Adenocarcinoma sebaceous. Medical search

A malignant epithelial tumor with a glandular organization.

An adenocarcinoma producing mucin in significant amounts. (From Dorland, 27th ed)

Tumors or cancer of the LUNG.

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).

Tumors or cancer of the ESOPHAGUS.

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)

A condition with damage to the lining of the lower ESOPHAGUS resulting from chronic acid reflux (ESOPHAGITIS, REFLUX). Through the process of metaplasia, the squamous cells are replaced by a columnar epithelium with cells resembling those of the INTESTINE or the salmon-pink mucosa of the STOMACH. Barrett's columnar epithelium is a marker for severe reflux and precursor to ADENOCARCINOMA of the esophagus.

Carcinoma that arises from the PANCREATIC DUCTS. It accounts for the majority of cancers derived from the PANCREAS.

A carcinoma thought to be derived from epithelium of terminal bronchioles, in which the neoplastic tissue extends along the alveolar walls and grows in small masses within the alveoli. Involvement may be uniformly diffuse and massive, or nodular, or lobular. The neoplastic cells are cuboidal or columnar and form papillary structures. Mucin may be demonstrated in some of the cells and in the material in the alveoli, which also includes denuded cells. Metastases in regional lymph nodes, and in even more distant sites, are known to occur, but are infrequent. (From Stedman, 25th ed)

Tumors or cancer of the STOMACH.

That part of the STOMACH close to the opening from ESOPHAGUS into the stomach (cardiac orifice), the ESOPHAGOGASTRIC JUNCTION. The cardia is so named because of its closeness to the HEART. Cardia is characterized by the lack of acid-forming cells (GASTRIC PARIETAL CELLS).

Histochemical localization of immunoreactive substances using labeled antibodies as reagents.

Tumors or cancer of the COLON.

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.

The area covering the terminal portion of ESOPHAGUS and the beginning of STOMACH at the cardiac orifice.

Methods which attempt to express in replicable terms the extent of the neoplasm in the patient.

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.

A type II keratin found associated with KERATIN-19 in ductal epithelia and gastrointestinal epithelia.

Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.

A cell line derived from cultured tumor cells.

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)

Tumors or cancer of ENDOMETRIUM, the mucous lining of the UTERUS. These neoplasms can be benign or malignant. Their classification and grading are based on the various cell types and the percent of undifferentiated cells.

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.

Pathological processes that tend eventually to become malignant. (From Dorland, 27th ed)

Tumors or cancer of the INTESTINES.

Tumors or cancer of the PROSTATE.

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.

Tumors or cancer of the DUODENUM.

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.

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.

Tumors or cancer of the CECUM.

Experimentally induced mammary neoplasms in animals to provide a model for studying human BREAST NEOPLASMS.

Ability of neoplasms to infiltrate and actively destroy surrounding tissue.

An adenocarcinoma characterized by the presence of varying combinations of clear and hobnail-shaped tumor cells. There are three predominant patterns described as tubulocystic, solid, and papillary. These tumors, usually located in the female reproductive organs, have been seen more frequently in young women since 1970 as a result of the association with intrauterine exposure to diethylstilbestrol. (From Holland et al., Cancer Medicine, 3d ed)

A condition in which there is a change of one adult cell type to another similar adult cell type.

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.

Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ULCERATIVE COLITIS; FAMILIAL POLYPOSIS COLI; exposure to ASBESTOS; and irradiation of the CERVIX UTERI.

Tumors or cancer of the RECTUM.

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.

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.

Tumor or cancer of the COMMON BILE DUCT including the AMPULLA OF VATER and the SPHINCTER OF ODDI.

A type I keratin expressed predominately in gastrointestinal epithelia, MERKEL CELLS, and the TASTE BUDS of the oral mucosa.

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.

Tumors or cancer in the ILEUM region of the small intestine (INTESTINE, SMALL).

A benign epithelial tumor with a glandular organization.

The excision of the head of the pancreas and the encircling loop of the duodenum to which it is connected.

DNA present in neoplastic tissue.

Tumors or cancer in the JEJUNUM region of the small intestine (INTESTINE, SMALL).

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.

The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.

Transfer of a neoplasm from its primary site to lymph nodes or to distant parts of the body by way of the lymphatic system.

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.

A heterogeneous aggregate of at least three distinct histological types of lung cancer, including SQUAMOUS CELL CARCINOMA; ADENOCARCINOMA; and LARGE CELL CARCINOMA. They are dealt with collectively because of their shared treatment strategy.

A mixed adenocarcinoma and squamous cell or epidermoid carcinoma.

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.

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)

Experimental transplantation of neoplasms in laboratory animals for research purposes.

The muscular membranous segment between the PHARYNX and the STOMACH in the UPPER GASTROINTESTINAL TRACT.

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.

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.

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.

Excision of the whole (total gastrectomy) or part (subtotal gastrectomy, partial gastrectomy, gastric resection) of the stomach. (Dorland, 28th ed)

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.

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.

Tumors or cancer of the PARANASAL SINUSES.

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.

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.

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.

Substances that inhibit or prevent the proliferation of NEOPLASMS.

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)

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.

Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.

Surgical removal of the pancreas. (Dorland, 28th ed)

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.

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.

Tumors or cancer of the UTERINE CERVIX.

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.

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.

Tumors or cancer of the GASTROINTESTINAL TRACT, from the MOUTH to the ANAL CANAL.

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.

Tumors or cancer of the APPENDIX.

Ducts that collect PANCREATIC JUICE from the PANCREAS and supply it to the DUODENUM.

All of the processes involved in increasing CELL NUMBER including CELL DIVISION.

The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.

Tumors or cancer of the gallbladder.

Tumors or cancer of the SIGMOID COLON.

Excision of part (partial) or all (total) of the esophagus. (Dorland, 28th ed)

Benign proliferation of the ENDOMETRIUM in the UTERUS. Endometrial hyperplasia is classified by its cytology and glandular tissue. There are simple, complex (adenomatous without atypia), and atypical hyperplasia representing also the ascending risk of becoming malignant.

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.

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.

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.

A premalignant change arising in the prostatic epithelium, regarded as the most important and most likely precursor of prostatic adenocarcinoma. The neoplasia takes the form of an intra-acinar or ductal proliferation of secretory cells with unequivocal nuclear anaplasia, which corresponds to nuclear grade 2 and 3 invasive prostate cancer.

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.

A tumor of undifferentiated (anaplastic) cells of large size. It is usually bronchogenic. (From Dorland, 27th ed)

Experimentally induced new abnormal growth of TISSUES in animals to provide models for studying human neoplasms.

A pyrimidine analog that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the THYMIDYLATE SYNTHETASE conversion of deoxyuridylic acid to thymidylic acid.

In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.

Sialylated Lewis blood group carbohydrate antigen found in many adenocarcinomas of the digestive tract, especially pancreatic tumors.

Tumors or cancer of the UTERUS.

Tumors or cancer of the MAMMARY GLAND in animals (MAMMARY GLANDS, ANIMAL).

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.

Lining of the STOMACH, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. The surface cells produce MUCUS that protects the stomach from attack by digestive acid and enzymes. When the epithelium invaginates into the LAMINA PROPRIA at various region of the stomach (CARDIA; GASTRIC FUNDUS; and PYLORUS), different tubular gastric glands are formed. These glands consist of cells that secrete mucus, enzymes, HYDROCHLORIC ACID, or hormones.

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.

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.

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)

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.

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.

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)

An adenoma of the large intestine. It is usually a solitary, sessile, often large, tumor of colonic mucosa composed of mucinous epithelium covering delicate vascular projections. Hypersecretion and malignant changes occur frequently. (Stedman, 25th ed)

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.

Elements of limited time intervals, contributing to particular results or situations.

A gland in males that surrounds the neck of the URINARY BLADDER and the URETHRA. It secretes a substance that liquefies coagulated semen. It is situated in the pelvic cavity behind the lower part of the PUBIC SYMPHYSIS, above the deep layer of the triangular ligament, and rests upon the RECTUM.

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.

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.

Tomography using x-ray transmission and a computer algorithm to reconstruct the image.

Transplantation between animals of different species.

The use of two or more chemicals simultaneously or sequentially in the drug therapy of neoplasms. The drugs need not be in the same dosage form.

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)

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.

The loss of one allele at a specific locus, caused by a deletion mutation; or loss of a chromosome from a chromosome pair, resulting in abnormal HEMIZYGOSITY. It is detected when heterozygous markers for a locus appear monomorphic because one of the ALLELES was deleted.

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.

RNA present in neoplastic tissue.

A malignant neoplasm derived from glandular epithelium, in which cystic accumulations of retained secretions are formed. The neoplastic cells manifest varying degrees of anaplasia and invasiveness, and local extension and metastases occur. Cystadenocarcinomas develop frequently in the ovaries, where pseudomucinous and serous types are recognized. (Stedman, 25th ed)

Antimetabolites that are useful in cancer chemotherapy.

Endoscopic examination, therapy or surgery of the esophagus.

The proto-oncogene c-erbB-1 codes for the epidermal growth factor receptor. Its name originates from the viral homolog v-erbB which was isolated from an avian erythroblastosis virus (AEV) where it was contained as a fragment of the chicken c-ErbB-1 gene lacking the amino-terminal ligand-binding domain. Overexpression of erbB-1 genes occurs in a wide range of tumors, commonly squamous carcinomas of various sites and less commonly adenocarcinomas. The human c-erbB-1 gene is located in the chromosomal region 7p14 and 7p12.

A tumor derived from mesothelial tissue (peritoneum, pleura, pericardium). It appears as broad sheets of cells, with some regions containing spindle-shaped, sarcoma-like cells and other regions showing adenomatous patterns. Pleural mesotheliomas have been linked to exposure to asbestos. (Dorland, 27th ed)

An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.

An inorganic and water-soluble platinum complex. After undergoing hydrolysis, it reacts with DNA to produce both intra and interstrand crosslinks. These crosslinks appear to impair replication and transcription of DNA. The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle.

Removal and examination of tissue obtained through a transdermal needle inserted into the specific region, organ, or tissue being analyzed.

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.

A pair of anal glands or sacs, located on either side of the ANUS, that produce and store a dark, foul-smelling fluid in carnivorous animals such as MEPHITIDAE and DOGS. The expelled fluid is used as a defensive repellent (in skunks) or a material to mark territory (in dogs).

A malignant cystic or semicystic neoplasm. It often occurs in the ovary and usually bilaterally. The external surface is usually covered with papillary excrescences. Microscopically, the papillary patterns are predominantly epithelial overgrowths with differentiated and undifferentiated papillary serous cystadenocarcinoma cells. Psammoma bodies may be present. The tumor generally adheres to surrounding structures and produces ascites. (From Hughes, Obstetric-Gynecologic Terminology, 1972, p185)

The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.

Period after successful treatment in which there is no appearance of the symptoms or effects of the disease.

Antibodies produced by a single clone of cells.

Metastases in which the tissue of origin is unknown.

Inhaling and exhaling the smoke of burning TOBACCO.

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.

An inducibly-expressed subtype of prostaglandin-endoperoxide synthase. It plays an important role in many cellular processes and INFLAMMATION. It is the target of COX2 INHIBITORS.

Biochemical identification of mutational changes in a nucleotide sequence.

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.

Carbohydrate antigens expressed by malignant tissue. They are useful as tumor markers and are measured in the serum by means of a radioimmunoassay employing monoclonal antibodies.

Drug therapy given to augment or stimulate some other form of treatment such as surgery or radiation therapy. Adjuvant chemotherapy is commonly used in the therapy of cancer and can be administered before or after the primary treatment.

Human colonic ADENOCARCINOMA cells that are able to express differentiation features characteristic of mature intestinal cells such as the GOBLET CELLS.

Presence of fluid in the PLEURAL CAVITY as a complication of malignant disease. Malignant pleural effusions often contain actual malignant cells.

A transmembrane mucin that is found in a broad variety of epithelial tissue. Mucin-4 may play a role in regulating cellular adhesion and in cell surface signaling from the ERBB-2 RECEPTOR PROTEIN-TYROSINE KINASE. Mucin-4 is a heterodimer of alpha and beta chains. The alpha and beta chains result from the proteolytic cleavage of a precursor protein.

A type of IN SITU HYBRIDIZATION in which target sequences are stained with fluorescent dye so their location and size can be determined using fluorescence microscopy. This staining is sufficiently distinct that the hybridization signal can be seen both in metaphase spreads and in interphase nuclei.

Retrograde flow of gastric juice (GASTRIC ACID) and/or duodenal contents (BILE ACIDS; PANCREATIC JUICE) into the distal ESOPHAGUS, commonly due to incompetence of the LOWER ESOPHAGEAL SPHINCTER.

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.

Excision of the uterus.

A selective increase in the number of copies of a gene coding for a specific protein without a proportional increase in other genes. It occurs naturally via the excision of a copy of the repeating sequence from the chromosome and its extrachromosomal replication in a plasmid, or via the production of an RNA transcript of the entire repeating sequence of ribosomal RNA followed by the reverse transcription of the molecule to produce an additional copy of the original DNA sequence. Laboratory techniques have been introduced for inducing disproportional replication by unequal crossing over, uptake of DNA from lysed cells, or generation of extrachromosomal sequences from rolling circle replication.

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.

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)

An embryonic structure originating from the ALLANTOIS. It is a canal connecting the fetal URINARY BLADDER and the UMBILICUS. It is normally converted into a fibrous cord postnatally. When the canal fails to be filled and remains open (patent urachus), urine leaks through the umbilicus.

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.

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.

Substances that increase the risk of NEOPLASMS in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included.

Tumors or cancer of the LIVER.

Radiotherapy given to augment some other form of treatment such as surgery or chemotherapy. Adjuvant radiotherapy is commonly used in the therapy of cancer and can be administered before or after the primary treatment.

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.

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.

Neoplasms composed of more than one type of neoplastic tissue.

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)

Tumors or cancer of the NOSE.

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.

Tumors or cancer of the SALIVARY GLANDS.

The number of new cases of a given disease during a given period in a specified population. It also is used for the rate at which new events occur in a defined population. It is differentiated from PREVALENCE, which refers to all cases, new or old, in the population at a given time.

The segment of LARGE INTESTINE between the CECUM and the RECTUM. It includes the ASCENDING COLON; the TRANSVERSE COLON; the DESCENDING COLON; and the SIGMOID COLON.

A usually small, slow-growing neoplasm composed of islands of rounded, oxyphilic, or spindle-shaped cells of medium size, with moderately small vesicular nuclei, and covered by intact mucosa with a yellow cut surface. The tumor can occur anywhere in the gastrointestinal tract (and in the lungs and other sites); approximately 90% arise in the appendix. It is now established that these tumors are of neuroendocrine origin and derive from a primitive stem cell. (From Stedman, 25th ed & Holland et al., Cancer Medicine, 3d ed, p1182)

Addition of methyl groups to DNA. DNA methyltransferases (DNA methylases) perform this reaction using S-ADENOSYLMETHIONINE as the methyl group donor.

Tumors or cancer of the BILE DUCTS.

A BETARETROVIRUS that causes pulmonary adenomatosis in sheep (PULMONARY ADENOMATOSIS, OVINE).

Lining of the INTESTINES, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. In the SMALL INTESTINE, the mucosa is characterized by a series of folds and abundance of absorptive cells (ENTEROCYTES) with MICROVILLI.

Tumors or cancer of the DIGESTIVE SYSTEM.

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.

Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.

The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.

A class of compounds that contain a -NH2 and a -NO radical. Many members of this group have carcinogenic and mutagenic properties.

The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.

Tumor suppressor genes located on the short arm of human chromosome 17 and coding for the phosphoprotein p53.

A malignant neoplasm that contains elements of carcinoma and sarcoma so extensively intermixed as to indicate neoplasia of epithelial and mesenchymal tissue. (Stedman, 25th ed)

Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.

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.

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.

Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.

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.

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.

Tumors or cancer of the VAGINA.

Preliminary cancer therapy (chemotherapy, radiation therapy, hormone/endocrine therapy, immunotherapy, hyperthermia, etc.) that precedes a necessary second modality of treatment.

A contagious, neoplastic, pulmonary disease of sheep characterized by hyperplasia and hypertrophy of pneumocytes and epithelial cells of the lung. It is caused by JAAGSIEKTE SHEEP RETROVIRUS.

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.

Study of intracellular distribution of chemicals, reaction sites, enzymes, etc., by means of staining reactions, radioactive isotope uptake, selective metal distribution in electron microscopy, or other methods.

Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.

One or more layers of EPITHELIAL CELLS, supported by the basal lamina, which covers the inner or outer surfaces of the body.

Retrograde flow of duodenal contents (BILE ACIDS; PANCREATIC JUICE) into the STOMACH.

Loss of p21(WAF1) compartmentalisation in sebaceous carcinoma compared with sebaceous hyperplasia and sebaceous adenoma. (1/35)

AIMS: Regulation of cell cycle progression is a fundamental control process, linked to cellular differentiation and apoptosis in normal tissues. p21(WAF1) is a nuclear protein that regulates cell cycle progression. p21(WAF1) can be transcriptionally upregulated by p53, but may be activated independently of p53-for example, during terminal differentiation. Loss of topological control of p21(WAF1) expression is an early feature of malignancy in the colorectal system. Similar to the colonic mucosa, sebaceous glands contain cells that are constantly going through a process of cell division, differentiation, and cell death. This study investigated the expression of p53, p21(WAF1), and the proliferation marker Ki67 in normal sebaceous glands, sebaceous adenoma, sebaceoma, and sebaceous carcinoma. METHODS: Serial sections were stained with monoclonal antibodies to p21(WAF1), p53, and Ki67 (MIB1) using standard immunohistochemical techniques. RESULTS: In normal sebaceous glands, p21(WAF1) positive cells were only seen within the differentiating compartment, which was spatially distinct from the cycling peripheral Ki67 positive cells. In sebaceous adenoma and sebaceoma, topological control was maintained, with the distribution of markers being similar to that seen in normal sebaceous glands. Loss of topological control of markers of cellular control was seen in sebaceous carcinoma only. This contrasts with colonic tumours, in which loss of p21 compartmentalisation is seen in adenomas at an early stage of tumour progression. CONCLUSION: This work confirms the hypothesis that the dysregulation of cell cycle progression is an important process in the development of malignancy within sebaceous glands, although loss of topological control was seen only in sebaceous carcinoma. (+info)

Immunohistochemical staining for adipophilin, perilipin and TIP47. (2/35)

BACKGROUND: The presence of lipid in the cell cytoplasm is useful for supporting the diagnosis of sebaceous gland carcinoma (SGC). Currently this requires histochemical stains that are carried out on frozen sections of unprocessed tissue. Recently, several anti-adipocytic antibodies that recognise proteins associated with lipid vesicles have been described. These antibodies can be applied to paraffin-wax sections. AIM: To assess the ability of anti-adipocytic antibodies to identify intracytoplasmic lipid in SGC. METHODS: Immunohistochemistry with a monoclonal antibody to adipophilin and polyclonal antibodies to perilipin and TIP47/PP17 was carried out on archival, formalin-fixed, paraffin-wax-embedded sections of 26 samples of SGC. The immunostaining was compared with 22 other eyelid tumours (11 basal cell carcinomas (BCC), 10 squamous cell carcinomas (SCC) and 1 Merkel cell tumour). RESULTS: Immunohistochemical staining was positive in 23, 10 and 2 cases of 26 SGC with adipophilin, perilipin and TIP47, respectively. The positive staining identified cytoplasmic lipid vesicles. Anti-adipophilin was positive in five other eyelid tumours (4 BCC and 1 SCC) staining small cytoplasmic granules that can be easily distinguished from the staining in SGC. CONCLUSIONS: Immunohistochemical staining for adipophilin and perilipin is a useful ancillary technique for the demonstration of lipid in SGC that may be applied to paraffin-wax sections. (+info)

Complications of mitomycin C therapy in 100 eyes with ocular surface neoplasia. (3/35)

AIM: To determine the complications associated with mitomycin C (MMC) in the treatment of ocular surface neoplasia. METHODS: A retrospective and consecutive study of 100 eyes in 91 patients with ocular surface neoplasia treated with MMC in a single centre between November 1998 and January 2005. Outcome measures included complications of MMC and the treatment required for these complications. RESULTS: One to three 7 day cycles of topical MMC 0.04% four times a day were given to 59 eyes with localised corneal-conjunctival intraepithelial neoplasia (CIN), 19 eyes with diffuse CIN, six eyes with recurrent CIN, one eye with ocular surface squamous cell carcinoma, three eyes with primary acquired melanosis (PAM) with atypia, nine eyes with conjunctival malignant melanoma (MM), two eyes with sebaceous carcinoma with pagetoid spread, and one eye with recurrent atypical fibroxanthoma. Nine patients had bilateral CIN. 31 (34%) cases developed an allergic reaction to MMC and 14 (14%) eyes had epiphora secondary to punctal stenosis at a mean follow up period of 26.5 months. CONCLUSION: In the largest study looking at complications of topical MMC in the treatment of ocular surface neoplasia, allergic reaction and punctal stenosis are relatively common. Serious complications were not observed suggesting the safe use of MMC in mid-term follow up. (+info)

Activator protein-1 activity regulates epithelial tumor cell identity. (4/35)

To examine the consequences of inhibiting activator protein-1 (AP-1) transcription factors in skin, transgenic mice were generated, which use the tetracycline system to conditionally express A-FOS, a dominant negative that inhibits AP-1 DNA binding. Older mice develop mild alopecia and hyperplasia of sebaceous glands, particularly around the eyes. When A-FOS was expressed during chemical-induced skin carcinogenesis, mice do not develop characteristic benign and malignant squamous lesions but instead develop benign sebaceous adenomas containing a signature mutation in the H-ras proto-oncogene. Inhibiting AP-1 activity after tumor formation caused squamous tumors to transdifferentiate into sebaceous tumors. Furthermore, reactivating AP-1 in sebaceous tumors results in a reciprocal transdifferentiation into squamous tumors. In both cases of transdifferentiation, individual cells express molecular markers for both cell types, indicating individual tumor cells have the capacity to express multiple lineages. Molecular characterization of cultured keratinocytes and tumor material indicates that AP-1 regulates the balance between the wnt/beta-catenin and hedgehog signaling pathways that determine squamous and sebaceous lineages, respectively. Chromatin immunoprecipitation analysis indicates that c-Jun binds several wnt promoters, which are misregulated by A-FOS expression, suggesting that members of the wnt pathway can be a primary targets of AP-1 transcriptional regulation. Thus, AP-1 activity regulates tumor cell lineage and is essential to maintain the squamous tumor cell identity. (+info)

A clinicopathological study of eyelid malignancies from central India. (5/35)

BACKGROUND: Eyelid malignancies are completely treatable if detected early. The treatment depends on the invasiveness of the cancer which in turn depends on the type of malignancy. AIM: The aim of the study was to characterize the distribution of the types of eyelid malignancies in central India. SETTINGS AND DESIGN: The study was conducted in the Department of Plastic and Maxillofacial Surgery at a tertiary care hospital. MATERIALS AND METHODS: We report a series of 27 cases of eyelid malignancies. In the same case series, we also include a case of malignant hemangiopericytoma which is an extremely rare form of eyelid malignancy worldwide. STATISTICAL ANALYSIS: Depending on the underlying statistical distribution, either analysis of variance (ANOVA) or the Kruskal-Wallis (K-W) test was used to assess the differential distribution of these variables across the types of eyelid malignancies observed in this study. RESULTS: We observed that sebaceous cell carcinoma (approximately 37%) was almost as prevalent as basal cell carcinoma (approximately 44%) in the study subjects and had an earlier age of occurrence and a more rapid clinical course. CONCLUSIONS: Sebaceous cell carcinoma of the eyelid is almost as common as basal cell carcinoma in a large tertiary care centre in central India. (+info)

Dual role of inactivating Lef1 mutations in epidermis: tumor promotion and specification of tumor type. (6/35)

The NH(2) terminus of LEF1 is frequently mutated in human sebaceous tumors. To investigate how this contributes to cancer, we did two-stage chemical carcinogenesis on K14DeltaNLef1 transgenic mice, which express NH(2)-terminally truncated Lef1 in the epidermal basal layer. Transgenic mice developed more tumors, more rapidly than littermate controls, even without exposure to tumor promoter. They developed sebaceous tumors, whereas controls developed squamous cell carcinomas. K14DeltaNLef1 epidermis failed to up-regulate p53 and p21 proteins during tumorigenesis or in response to UV irradiation, and this correlated with impaired p14ARF induction. We propose that LEF1 NH(2)-terminal mutations play a dual role in skin cancer, specifying tumor type by inhibiting Wnt signaling and acting as a tumor promoter by preventing induction of p53. (+info)

Role of fine needle aspiration cytology in diagnosis of eyelid sebaceous carcinoma. (7/35)

Sebaceous carcinoma of the ocular adnexa is a malignant neoplasm which can exhibit aggressive local behavior and can metastasize to regional lymph nodes and distant organs. The neoplasm is known to masquerade as other benign and less malignant lesions, resulting in delay in diagnosis and relative high morbidity and mortality. Fine needle aspiration cytology (FNAC) of recurrent upper eyelid nodules treated elsewhere as chalazion was done. Cytological smears were suggestive of malignancy. Subsequently histopathology confirmed the diagnosis of sebaceous gland carcinoma. Eyelid reconstruction was done after histopathologically confirmed tumor-free margins. The article highlights the role of FNAC in early diagnosis and subsequent appropriate surgical management of eyelid sebaceous gland carcinoma to prevent recurrence and metastasis. (+info)

Adnexal skin tumors in Zaria, Nigeria. (8/35)

BACKGROUND: Adnexal skin tumors share many features in common and differentiate along one line. Their detailed morphological classification is difficult because of the variety of tissue elements and patterns seen. They may be clinically confused with other cutaneous tumors. The aim of this report is to review and classify all adnexal tumors seen in a pathology department over a 16-year period. METHOD: A 16-year retrospective analysis of all adnexal skin tumors seen in a large University Teaching Hospital in Nigeria from January 1991- December 2006. All tissue specimens were fixed in 10% formalin, processed in paraffin wax and stained with Haematoxylin and Eosin. Histology slides were retrieved, studied and lesions characterized. RESULTS: Fifty-two adnexal tumors were seen, accounting for 0.9% of all cutaneous tumors seen within the same period. The median age was 33 years (range: 4 days-70 years). Clinical presentations varied from discreet swellings and nodules to ulcerated masses. Five patients presented with recurrent lesions. Only two cases had a clinical diagnosis of adnexal tumor. Twenty-four (46%) of the lesions were distributed in the head and neck region. Duration of symptoms was 2 months to 15 years (median: 12 months). Tumours of the sweat gland were the commonest--41 (78.8%); they comprised predominantly eccrine acrospiroma (17), characterized histologically by solid nests of round to polygonal cells with clear to eosinophilic cytoplasm, forming tubules in areas. Tumours of sebaceous gland were 7 (13.5%); they comprised mainly Nevus sebaceous of Jadassohn (6), composed of immature sebaceous glands and pilar structures microscopically and a solitary sebaceous adenoma. Tumours of hair follicle were 4 (7.7%) and included trichoepithelioma, characterized microscopically by multiple horn cysts and epithelial tracts connecting abortive pilar structures and a trichofolliculoma. Forty-six lesions (88.5%) were benign and six (11.5%) malignant. CONCLUSION: Adnexal skin tumors have distinct histological patterns which differentiates them from other cutaneous tumors. They are commonly distributed in the head, neck and trunk. The commonest variants are those of eccrine sweat gland origin. Malignant adnexal tumors are uncommon in our setting. (+info)

Adenocarcinoma is a term used to describe a variety of different types of cancer that arise in glandular tissue, including:

1. Colorectal adenocarcinoma (cancer of the colon or rectum)
2. Breast adenocarcinoma (cancer of the breast)
3. Prostate adenocarcinoma (cancer of the prostate gland)
4. Pancreatic adenocarcinoma (cancer of the pancreas)
5. Lung adenocarcinoma (cancer of the lung)
6. Thyroid adenocarcinoma (cancer of the thyroid gland)
7. Skin adenocarcinoma (cancer of the skin)

The symptoms of adenocarcinoma depend on the location of the cancer and can include:

1. Blood in the stool or urine
2. Abdominal pain or discomfort
3. Changes in bowel habits
4. Unusual vaginal bleeding (in the case of endometrial adenocarcinoma)
5. A lump or thickening in the breast or elsewhere
6. Weight loss
7. Fatigue
8. Coughing up blood (in the case of lung adenocarcinoma)

The diagnosis of adenocarcinoma is typically made through a combination of imaging tests, such as CT scans, MRI scans, and PET scans, and a biopsy, which involves removing a sample of tissue from the affected area and examining it under a microscope for cancer cells.

Treatment options for adenocarcinoma depend on the location of the cancer and can include:

1. Surgery to remove the tumor
2. Chemotherapy, which involves using drugs to kill cancer cells
3. Radiation therapy, which involves using high-energy X-rays or other particles to kill cancer cells
4. Targeted therapy, which involves using drugs that target specific molecules on cancer cells to kill them
5. Immunotherapy, which involves using drugs that stimulate the immune system to fight cancer cells.

The prognosis for adenocarcinoma is generally good if the cancer is detected and treated early, but it can be more challenging to treat if the cancer has spread to other parts of the body.

Examples of 'Adenocarcinoma, Mucinous' in medical literature:

* The patient was diagnosed with adenocarcinoma, mucinous type, in their colon after undergoing a colonoscopy and biopsy. (From the Journal of Clinical Oncology)

* The patient had a history of adenocarcinoma, mucinous type, in their breast and was being monitored for potential recurrence. (From the Journal of Surgical Oncology)

* The tumor was found to be an adenocarcinoma, mucinous type, with a high grade and was treated with surgery and chemotherapy. (From the Journal of Gastrointestinal Oncology)

Synonyms for 'Adenocarcinoma, Mucinous' include:

* Mucinous adenocarcinoma
* Colon adenocarcinoma, mucinous type
* Rectal adenocarcinoma, mucinous type
* Adenocarcinoma of the colon and rectum, mucinous type.

There are several types of lung neoplasms, including:

1. Adenocarcinoma: This is the most common type of lung cancer, accounting for approximately 40% of all lung cancers. It is a malignant tumor that originates in the glands of the respiratory tract and can be found in any part of the lung.
2. Squamous cell carcinoma: This type of lung cancer accounts for approximately 25% of all lung cancers and is more common in men than women. It is a malignant tumor that originates in the squamous cells lining the airways of the lungs.
3. Small cell lung cancer (SCLC): This is a highly aggressive form of lung cancer that accounts for approximately 15% of all lung cancers. It is often found in the central parts of the lungs and can spread quickly to other parts of the body.
4. Large cell carcinoma: This is a rare type of lung cancer that accounts for only about 5% of all lung cancers. It is a malignant tumor that originates in the large cells of the respiratory tract and can be found in any part of the lung.
5. Bronchioalveolar carcinoma (BAC): This is a rare type of lung cancer that originates in the cells lining the airways and alveoli of the lungs. It is more common in women than men and tends to affect older individuals.
6. Lymphangioleiomyomatosis (LAM): This is a rare, progressive, and often fatal lung disease that primarily affects women of childbearing age. It is characterized by the growth of smooth muscle-like cells in the lungs and can lead to cysts, lung collapse, and respiratory failure.
7. Hamartoma: This is a benign tumor that originates in the tissue of the lungs and is usually found in children. It is characterized by an overgrowth of normal lung tissue and can be treated with surgery.
8. Secondary lung cancer: This type of cancer occurs when cancer cells from another part of the body spread to the lungs through the bloodstream or lymphatic system. It is more common in people who have a history of smoking or exposure to other carcinogens.
9. Metastatic cancer: This type of cancer occurs when cancer cells from another part of the body spread to the lungs through the bloodstream or lymphatic system. It is more common in people who have a history of smoking or exposure to other carcinogens.
10. Mesothelioma: This is a rare and aggressive form of cancer that originates in the lining of the lungs or abdomen. It is caused by asbestos exposure and can be treated with surgery, chemotherapy, and radiation therapy.

Lung diseases can also be classified based on their cause, such as:

1. Infectious diseases: These are caused by bacteria, viruses, or other microorganisms and can include pneumonia, tuberculosis, and bronchitis.
2. Autoimmune diseases: These are caused by an overactive immune system and can include conditions such as sarcoidosis and idiopathic pulmonary fibrosis.
3. Genetic diseases: These are caused by inherited mutations in genes that affect the lungs and can include cystic fibrosis and primary ciliary dyskinesia.
4. Environmental diseases: These are caused by exposure to harmful substances such as tobacco smoke, air pollution, and asbestos.
5. Radiological diseases: These are caused by exposure to ionizing radiation and can include conditions such as radiographic breast cancer and lung cancer.
6. Vascular diseases: These are caused by problems with the blood vessels in the lungs and can include conditions such as pulmonary embolism and pulmonary hypertension.
7. Tumors: These can be benign or malignant and can include conditions such as lung metastases and lung cancer.
8. Trauma: This can include injuries to the chest or lungs caused by accidents or other forms of trauma.
9. Congenital diseases: These are present at birth and can include conditions such as bronchopulmonary foregut malformations and congenital cystic adenomatoid malformation.

Each type of lung disease has its own set of symptoms, diagnosis, and treatment options. It is important to seek medical attention if you experience any persistent or severe respiratory symptoms, as early diagnosis and treatment can improve outcomes and quality of life.

Pancreatic adenocarcinoma is the most common type of malignant pancreatic neoplasm and accounts for approximately 85% of all pancreatic cancers. It originates in the glandular tissue of the pancreas and has a poor prognosis, with a five-year survival rate of less than 10%.

Pancreatic neuroendocrine tumors (PNETs) are less common but more treatable than pancreatic adenocarcinoma. These tumors originate in the hormone-producing cells of the pancreas and can produce excess hormones that cause a variety of symptoms, such as diabetes or high blood sugar. PNETs are classified into two main types: functional and non-functional. Functional PNETs produce excess hormones and are more aggressive than non-functional tumors.

Other rare types of pancreatic neoplasms include acinar cell carcinoma, ampullary cancer, and oncocytic pancreatic neuroendocrine tumors. These tumors are less common than pancreatic adenocarcinoma and PNETs but can be equally aggressive and difficult to treat.

The symptoms of pancreatic neoplasms vary depending on the type and location of the tumor, but they often include abdominal pain, weight loss, jaundice, and fatigue. Diagnosis is typically made through a combination of imaging tests such as CT scans, endoscopic ultrasound, and biopsy. Treatment options for pancreatic neoplasms depend on the type and stage of the tumor but may include surgery, chemotherapy, radiation therapy, or a combination of these.

Prognosis for patients with pancreatic neoplasms is generally poor, especially for those with advanced stages of disease. However, early detection and treatment can improve survival rates. Research into the causes and mechanisms of pancreatic neoplasms is ongoing, with a focus on developing new and more effective treatments for these devastating diseases.

Types of Esophageal Neoplasms:

1. Barrett's Esophagus: This is a precancerous condition that occurs when the cells lining the esophagus undergo abnormal changes, increasing the risk of developing esophageal cancer.
2. Adenocarcinoma: This is the most common type of esophageal cancer, accounting for approximately 70% of all cases. It originates in the glands that line the esophagus.
3. Squamous Cell Carcinoma: This type of cancer accounts for about 20% of all esophageal cancers and originates in the squamous cells that line the esophagus.
4. Other rare types: Other rare types of esophageal neoplasms include lymphomas, sarcomas, and carcinoid tumors.

Causes and Risk Factors:

1. Gastroesophageal reflux disease (GERD): Long-standing GERD can lead to the development of Barrett's esophagus, which is a precancerous condition that increases the risk of developing esophageal cancer.
2. Obesity: Excess body weight is associated with an increased risk of developing esophageal cancer.
3. Diet: A diet high in processed meats and low in fruits and vegetables may increase the risk of developing esophageal cancer.
4. Alcohol consumption: Heavy alcohol consumption is a known risk factor for esophageal cancer.
5. Smoking: Cigarette smoking is a major risk factor for esophageal cancer.
6. Family history: Having a family history of esophageal cancer or other cancers may increase an individual's risk.
7. Age: The risk of developing esophageal cancer increases with age, with most cases occurring in people over the age of 50.
8. Other medical conditions: Certain medical conditions, such as achalasia, may increase the risk of developing esophageal cancer.

Symptoms and Diagnosis:

1. Dysphagia (difficulty swallowing): This is the most common symptom of esophageal cancer, and can be caused by a narrowing or blockage of the esophagus due to the tumor.
2. Chest pain or discomfort: Pain in the chest or upper back can be a symptom of esophageal cancer.
3. Weight loss: Losing weight without trying can be a symptom of esophageal cancer.
4. Coughing or hoarseness: If the tumor is obstructing the airway, it can cause coughing or hoarseness.
5. Fatigue: Feeling tired or weak can be a symptom of esophageal cancer.
6. Diagnosis: A diagnosis of esophageal cancer is typically made through a combination of endoscopy, imaging tests (such as CT scans), and biopsies.

Treatment Options:

1. Surgery: Surgery is the primary treatment for esophageal cancer, and can involve removing the tumor and some surrounding tissue, or removing the entire esophagus and replacing it with a section of stomach or intestine.
2. Chemotherapy: Chemotherapy involves using drugs to kill cancer cells, and is often used in combination with surgery to treat esophageal cancer.
3. Radiation therapy: Radiation therapy uses high-energy X-rays to kill cancer cells, and can be used alone or in combination with surgery or chemotherapy.
4. Targeted therapy: Targeted therapy drugs are designed to target specific molecules that are involved in the growth and spread of cancer cells, and can be used in combination with other treatments.

Prognosis and Survival Rate:

1. The prognosis for esophageal cancer is generally poor, with a five-year survival rate of around 20%.
2. Factors that can improve the prognosis include early detection, small tumor size, and absence of spread to lymph nodes or other organs.
3. The overall survival rate for esophageal cancer has not improved much over the past few decades, but advances in treatment have led to a slight increase in survival time for some patients.

Lifestyle Changes and Prevention:

1. Avoiding tobacco and alcohol: Tobacco and alcohol are major risk factors for esophageal cancer, so avoiding them can help reduce the risk of developing the disease.
2. Maintaining a healthy diet: Eating a balanced diet that is high in fruits, vegetables, and whole grains can help protect against esophageal cancer.
3. Managing obesity: Obesity is a risk factor for esophageal cancer, so maintaining a healthy weight through diet and exercise can help reduce the risk of developing the disease.
4. Reducing exposure to pollutants: Exposure to certain chemicals and pollutants, such as pesticides and asbestos, has been linked to an increased risk of esophageal cancer. Avoiding these substances can help reduce the risk of developing the disease.
5. Getting regular screening: Regular screening for Barrett's esophagus, a precancerous condition that can develop in people with gastroesophageal reflux disease (GERD), can help detect and treat esophageal cancer early, when it is most treatable.

Current Research and Future Directions:

1. Targeted therapies: Researchers are working on developing targeted therapies that can specifically target the genetic mutations that drive the growth of esophageal cancer cells. These therapies may be more effective and have fewer side effects than traditional chemotherapy.
2. Immunotherapy: Immunotherapy, which uses the body's immune system to fight cancer, is being studied as a potential treatment for esophageal cancer. Researchers are working on developing vaccines and other immunotherapies that can help the body recognize and attack cancer cells.
3. Precision medicine: With the help of advanced genomics and precision medicine, researchers are working to identify specific genetic mutations that drive the growth of esophageal cancer in each patient. This information can be used to develop personalized treatment plans that are tailored to the individual patient's needs.
4. Early detection: Researchers are working on developing new methods for early detection of esophageal cancer, such as using machine learning algorithms to analyze medical images and detect signs of cancer at an early stage.
5. Lifestyle modifications: Studies have shown that lifestyle modifications, such as quitting smoking and maintaining a healthy diet, can help reduce the risk of developing esophageal cancer. Researchers are working on understanding the specific mechanisms by which these modifications can help prevent the disease.

In conclusion, esophageal cancer is a complex and aggressive disease that is often diagnosed at an advanced stage. However, with advances in technology, research, and treatment options, there is hope for improving outcomes for patients with this disease. By understanding the risk factors, early detection methods, and current treatments, as well as ongoing research and future directions, we can work towards a future where esophageal cancer is more manageable and less deadly.

The term "papillary" refers to the fact that the cancer cells grow in a finger-like shape, with each cell forming a small papilla (bump) on the surface of the tumor. APC is often slow-growing and may not cause any symptoms in its early stages.

APC is generally considered to be less aggressive than other types of cancer, such as ductal carcinoma in situ (DCIS) or invasive breast cancer. However, it can still spread to other parts of the body if left untreated. Treatment options for APC may include surgery, radiation therapy, and/or hormone therapy, depending on the location and stage of the cancer.

It's worth noting that APC is sometimes referred to as "papillary adenocarcinoma" or simply "papillary cancer." However, these terms are often used interchangeably with "adenocarcinoma, papillary" in medical literature and clinical practice.

The condition is named after Dr. Norman Barrett, who first described it in 1956. It is a precancerous condition, meaning that if left untreated, it can progress to esophageal cancer over time. The exact cause of Barrett esophagus is not fully understood, but chronic acid reflux is thought to play a role in its development.

The symptoms of Barrett esophagus are similar to those of GERD and may include heartburn, difficulty swallowing, chest pain, and regurgitation of food. The condition can be diagnosed through an endoscopy, which involves inserting a flexible tube with a camera into the esophagus to visualize the cells lining the esophagus.

Treatment for Barrett esophagus typically involves controlling the underlying acid reflux through lifestyle changes and medications. In some cases, surgery may be necessary to repair any damage to the esophageal lining or to strengthen the lower esophageal sphincter (LES), which is the muscle that separates the esophagus from the stomach and prevents acid reflux.

It's important for individuals with chronic acid reflux to be screened regularly for Barrett esophagus, as early detection and treatment can help prevent the development of esophageal cancer.

The carcinogenesis process of PDAC usually starts with the accumulation of genetic mutations in the pancreatic duct cells, which progressively leads to the formation of a premalignant lesion called PanIN (pancreatic intraepithelial neoplasia). Over time, these lesions can develop into invasive adenocarcinoma, which is PDAC.

The main risk factor for developing PDAC is smoking, but other factors such as obesity, diabetes, and family history of pancreatic cancer also contribute to the development of the disease. Symptoms of PDAC are often non-specific and late-stage, which makes early diagnosis challenging.

The treatment options for PDAC are limited, and the prognosis is generally poor. Surgery is the only potentially curative treatment, but only a small percentage of patients are eligible for surgical resection due to the locally advanced nature of the disease at the time of diagnosis. Chemotherapy, radiation therapy, and targeted therapies are used to palliate symptoms and improve survival in non-surgical cases.

PDAC is an aggressive and lethal cancer, and there is a need for better diagnostic tools and more effective treatment strategies to improve patient outcomes.

There are several types of stomach neoplasms, including:

1. Adenocarcinoma: This is the most common type of stomach cancer, accounting for approximately 90% of all cases. It begins in the glandular cells that line the stomach and can spread to other parts of the body.
2. Squamous cell carcinoma: This type of cancer begins in the squamous cells that cover the outer layer of the stomach. It is less common than adenocarcinoma but more likely to be found in the upper part of the stomach.
3. Gastric mixed adenocarcinomasquamous cell carcinoma: This type of cancer is a combination of adenocarcinoma and squamous cell carcinoma.
4. Lymphoma: This is a cancer of the immune system that can occur in the stomach. It is less common than other types of stomach cancer but can be more aggressive.
5. Carcinomas of the stomach: These are malignant tumors that arise from the epithelial cells lining the stomach. They can be subdivided into adenocarcinoma, squamous cell carcinoma, and others.
6. Gastric brunner's gland adenoma: This is a rare type of benign tumor that arises from the Brunner's glands in the stomach.
7. Gastric polyps: These are growths that occur on the lining of the stomach and can be either benign or malignant.

The symptoms of stomach neoplasms vary depending on the location, size, and type of tumor. Common symptoms include abdominal pain, nausea, vomiting, weight loss, and difficulty swallowing. Diagnosis is usually made through a combination of endoscopy, imaging studies (such as CT or PET scans), and biopsy. Treatment depends on the type and stage of the tumor and may include surgery, chemotherapy, radiation therapy, or a combination of these. The prognosis for stomach neoplasms varies depending on the type and stage of the tumor, but early detection and treatment can improve outcomes.

There are several types of colonic neoplasms, including:

1. Adenomas: These are benign growths that are usually precursors to colorectal cancer.
2. Carcinomas: These are malignant tumors that arise from the epithelial lining of the colon.
3. Sarcomas: These are rare malignant tumors that arise from the connective tissue of the colon.
4. Lymphomas: These are cancers of the immune system that can affect the colon.

Colonic neoplasms can cause a variety of symptoms, including bleeding, abdominal pain, and changes in bowel habits. They are often diagnosed through a combination of medical imaging tests (such as colonoscopy or CT scan) and biopsy. Treatment for colonic neoplasms depends on the type and stage of the tumor, and may include surgery, chemotherapy, and/or radiation therapy.

Overall, colonic neoplasms are a common condition that can have serious consequences if left untreated. It is important for individuals to be aware of their risk factors and to undergo regular screening for colon cancer to help detect and treat any abnormal growths or tumors in the colon.

SCC typically appears as a firm, flat, or raised bump on the skin, and may be pink, red, or scaly. The cancer cells are usually well-differentiated, meaning they resemble normal squamous cells, but they can grow rapidly and invade surrounding tissues if left untreated.

SCC is more common in fair-skinned individuals and those who spend a lot of time in the sun, as UV radiation can damage the skin cells and increase the risk of cancer. The cancer can also spread to other parts of the body, such as lymph nodes or organs, and can be life-threatening if not treated promptly and effectively.

Treatment for SCC usually involves surgery to remove the cancerous tissue, and may also include radiation therapy or chemotherapy to kill any remaining cancer cells. Early detection and treatment are important to improve outcomes for patients with SCC.

Endometrial neoplasms are abnormal growths or tumors that develop in the lining of the uterus, known as the endometrium. These growths can be benign (non-cancerous) or malignant (cancerous). The most common type of endometrial neoplasm is endometrial hyperplasia, which is a condition where the endometrium grows too thick and can become cancerous if left untreated. Other types of endometrial neoplasms include endometrial adenocarcinoma, which is the most common type of uterine cancer, and endometrial sarcoma, which is a rare type of uterine cancer that develops in the muscle or connective tissue of the uterus.

Endometrial neoplasms can be caused by a variety of factors, including hormonal imbalances, genetic mutations, and exposure to certain chemicals or radiation. Risk factors for developing endometrial neoplasms include obesity, early onset of menstruation, late onset of menopause, never being pregnant or having few or no full-term pregnancies, and taking hormone replacement therapy or other medications that can increase estrogen levels.

Symptoms of endometrial neoplasms can include abnormal vaginal bleeding, painful urination, and pelvic pain or discomfort. Treatment for endometrial neoplasms depends on the type and stage of the condition, and may involve surgery, radiation therapy, chemotherapy, or hormone therapy. In some cases, a hysterectomy (removal of the uterus) may be necessary.

In summary, endometrial neoplasms are abnormal growths that can develop in the lining of the uterus and can be either benign or malignant. They can be caused by a variety of factors and can cause symptoms such as abnormal bleeding and pelvic pain. Treatment depends on the type and stage of the condition, and may involve surgery, radiation therapy, chemotherapy, or hormone therapy.

Multiple primary neoplasms can arise in different organs or tissues throughout the body, such as the breast, colon, prostate, lung, or skin. Each tumor is considered a separate entity, with its own unique characteristics, including size, location, and aggressiveness. Treatment for multiple primary neoplasms typically involves surgery, chemotherapy, radiation therapy, or a combination of these modalities.

The diagnosis of multiple primary neoplasms can be challenging due to the overlapping symptoms and radiological findings between the different tumors. Therefore, it is essential to have a thorough clinical evaluation and diagnostic workup to rule out other possible causes of the symptoms and confirm the presence of multiple primary neoplasms.

Multiple primary neoplasms are more common than previously thought, with an estimated prevalence of 2% to 5% in some populations. The prognosis for patients with multiple primary neoplasms varies depending on the location, size, and aggressiveness of each tumor, as well as the patient's overall health status.

It is important to note that multiple primary neoplasms are not the same as metastatic cancer, in which a single primary tumor spreads to other parts of the body. Multiple primary neoplasms are distinct tumors that arise independently from different primary sites within the body.

Examples of precancerous conditions include:

1. Dysplasia: This is a condition where abnormal cells are present in the tissue, but have not yet invaded surrounding tissues. Dysplasia can be found in organs such as the cervix, colon, and breast.
2. Carcinoma in situ (CIS): This is a condition where cancer cells are present in the tissue, but have not yet invaded surrounding tissues. CIS is often found in organs such as the breast, prostate, and cervix.
3. Atypical hyperplasia: This is a condition where abnormal cells are present in the tissue, but they are not yet cancerous. Atypical hyperplasia can be found in organs such as the breast and uterus.
4. Lobular carcinoma in situ (LCIS): This is a condition where cancer cells are present in the milk-producing glands of the breasts, but have not yet invaded surrounding tissues. LCIS is often found in both breasts and can increase the risk of developing breast cancer.
5. Adenomas: These are small growths on the surface of the colon that can become malignant over time if left untreated.
6. Leukoplakia: This is a condition where thick, white patches develop on the tongue or inside the mouth. Leukoplakia can be a precancerous condition and may increase the risk of developing oral cancer.
7. Oral subsquamous carcinoma: This is a type of precancerous lesion that develops in the mouth and can progress to squamous cell carcinoma if left untreated.
8. Cervical intraepithelial neoplasia (CIN): This is a condition where abnormal cells are present on the surface of the cervix, but have not yet invaded surrounding tissues. CIN can progress to cancer over time if left untreated.
9. Vulvar intraepithelial neoplasia (VIN): This is a condition where abnormal cells are present on the vulva, but have not yet invaded surrounding tissues. VIN can progress to cancer over time if left untreated.
10. Penile intraepithelial neoplasia (PIN): This is a condition where abnormal cells are present on the penis, but have not yet invaded surrounding tissues. PIN can progress to cancer over time if left untreated.

It is important to note that not all precancerous conditions will develop into cancer, and some may resolve on their own without treatment. However, it is important to follow up with a healthcare provider to monitor any changes and determine the best course of treatment.

Types of Intestinal Neoplasms:

1. Adenomas: These are benign tumors that grow on the inner lining of the intestine. They can become malignant over time if left untreated.
2. Carcinomas: These are malignant tumors that develop in the inner lining of the intestine. They can be subdivided into several types, including colon cancer and rectal cancer.
3. Lymphoma: This is a type of cancer that affects the immune system and can occur in the intestines.
4. Leiomyosarcomas: These are rare malignant tumors that develop in the smooth muscle layers of the intestine.

Causes and Risk Factors:

The exact cause of intestinal neoplasms is not known, but several factors can increase the risk of developing these growths. These include:

1. Age: The risk of developing intestinal neoplasms increases with age.
2. Family history: Having a family history of colon cancer or other intestinal neoplasms can increase the risk of developing these growths.
3. Inflammatory bowel disease: People with inflammatory bowel diseases, such as ulcerative colitis and Crohn's disease, are at higher risk of developing intestinal neoplasms.
4. Genetic mutations: Certain genetic mutations can increase the risk of developing intestinal neoplasms.
5. Diet and lifestyle factors: A diet high in fat and low in fiber, as well as lack of physical activity, may increase the risk of developing intestinal neoplasms.

Symptoms:

Intestinal neoplasms can cause a variety of symptoms, including:

1. Abdominal pain or discomfort
2. Changes in bowel habits, such as diarrhea or constipation
3. Blood in the stool
4. Weight loss
5. Fatigue
6. Loss of appetite

Diagnosis:

To diagnose intestinal neoplasms, a doctor may perform several tests, including:

1. Colonoscopy: A colonoscope is inserted through the rectum and into the colon to visualize the inside of the colon and detect any abnormal growths.
2. Biopsy: A small sample of tissue is removed from the colon and examined under a microscope for cancer cells.
3. Imaging tests: Such as X-rays, CT scans, or MRI scans to look for any abnormalities in the colon.
4. Blood tests: To check for certain substances in the blood that are associated with intestinal neoplasms.

Treatment:

The treatment of intestinal neoplasms depends on the type and location of the growth, as well as the stage of the cancer. Treatment options may include:

1. Surgery: To remove the tumor and any affected tissue.
2. Chemotherapy: To kill any remaining cancer cells with drugs.
3. Radiation therapy: To kill cancer cells with high-energy X-rays or other forms of radiation.
4. Targeted therapy: To use drugs that target specific molecules on cancer cells to kill them.
5. Immunotherapy: To use drugs that stimulate the immune system to fight cancer cells.

Prognosis:

The prognosis for intestinal neoplasms depends on several factors, including the type and stage of the cancer, the location of the growth, and the effectiveness of treatment. In general, early detection and treatment improve the prognosis, while later-stage cancers have a poorer prognosis.

Complications:

Intestinal neoplasms can cause several complications, including:

1. Obstruction: The tumor can block the normal flow of food through the intestine, leading to abdominal pain and other symptoms.
2. Bleeding: The tumor can cause bleeding in the intestine, which can lead to anemia and other complications.
3. Perforation: The tumor can create a hole in the wall of the intestine, leading to peritonitis (inflammation of the lining of the abdomen) and other complications.
4. Metastasis: The cancer cells can spread to other parts of the body, such as the liver or lungs, and cause further complications.
5. Malnutrition: The tumor can make it difficult for the body to absorb nutrients, leading to malnutrition and other health problems.

Prevention:

There is no sure way to prevent intestinal neoplasms, but there are several steps that may help reduce the risk of developing these types of cancer. These include:

1. Avoiding known risk factors: Avoiding known risk factors such as smoking, excessive alcohol consumption, and a diet high in processed meat can help reduce the risk of developing intestinal neoplasms.
2. Maintaining a healthy diet: Eating a balanced diet that is high in fruits, vegetables, and whole grains can help keep the intestines healthy and may reduce the risk of cancer.
3. Exercise regularly: Regular exercise can help maintain a healthy weight, improve digestion, and may reduce the risk of developing intestinal neoplasms.
4. Managing chronic conditions: Managing chronic conditions such as inflammatory bowel disease, diabetes, and obesity can help reduce the risk of developing intestinal neoplasms.
5. Screening tests: Regular screening tests such as colonoscopy, CT scan, or barium enema can help detect precancerous polyps or early-stage cancer, allowing for early treatment and prevention of advanced disease.

Early detection and diagnosis are crucial for effective treatment and survival rates for intestinal neoplasms. If you have any of the risk factors or symptoms mentioned above, it is essential to consult a doctor as soon as possible. A thorough examination and diagnostic tests can help determine the cause of your symptoms and recommend appropriate treatment.

Malignant prostatic neoplasms are cancerous tumors that can be aggressive and spread to other parts of the body (metastasize). The most common type of malignant prostatic neoplasm is adenocarcinoma of the prostate, which accounts for approximately 95% of all prostate cancers. Other types of malignant prostatic neoplasms include sarcomas and small cell carcinomas.

Prostatic neoplasms can be diagnosed through a variety of tests such as digital rectal examination (DRE), prostate-specific antigen (PSA) test, imaging studies (ultrasound, CT scan or MRI), and biopsy. Treatment options for prostatic neoplasms depend on the type, stage, and grade of the tumor, as well as the patient's age and overall health. Treatment options can include active surveillance, surgery (robotic-assisted laparoscopic prostatectomy or open prostatectomy), radiation therapy (external beam radiation therapy or brachytherapy), and hormone therapy.

In summary, Prostatic Neoplasms are tumors that occur in the prostate gland, which can be benign or malignant. The most common types of malignant prostatic neoplasms are adenocarcinoma of the prostate, and other types include sarcomas and small cell carcinomas. Diagnosis is done through a variety of tests, and treatment options depend on the type, stage, and grade of the tumor, as well as the patient's age and overall health.

Symptoms of duodenal neoplasms can vary depending on the location and size of the tumor, but may include abdominal pain, weight loss, nausea, vomiting, and abdominal distension. Diagnosis is typically made through a combination of endoscopy, imaging studies such as CT scans or MRI, and biopsy. Treatment options for duodenal neoplasms depend on the type and stage of the tumor, but may include surgery, chemotherapy, and/or radiation therapy.

Duodenal Neoplasms are relatively rare, accounting for only about 1-2% of all gastrointestinal cancers. However, they can be aggressive and difficult to treat if not detected early. The prognosis for duodenal neoplasms is generally poor, with a 5-year survival rate of approximately 20-30%.

A rare type of carcinoma that develops in the gastrointestinal tract (GI tract) such as stomach, small intestine, or large intestine is known as signet ring cell carcinoma. This cancerous tumor is characterized by its appearance under a microscope, which displays cells arranged in a signet ring pattern.

These cells have a distinctive round nucleus and prominent nucleoli that give them a characteristic signet ring appearance. Signet ring cell carcinomas tend to grow slowly, and they do not typically cause any symptoms until they reach an advanced stage.

Signet ring cell carcinoma can be difficult to diagnose because it often looks like other types of noncancerous conditions, such as inflammation or infection. To diagnose this condition, a healthcare provider will need to perform tests such as endoscopy, imaging studies (such as CT scan or MRI), and biopsy.

Treatment options for signet ring cell carcinoma include surgery to remove the tumor, chemotherapy, radiation therapy, or a combination of these. Treatment decisions depend on the stage of the cancer, location, and other factors such as patient's overall health status and personal preferences.

In summary, signet ring cell carcinoma is a rare type of gastrointestinal tract cancer characterized by its distinctive signet ring appearance under a microscope. It tends to grow slowly and can be difficult to diagnose until it reaches an advanced stage. Treatment options include surgery, chemotherapy, radiation therapy, or combination of these depending on the stage of the cancer and other factors.

Sources:
American Cancer Society. (2022). Signet Ring Cell Carcinoma of the Stomach. Retrieved from
National Cancer Institute. (2022). Signet Ring Cell Carcinoma of the Gastrointestinal Tract. Retrieved from

Cecal neoplasms refer to abnormal growths or tumors that occur in the cecum, which is a part of the large intestine. The cecum is a pouch-like structure located at the junction of the small and large intestines. Cecal neoplasms can be benign (non-cancerous) or malignant (cancerous).

Types of Cecal Neoplasms

There are several types of cecal neoplasms, including:

1. Adenoma: A benign tumor that arises from the glandular cells lining the cecum.
2. Villous adenoma: A type of adenoma that is characterized by the growth of villi, which are finger-like projections of epithelial tissue.
3. Tubulovillous adenoma: A type of adenoma that is characterized by the growth of tubular and villous structures.
4. Mucinous cystic neoplasm: A benign tumor that arises from the mucin-secreting cells lining the cecum.
5. Intraepithelial neoplasms: Precancerous changes that occur in the epithelial cells lining the cecum.
6. Carcinoma: A malignant tumor that arises from the epithelial cells lining the cecum.
7. Squamous cell carcinoma: A type of carcinoma that is characterized by the growth of squamous cells.
8. Adenocarcinoma: A type of carcinoma that is characterized by the growth of glandular cells.

Causes and Risk Factors

The exact causes of cecal neoplasms are not known, but several risk factors have been identified, including:

1. Age: The risk of developing cecal neoplasms increases with age.
2. Family history: Having a family history of colon cancer or other gastrointestinal cancers increases the risk of developing cecal neoplasms.
3. Inflammatory bowel disease: People with inflammatory bowel diseases, such as ulcerative colitis and Crohn's disease, are at higher risk of developing cecal neoplasms.
4. Genetic mutations: Some genetic mutations, such as those associated with familial adenomatous polyposis (FAP) and Lynch syndrome, increase the risk of developing cecal neoplasms.
5. Diet and lifestyle factors: A diet high in processed meat and low in fiber may increase the risk of developing cecal neoplasms.

Symptoms

Cecal neoplasms may not cause any symptoms in the early stages, but as they grow, they can cause a variety of symptoms, including:

1. Abdominal pain or discomfort
2. Changes in bowel movements (such as diarrhea or constipation)
3. Blood in the stool
4. Weakness and fatigue
5. Loss of appetite
6. Unexplained weight loss

Diagnosis

The diagnosis of cecal neoplasms is based on a combination of clinical findings, imaging studies, and pathological examination of tissue samples. The following tests may be used to diagnose cecal neoplasms:

1. Endoscopy: A flexible tube with a camera and light on the end is inserted through the mouth or rectum to visualize the inside of the cecum and collect tissue samples.
2. Imaging studies: Computed tomography (CT) scans, magnetic resonance imaging (MRI), or positron emission tomography (PET) scans may be used to identify any abnormalities in the cecum and surrounding tissues.
3. Biopsy: A sample of tissue is taken from the cecum during endoscopy or surgery and examined under a microscope for cancer cells.
4. Blood tests: Blood tests may be used to check for certain substances in the blood that are associated with cancer, such as carcinoembryonic antigen (CEA).

Treatment

The treatment of cecal neoplasms depends on the type and stage of the cancer. The following options may be considered:

1. Surgery: Surgical removal of the cancerous tissue may be recommended for early-stage cancers.
2. Chemotherapy: Chemotherapy may be used in combination with surgery or as a standalone treatment for more advanced cancers.
3. Radiation therapy: Radiation therapy may be used in combination with chemotherapy or surgery to treat cancer that has spread to other parts of the body.
4. Targeted therapy: Targeted therapy may be used to treat specific genetic mutations that are driving the growth of the cancer.

Prognosis

The prognosis for cecal neoplasms depends on the type and stage of the cancer at the time of diagnosis. In general, early-stage cancers have a better prognosis than more advanced cancers. Factors that may affect prognosis include:

1. Type of cancer: The type of cancer present in the cecum can impact prognosis. For example, adenocarcinoma has a better prognosis than squamous cell carcinoma.
2. Stage of cancer: Cancers that have spread to other parts of the body (metastasized) have a poorer prognosis than those that are localized to the cecum.
3. Age and overall health: Older patients or those with underlying health conditions may have a poorer prognosis than younger, healthier individuals.
4. Treatment options: The effectiveness of treatment can also impact prognosis. Patients who receive early and appropriate treatment may have a better prognosis than those who do not receive timely treatment.

Survival rate

The survival rate for cecal neoplasms is generally lower than for other types of gastrointestinal cancers. According to the American Cancer Society, the 5-year survival rate for cecal cancer is approximately 20%. This means that of patients diagnosed with cecal cancer, about 20% are still alive 5 years after their initial diagnosis. However, it's important to note that this is a general estimate and individual prognosis can vary based on a variety of factors.

Lifestyle changes

There are several lifestyle changes that may help reduce the risk of developing cecal neoplasms or improve outcomes for those who have been diagnosed:

1. Maintain a healthy diet and weight: Eating a balanced diet high in fruits, vegetables, and whole grains can help reduce the risk of developing cecal cancer. Additionally, maintaining a healthy weight can help reduce the risk of developing many types of cancer.
2. Exercise regularly: Regular physical activity has been shown to reduce the risk of developing many types of cancer, including cecal cancer.
3. Avoid tobacco and excessive alcohol consumption: Tobacco use and excessive alcohol consumption have both been linked to an increased risk of developing cecal cancer. Quitting smoking and limiting alcohol intake can help reduce the risk of developing this disease.
4. Manage chronic conditions: Chronic conditions such as diabetes, obesity, and inflammatory bowel disease can increase the risk of developing cecal cancer. Managing these conditions through lifestyle changes and medication can help reduce the risk of developing this disease.
5. Get regular screenings: Regular screenings for colon cancer, such as colonoscopies, can help detect cecal cancer at an early stage when it is more treatable.
6. Consider aspirin therapy: Some studies have suggested that taking a low-dose aspirin every day may help reduce the risk of developing colorectal cancer, including cecal cancer. However, aspirin therapy is not right for everyone, and individuals should talk to their doctor before starting any new medication.
7. Don't delay symptoms: If you experience any symptoms that may be related to cecal cancer, such as abdominal pain or changes in bowel movements, don't delay seeking medical attention. These symptoms can also be caused by other conditions, but it is important to get them checked out by a healthcare professional.

It is important to note that these recommendations are not a guarantee against developing cecal cancer, and individuals should talk to their doctor about their specific risk factors and any additional steps they can take to reduce their risk of developing this disease.

Examples of 'Mammary Neoplasms, Experimental' in a sentence:

1. The researchers studied the effects of hormone therapy on mammary neoplasms in experimental animals to better understand its potential role in human breast cancer.
2. The lab used mice with genetic mutations that predispose them to developing mammary neoplasms to test the efficacy of new cancer drugs.
3. In order to investigate the link between obesity and breast cancer, the researchers conducted experiments on mammary neoplasms in rats with diet-induced obesity.

1. Tumor size and location: Larger tumors that have spread to nearby tissues or organs are generally considered more invasive than smaller tumors that are confined to the original site.
2. Cellular growth patterns: The way in which cancer cells grow and divide can also contribute to the overall invasiveness of a neoplasm. For example, cells that grow in a disorganized or chaotic manner may be more likely to invade surrounding tissues.
3. Mitotic index: The mitotic index is a measure of how quickly the cancer cells are dividing. A higher mitotic index is generally associated with more aggressive and invasive cancers.
4. Necrosis: Necrosis, or the death of cells, can be an indication of the level of invasiveness of a neoplasm. The presence of significant necrosis in a tumor is often a sign that the cancer has invaded surrounding tissues and organs.
5. Lymphovascular invasion: Cancer cells that have invaded lymphatic vessels or blood vessels are considered more invasive than those that have not.
6. Perineural invasion: Cancer cells that have invaded nerve fibers are also considered more invasive.
7. Histological grade: The histological grade of a neoplasm is a measure of how abnormal the cancer cells look under a microscope. Higher-grade cancers are generally considered more aggressive and invasive than lower-grade cancers.
8. Immunohistochemical markers: Certain immunohistochemical markers, such as Ki-67, can be used to evaluate the proliferative activity of cancer cells. Higher levels of these markers are generally associated with more aggressive and invasive cancers.

Overall, the degree of neoplasm invasiveness is an important factor in determining the likelihood of the cancer spreading to other parts of the body (metastasizing) and in determining the appropriate treatment strategy for the patient.

Clear cell adenocarcinomas can occur in various parts of the body, such as the ovary, pancreas, and lung. In general, clear cell adenocarcinomas tend to grow more slowly than other types of cancer and are less aggressive. However, they can still be malignant and may require treatment.

The prognosis for clear cell adenocarcinoma depends on various factors, such as the stage of the cancer (how far it has spread) and the specific location of the tumor. In general, the prognosis for clear cell adenocarcinoma is good if the cancer is caught early and treated appropriately. However, if the cancer has spread to other parts of the body, the prognosis may be poorer.

There are several treatment options for clear cell adenocarcinoma, including surgery, chemotherapy, radiation therapy, and targeted therapy. The specific treatment plan will depend on the stage and location of the cancer, as well as other individual factors such as age and overall health.

In summary, clear cell adenocarcinoma is a type of cancer that begins in glandular cells and has clear cells. It can occur in various parts of the body and tends to grow slowly, but it can still be malignant and require treatment. The prognosis for clear cell adenocarcinoma depends on various factors, and there are several treatment options available.

Examples and Observations:

1. Gastric metaplasia: This is a condition where the stomach lining is replaced by cells that are similar to those found in the esophagus. This can occur as a result of chronic acid reflux, leading to an increased risk of developing esophageal cancer.
2. Bronchial metaplasia: This is a condition where the airways in the lungs are replaced by cells that are similar to those found in the trachea. This can occur as a result of chronic inflammation, leading to an increased risk of developing lung cancer.
3. Pancreatic metaplasia: This is a condition where the pancreas is replaced by cells that are similar to those found in the ducts of the pancreas. This can occur as a result of chronic inflammation, leading to an increased risk of developing pancreatic cancer.
4. Breast metaplasia: This is a condition where the breast tissue is replaced by cells that are similar to those found in the salivary glands. This can occur as a result of chronic inflammation, leading to an increased risk of developing salivary gland cancer.

Etiology and Pathophysiology:

Metaplasia is thought to be caused by chronic inflammation, which can lead to the replacement of one type of cell or tissue with another. This can occur as a result of a variety of factors, including infection, injury, or exposure to carcinogens. Once the metaplastic changes have occurred, there is an increased risk of developing cancer if the underlying cause is not addressed.

Clinical Presentation:

Patients with metaplasia may present with a variety of symptoms, depending on the location and extent of the condition. These can include pain, difficulty swallowing or breathing, coughing up blood, and weight loss. In some cases, patients may be asymptomatic and the condition may be detected incidentally during diagnostic testing for another condition.

Diagnosis:

The diagnosis of metaplasia is typically made based on a combination of clinical findings, radiologic imaging (such as CT scans or endoscopies), and histopathological examination of biopsy specimens. Imaging studies can help to identify the location and extent of the metaplastic changes, while histopathology can confirm the presence of the metaplastic cells and rule out other potential diagnoses.

Treatment:

Treatment for metaplasia depends on the underlying cause and the severity of the condition. In some cases, treatment may involve addressing the underlying cause, such as removing a tumor or treating an infection. In other cases, treatment may be directed at managing symptoms and preventing complications. This can include medications to reduce inflammation and pain, as well as surgery to remove affected tissue.

Prognosis:

The prognosis for metaplasia varies depending on the underlying cause and the severity of the condition. In general, the prognosis is good for patients with benign metaplastic changes, while those with malignant changes may have a poorer prognosis if the cancer is not treated promptly and effectively.

Complications:

Metaplasia can lead to a number of complications, including:

1. Cancer: Metaplastic changes can sometimes progress to cancer, which can be life-threatening.
2. Obstruction: The growth of metaplastic cells can block the normal functioning of the organ or gland, leading to obstruction and potentially life-threatening complications.
3. Inflammation: Metaplasia can lead to chronic inflammation, which can cause scarring and further damage to the affected tissue.
4. Bleeding: Metaplastic changes can increase the risk of bleeding, particularly if they occur in the digestive tract or other organs.

The causes of colorectal neoplasms are not fully understood, but factors such as age, genetics, diet, and lifestyle have been implicated. Symptoms of colorectal cancer can include changes in bowel habits, blood in the stool, abdominal pain, and weight loss. Screening for colorectal cancer is recommended for adults over the age of 50, as it can help detect early-stage tumors and improve survival rates.

There are several subtypes of colorectal neoplasms, including adenomas (which are precancerous polyps), carcinomas (which are malignant tumors), and lymphomas (which are cancers of the immune system). Treatment options for colorectal cancer depend on the stage and location of the tumor, but may include surgery, chemotherapy, radiation therapy, or a combination of these.

Research into the causes and treatment of colorectal neoplasms is ongoing, and there has been significant progress in recent years. Advances in screening and treatment have improved survival rates for patients with colorectal cancer, and there is hope that continued research will lead to even more effective treatments in the future.

Rectal neoplasms refer to abnormal growths or tumors that occur in the rectum, which is the lower part of the digestive system. These growths can be benign (non-cancerous) or malignant (cancerous).

Types of Rectal Neoplasms:

There are several types of rectal neoplasms, including:

1. Adenoma: A benign growth that is usually found in the colon and rectum. It is a common precursor to colorectal cancer.
2. Carcinoma: A malignant tumor that arises from the epithelial cells lining the rectum. It is the most common type of rectal cancer.
3. Rectal adenocarcinoma: A type of carcinoma that originates in the glandular cells lining the rectum.
4. Rectal squamous cell carcinoma: A type of carcinoma that originates in the squamous cells lining the rectum.
5. Rectal melanoma: A rare type of carcinoma that originates in the pigment-producing cells (melanocytes) of the rectum.

Causes and Risk Factors:

The exact causes of rectal neoplasms are not known, but several factors can increase the risk of developing these growths. These include:

1. Age: The risk of developing rectal neoplasms increases with age, with most cases occurring in people over the age of 50.
2. Family history: Having a family history of colorectal cancer or polyps can increase the risk of developing rectal neoplasms.
3. Inflammatory bowel disease: People with inflammatory bowel disease, such as ulcerative colitis and Crohn's disease, are at higher risk of developing rectal neoplasms.
4. Diet: A diet high in fat and low in fiber may increase the risk of developing rectal neoplasms.
5. Lifestyle factors: Factors such as smoking, obesity, and lack of physical activity may also increase the risk of developing rectal neoplasms.

Symptoms:

The symptoms of rectal neoplasms can vary depending on the type and location of the growth. Some common symptoms include:

1. Blood in the stool
2. Changes in bowel movements (such as diarrhea or constipation)
3. Abdominal pain or discomfort
4. Weakness and fatigue
5. Loss of appetite

Diagnosis:

To diagnose rectal neoplasms, a doctor may perform several tests, including:

1. Digital rectal exam (DRE): A doctor will insert a gloved finger into the rectum to feel for any abnormalities.
2. Colonoscopy: A flexible tube with a camera and light on the end is inserted through the anus and into the rectum to examine the inside of the rectum and colon for polyps or other abnormalities.
3. Imaging tests: Such as X-rays, CT scans, or MRI scans to visualize the growth and determine its location and size.
4. Biopsy: A sample of tissue is removed from the rectum and examined under a microscope for cancer cells.

Treatment:

The treatment of rectal neoplasms depends on the type, location, and stage of the growth. Some common treatments include:

1. Polypectomy: Removal of polyps through a colonoscopy or surgery.
2. Local excision: Surgical removal of the tumor and a small amount of surrounding tissue.
3. Radiation therapy: High-energy beams are used to kill cancer cells.
4. Chemotherapy: Drugs are used to kill cancer cells.
5. Immunotherapy: A treatment that uses the body's immune system to fight cancer.

Prognosis:

The prognosis for rectal neoplasms depends on the type, location, and stage of the growth. In general, the earlier the diagnosis and treatment, the better the prognosis. However, some types of rectal neoplasms can be more aggressive and difficult to treat, and may have a poorer prognosis.

Prevention:

There is no sure way to prevent rectal neoplasms, but there are several screening tests that can help detect them early, including:

1. Colonoscopy: A test in which a flexible tube with a camera and light on the end is inserted into the rectum and colon to examine for polyps or cancer.
2. Fecal occult blood test (FOBT): A test that checks for blood in the stool.
3. Flexible sigmoidoscopy: A test similar to a colonoscopy, but only examines the lower part of the colon and rectum.
4. Digital rectal exam (DRE): An examination of the rectum using a gloved finger to feel for any abnormalities.

It is important to talk to your doctor about your risk for rectal neoplasms and any screening tests that may be appropriate for you. Early detection and treatment can improve the prognosis for these types of growths.

Benign ileal neoplasms include:

1. Adenomas: These are growths that are similar to colon polyps and can develop into colon cancer if left untreated.
2. Villous adenomas: These are benign tumors that grow on the villi, which are small projections that line the inside of the intestine.
3. Lipomas: These are slow-growing, non-cancerous growths that are made up of fat cells.

Malignant ileal neoplasms include:

1. Adenocarcinoma: This is the most common type of small intestine cancer and accounts for about 95% of all cases. It can occur in any part of the small intestine, but is more common in the duodenum (the first part of the small intestine).
2. Squamous cell carcinoma: This type of cancer occurs in the upper parts of the small intestine and is less common than adenocarcinoma.
3. Neuroendocrine tumors: These are rare tumors that occur in the hormone-producing cells of the small intestine and can produce excess hormones that can cause symptoms such as diarrhea, abdominal pain, and weight loss.

Ileal neoplasms can cause a variety of symptoms depending on their size, location, and type. These may include:

* Abdominal pain or discomfort
* Diarrhea or constipation
* Weight loss or loss of appetite
* Fatigue or weakness
* Nausea or vomiting
* Abnormal bleeding or discharge from the rectum

If you suspect that you may have an ileal neoplasm, it is important to seek medical attention as soon as possible. A healthcare professional can perform a series of tests and examinations to diagnose and determine the appropriate treatment for your condition. These may include:

1. Endoscopy: A flexible tube with a camera and light on the end is inserted through the mouth or rectum to visualize the inside of the small intestine and look for any abnormalities.
2. Imaging tests: Such as X-rays, CT scans, or MRI scans to visualize the small intestine and look for any tumors or other abnormalities.
3. Biopsy: A sample of tissue is removed from the small intestine and examined under a microscope to determine if there are any cancer cells present.
4. Blood tests: To check for certain substances in the blood that can indicate the presence of a neoplasm.
5. Genetic testing: To look for genetic changes that may indicate the presence of a neoplasm.

Treatment for ileal neoplasms depends on the type, size, location, and stage of the tumor, as well as the patient's overall health. Treatment options may include:

1. Surgery: To remove the tumor and any affected tissue.
2. Chemotherapy: To kill cancer cells with drugs.
3. Radiation therapy: To kill cancer cells with high-energy X-rays or other forms of radiation.
4. Targeted therapy: To use drugs or other substances to target specific molecules on the surface of cancer cells.
5. Supportive care: To manage symptoms and side effects, such as pain, nausea, and vomiting.

It's important for patients with ileal neoplasms to work closely with their healthcare team to determine the best course of treatment for their specific condition. With prompt and appropriate treatment, many people with ileal neoplasms can achieve long-term survival and a good quality of life.

Adenomas are caused by genetic mutations that occur in the DNA of the affected cells. These mutations can be inherited or acquired through exposure to environmental factors such as tobacco smoke, radiation, or certain chemicals.

The symptoms of an adenoma can vary depending on its location and size. In general, they may include abdominal pain, bleeding, or changes in bowel movements. If the adenoma becomes large enough, it can obstruct the normal functioning of the affected organ or cause a blockage that can lead to severe health complications.

Adenomas are usually diagnosed through endoscopy, which involves inserting a flexible tube with a camera into the affected organ to visualize the inside. Biopsies may also be taken to confirm the presence of cancerous cells.

Treatment for adenomas depends on their size, location, and severity. Small, non-pedunculated adenomas can often be removed during endoscopy through a procedure called endoscopic mucosal resection (EMR). Larger adenomas may require surgical resection, and in some cases, chemotherapy or radiation therapy may also be necessary.

In summary, adenoma is a type of benign tumor that can occur in glandular tissue throughout the body. While they are not cancerous, they have the potential to become malignant over time if left untreated. Therefore, it is important to seek medical attention if symptoms persist or worsen over time. Early detection and treatment can help prevent complications and improve outcomes for patients with adenomas.

Benign jejal neoplasms include:

1. Adenomas: These are benign tumors that grow on the lining of the jejunum and can become cancerous over time if left untreated.
2. Villous adenomas: These are benign tumors that grow on the villi, which are small projections on the lining of the small intestine that increase the surface area for nutrient absorption.
3. GISTs (gastrointestinal stromal tumors): These are rare benign tumors that can occur in the jejunum and other parts of the digestive system.

Malignant jejal neoplasms include:

1. Adenocarcinomas: These are cancerous tumors that grow on the lining of the jejunum and can invade surrounding tissues and organs.
2. Lymphoma: This is a type of cancer that affects the immune system and can occur in the jejunum.
3. Leiomyosarcomas: These are rare cancerous tumors that grow on the muscular walls of the jejunum.

Jejunal neoplasms can cause symptoms such as abdominal pain, diarrhea, nausea, and vomiting, depending on their location and size. They can also cause anemia, bleeding, and blockage of the intestine if they become large enough to obstruct the passage of food and fluids.

Jejunal neoplasms are diagnosed through a combination of endoscopy, imaging tests such as CT scans or MRI, and biopsy. Treatment options depend on the type and location of the neoplasm, and can include surgery, chemotherapy, and radiation therapy.

Neoplastic metastasis can occur in any type of cancer but are more common in solid tumors such as carcinomas (breast, lung, colon). It is important for cancer diagnosis and prognosis because metastasis indicates that the cancer has spread beyond its original site and may be more difficult to treat.

Metastases can appear at any distant location but commonly found sites include the liver, lungs, bones, brain, and lymph nodes. The presence of metastases indicates a higher stage of cancer which is associated with lower survival rates compared to localized cancer.

Lymphatic metastasis occurs when cancer cells enter the lymphatic vessels and are carried through the lymphatic system to other parts of the body. This can happen through several mechanisms, including:

1. Direct invasion: Cancer cells can invade the nearby lymphatic vessels and spread through them.
2. Lymphatic vessel embolization: Cancer cells can block the flow of lymphatic fluid and cause the formation of a clot-like structure, which can trap cancer cells and allow them to grow.
3. Lymphatic vessel invasion: Cancer cells can infiltrate the walls of lymphatic vessels and spread through them.

Lymphatic metastasis is a common mechanism for the spread of cancer, particularly in the breast, melanoma, and other cancers that have a high risk of lymphatic invasion. The presence of lymphatic metastasis in a patient's body can indicate a more aggressive cancer and a poorer prognosis.

Treatment for lymphatic metastasis typically involves a combination of surgery, chemotherapy, and radiation therapy. Surgery may be used to remove any affected lymph nodes or other tumors that have spread through the lymphatic system. Chemotherapy may be used to kill any remaining cancer cells, while radiation therapy may be used to shrink the tumors and relieve symptoms.

In summary, lymphatic metastasis is a common mechanism for the spread of cancer through the body, particularly in cancers that originate in organs with a high lymphatic drainage. Treatment typically involves a combination of surgery, chemotherapy, and radiation therapy to remove or shrink the tumors and relieve symptoms.

Adenocarcinoma is the most common subtype of NSCLC and is characterized by malignant cells that have glandular or secretory properties. Squamous cell carcinoma is less common and is characterized by malignant cells that resemble squamous epithelium. Large cell carcinoma is a rare subtype and is characterized by large, poorly differentiated cells.

The main risk factor for developing NSCLC is tobacco smoking, which is responsible for approximately 80-90% of all cases. Other risk factors include exposure to secondhand smoke, radon gas, asbestos, and certain chemicals in the workplace or environment.

Symptoms of NSCLC can include coughing, chest pain, shortness of breath, and fatigue. The diagnosis is typically made through a combination of imaging studies such as CT scans, PET scans, and biopsy. Treatment options for NSCLC can include surgery, chemotherapy, radiation therapy, or a combination of these. The prognosis for NSCLC depends on several factors, including the stage of the cancer, the patient's overall health, and the effectiveness of treatment.

Overall, NSCLC is a common and aggressive form of lung cancer that can be treated with a variety of therapies. Early detection and treatment are critical for improving outcomes in patients with this diagnosis.

Example Sentences:

The patient was diagnosed with adenosquamous carcinoma of the lung and underwent surgical resection.

The pathology report revealed that the tumor was an adenosquamous carcinoma, which is a rare type of lung cancer.

Note: Adenosquamous carcinoma is a rare subtype of non-small cell lung cancer (NSCLC), accounting for approximately 1-3% of all lung cancers. It has a more aggressive clinical course and poorer prognosis compared to other types of NSCLC.

Anatomy17

Organisms4

Diseases78

Chemicals and Drugs35

Analytical, Diagnostic and Therapeutic Techniques and Equipment48

Psychiatry and Psychology1

Phenomena and Processes19

Disciplines and Occupations2

Information Science5

Health Care15

Loss of p21(WAF1) compartmentalisation in sebaceous carcinoma compared with sebaceous hyperplasia and sebaceous adenoma. (1/35)

Immunohistochemical staining for adipophilin, perilipin and TIP47. (2/35)

Complications of mitomycin C therapy in 100 eyes with ocular surface neoplasia. (3/35)

Activator protein-1 activity regulates epithelial tumor cell identity. (4/35)

A clinicopathological study of eyelid malignancies from central India. (5/35)

Dual role of inactivating Lef1 mutations in epidermis: tumor promotion and specification of tumor type. (6/35)

Role of fine needle aspiration cytology in diagnosis of eyelid sebaceous carcinoma. (7/35)

Adnexal skin tumors in Zaria, Nigeria. (8/35)

Adenocarcinoma

Adenocarcinoma, Mucinous

Lung Neoplasms

Pancreatic Neoplasms

Esophageal Neoplasms

Adenocarcinoma, Papillary

Barrett Esophagus

Carcinoma, Pancreatic Ductal

Adenocarcinoma, Bronchiolo-Alveolar

Stomach Neoplasms

Cardia

Immunohistochemistry

Colonic Neoplasms

Tumor Markers, Biological

Esophagogastric Junction

Neoplasm Staging

Prognosis

Keratin-7

Gene Expression Regulation, Neoplastic

Cell Line, Tumor

Carcinoma, Squamous Cell

Endometrial Neoplasms

Neoplasms, Multiple Primary

Precancerous Conditions

Intestinal Neoplasms

Prostatic Neoplasms

Tumor Cells, Cultured

Duodenal Neoplasms

Carcinoma, Signet Ring Cell

Carcinoma, Endometrioid

Cecal Neoplasms

Mammary Neoplasms, Experimental

Neoplasm Invasiveness

Adenocarcinoma, Clear Cell

Metaplasia

Immunoenzyme Techniques

Colorectal Neoplasms

Rectal Neoplasms

Ampulla of Vater

Genes, ras

Common Bile Duct Neoplasms

Keratin-20

Tissue Array Analysis

Ileal Neoplasms

Adenoma

Pancreaticoduodenectomy

DNA, Neoplasm

Jejunal Neoplasms

Survival Rate

Neoplasm Metastasis

Lymphatic Metastasis

Neoplasm Proteins

Carcinoma, Non-Small-Cell Lung

Carcinoma, Adenosquamous

Carcinoembryonic Antigen

Carcinoma, Acinar Cell

Neoplasm Transplantation

Esophagus

Disease Progression

Survival Analysis

Retrospective Studies

Gastrectomy

Mice, Nude

RNA, Messenger

Paranasal Sinus Neoplasms

Mutation

Carcinoma in Situ

Receptor, Epidermal Growth Factor

Antineoplastic Agents

Kaplan-Meier Estimate

Reverse Transcriptase Polymerase Chain Reaction

Biopsy

Pancreatectomy

Fatal Outcome

Antigens, Neoplasm

Uterine Cervical Neoplasms

Treatment Outcome

Mucins

Gastrointestinal Neoplasms

Tumor Suppressor Protein p53