatic ductal adenocarcinoma. *For patients in Cohort 1: no prior ... A Study of Multiple Immunotherapy-Based Treatment Combinations in Participants With Metastatic Pancreatic Ductal Adenocarcinoma ... Pancreatic Adenocarcinoma Drug: Nab-Paclitaxel Drug: Gemcitabine Drug: Oxaliplatin Drug: Leucovorin Drug: Fluorouracil Drug: ...
Diagnosis of pancreatic islet neoplasm, acinar cell carcinoma, non-adenocarcinoma, adenocarcinoma originating from the biliary ... Metastatic Pancreatic Ductal Adenocarcinoma Drug: Momelotinib Drug: Placebo to match momelotinib Drug: Nab-paclitaxel Drug: ... Gemcitabine and Nab-paclitaxel Combined With Momelotinib in Participants With Previously Untreated Metastatic Pancreatic Ductal ... Presence of metastatic pancreatic adenocarcinoma plus 1 of the following:. *Histological diagnosis of pancreatic adenocarcinoma ...
Carcinoma, Pancreatic Ductal/blood supply. *Carcinoma, Pancreatic Ductal/genetics*. *Carcinoma, Pancreatic Ductal/pathology ... Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy. Long non-coding RNAs (lncRNAs) are important regulators in ... Linc00511 acts as a competing endogenous RNA to regulate VEGFA expression through sponging hsa-miR-29b-3p in pancreatic ductal ... Linc00511 acts as a competing endogenous RNA to regulate VEGFA expression through sponging hsa‐miR‐29b‐3p in pancreatic ductal ...
... the incidence of pancreatic cancer has been increasing in recent years. The disease shows multigene, multi-step co.. ... Progress in Animal Models of Pancreatic Ductal Adeno-carcinoma. As a common gastrointestinal tumor, the incidence of pancreatic ... Furthermore , pancreatic cancer has an insidious onset and an extremely poor prognosis, so it is difficult to obtain cinical ... A large number of animal models of pancreatic cancer are currently available, including a cancer cell line-based xenograft, a ...
"Proteomic profiling of pancreatic ductal carcinoma cell lines treated with trichostatin-A". ... "Proteomic profiling of pancreatic ductal carcinoma cell lines treated with trichostatin-A" ... A pancreatic adenocarcinoma cell line (Paca44) was treated with trichostatin-A (TSA), a potent inhibitor of histone ... A pancreatic adenocarcinoma cell line (Paca44) was treated with trichostatin-A (TSA), a potent inhibitor of histone ...
Pancreatic ductal adenocarcinoma (PDAC), which is considered incurable, accounts for more than 90% of pancreatic cancer cases. ... Resource Library Pancreatic Cancer Connections Symptoms Stages Videos What Is Standard of Care? Glossary ... Resource Library Pancreatic Cancer Connections Symptoms Stages Videos What Is Standard of Care? Glossary ... Lets Win! Pancreatic Cancer is an online community for sharing information about innovative, science-based treatments for ...
In this study, we found that the majority of pancreatic ductal adenocarcinoma tissues and cell lines had weak or no expression ... we found that overexpression of Net inhibited cell growth and survival and induced cell apoptosis in human pancreatic ductal ... Our data thus suggested that Net might play an important role in pancreatic carcinogenesis, possibly by acting as a tumor ... has been suspected of being involved in pancreatic cancer and other tumors biology. ...
Pancreatic cancer : with special focus on topical issues and surgical techniques. [Sun-Whe Kim; Hiroki Yamaue;] -- This book ... provides state of the art knowledge on a broad range of clinical issues in pancreatic cancer, covering topics from screening ... 3.1.1 Invasive Ductal Adenocarcinoma; 3.1.2 Pancreatic Intraepithelial Neoplasia (PanIN); 3.1.3 Other Carcinomas of Ductal ... Pancreatic Neoplasms a schema:Intangible ;. schema:name "Pancreatic Neoplasms"@en ;. . ...
Singh on invasive ductal carcinoma stage 2: Tubular carcinoma is a type of breast cancer that has a better prognosis. A ... carcinoma, unless stated to be in-situ, is by definition invasive. ... Prognosis for 3 pancreatic ampullary cancer tumors. 1 removed with whipple. Chemo 7months helped 1 shrink & 1 disappear. Liver ... Breast cancer: Tubular carcinoma is a type of breast cancer that has a better prognosis. A carcinoma, unless stated to be in- ...
Pancreatic ductal adenocarcinoma (PDA) is a lethal disease. Overall survival is typically 6 months from diagnosis. Numerous ... Carcinoma, Pancreatic Ductal / classification* * Carcinoma, Pancreatic Ductal / drug therapy * Carcinoma, Pancreatic Ductal / ... Subtypes of pancreatic ductal adenocarcinoma and their differing responses to therapy Nat Med. 2011 Apr;17(4):500-3. doi: ... Pancreatic ductal adenocarcinoma (PDA) is a lethal disease. Overall survival is typically 6 months from diagnosis. Numerous ...
Pancreatic ductal adenocarcinoma (PDAC) is characterized by near-universal mutations in KRAS and frequent deregulation of ... Carcinoma, Pancreatic Ductal / genetics* * Carcinoma, Pancreatic Ductal / pathology * Cell Lineage * Genes, ras* ... KRAS, Hedgehog, Wnt and the twisted developmental biology of pancreatic ductal adenocarcinoma Nat Rev Cancer. 2010 Oct;10(10): ... Pancreatic ductal adenocarcinoma (PDAC) is characterized by near-universal mutations in KRAS and frequent deregulation of ...
Pancreatic Ductal. Carcinoma. Neoplasms, Glandular and Epithelial. Neoplasms by Histologic Type. Neoplasms. Carcinoma, Ductal. ... Carcinoma, Pancreatic Ductal Drug: Napabucasin Drug: Nab-paclitaxel Drug: Gemcitabine Phase 3 ... Neoplasms, Ductal, Lobular, and Medullary. Pancreatic Neoplasms. Digestive System Neoplasms. Neoplasms by Site. Endocrine Gland ... Must have histologically or cytologically confirmed advanced pancreatic ductal adenocarcinoma (PDAC) that is metastatic. The ...
  • A phase IB/II randomized study of mFOLFIRINOX (mFFOX) + pegylated recombinant human hyaluronidase (PEGPH20) versus mFFOX alone in patients with good performance status metastatic pancreatic adenocarcinoma (mPC): SWOG S1313 (NCT #01959139). (google.com)
  • adeno = gland ) Refers to a carcinoma featuring microscopic glandular-related tissue cytology, tissue architecture, and/or gland-related molecular products, e.g., mucin . (wikipedia.org)
  • Cancers are usually named using -carcinoma, -sarcoma or -blastoma as a suffix, with the Latin or Greek word for the organ or tissue of origin as the root. (wikipedia.org)