The reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions. The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand; photoreactivation repair, in which the lethal and mutagenic effects of ultraviolet light are eliminated; and post-replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex. Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.
Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.
The repair of DOUBLE-STRAND DNA BREAKS by rejoining the broken ends of DNA to each other directly.
Enzymes that are involved in the reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule, which contained damaged regions.
Interruptions in the sugar-phosphate backbone of DNA, across both strands adjacently.
That portion of the electromagnetic spectrum immediately below the visible range and extending into the x-ray frequencies. The longer wavelengths (near-UV or biotic or vital rays) are necessary for the endogenous synthesis of vitamin D and are also called antirachitic rays; the shorter, ionizing wavelengths (far-UV or abiotic or extravital rays) are viricidal, bactericidal, mutagenic, and carcinogenic and are used as disinfectants.
Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.
Interruptions in one of the strands of the sugar-phosphate backbone of double-stranded DNA.
Penetrating, high-energy electromagnetic radiation emitted from atomic nuclei during NUCLEAR DECAY. The range of wavelengths of emitted radiation is between 0.1 - 100 pm which overlaps the shorter, more energetic hard X-RAYS wavelengths. The distinction between gamma rays and X-rays is based on their radiation source.
Immunologically detectable substances found in the CELL NUCLEUS.
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
Production of new arrangements of DNA by various mechanisms such as assortment and segregation, CROSSING OVER; GENE CONVERSION; GENETIC TRANSFORMATION; GENETIC CONJUGATION; GENETIC TRANSDUCTION; or mixed infection of viruses.
Poly(deoxyribonucleotide):poly(deoxyribonucleotide)ligases. Enzymes that catalyze the joining of preformed deoxyribonucleotides in phosphodiester linkage during genetic processes during repair of a single-stranded break in duplex DNA. The class includes both EC (ATP) and EC (NAD).
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).
Dimers found in DNA chains damaged by ULTRAVIOLET RAYS. They consist of two adjacent PYRIMIDINE NUCLEOTIDES, usually THYMINE nucleotides, in which the pyrimidine residues are covalently joined by a cyclobutane ring. These dimers block DNA REPLICATION.
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
An enzyme that catalyzes the reactivation by light of UV-irradiated DNA. It breaks two carbon-carbon bonds in PYRIMIDINE DIMERS in DNA.
An alkylating agent in cancer therapy that may also act as a mutagen by interfering with and causing damage to DNA.
Proteins that catalyze the unwinding of duplex DNA during replication by binding cooperatively to single-stranded regions of DNA or to short regions of duplex DNA that are undergoing transient opening. In addition DNA helicases are DNA-dependent ATPases that harness the free energy of ATP hydrolysis to translocate DNA strands.
A DNA repair enzyme that catalyzes DNA synthesis during base excision DNA repair. EC
A Rec A recombinase found in eukaryotes. Rad51 is involved in DNA REPAIR of double-strand breaks.
The ability of some cells or tissues to survive lethal doses of IONIZING RADIATION. Tolerance depends on the species, cell type, and physical and chemical variables, including RADIATION-PROTECTIVE AGENTS and RADIATION-SENSITIZING AGENTS.
The process by which a DNA molecule is duplicated.
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 group of enzymes catalyzing the endonucleolytic cleavage of DNA. They include members of EC 3.1.21.-, EC 3.1.22.-, EC 3.1.23.- (DNA RESTRICTION ENZYMES), EC 3.1.24.- (DNA RESTRICTION ENZYMES), and EC 3.1.25.-.
Neoplasms containing cyst-like formations or producing mucin or serum.
ELECTROMAGNETIC RADIATION or particle radiation (high energy ELEMENTARY PARTICLES) capable of directly or indirectly producing IONS in its passage through matter. The wavelengths of ionizing electromagnetic radiation are equal to or smaller than those of short (far) ultraviolet radiation and include gamma and X-rays.
A DNA repair pathway involved in correction of errors introduced during DNA replication when an incorrect base, which cannot form hydrogen bonds with the corresponding base in the parent strand, is incorporated into the daughter strand. Excinucleases recognize the BASE PAIR MISMATCH and cause a segment of polynucleotide chain to be excised from the daughter strand, thereby removing the mismatched base. (from Oxford Dictionary of Biochemistry and Molecular Biology, 2001)
The relationship between the dose of administered radiation and the response of the organism or tissue to the radiation.
Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes.
A serine-threonine protein kinase that, when activated by DNA, phosphorylates several DNA-binding protein substrates including the TUMOR SUPPRESSOR PROTEIN P53 and a variety of TRANSCRIPTION FACTORS.
Tumors or cancer of the SKIN.
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.
Established cell cultures that have the potential to propagate indefinitely.
Proteins found in the nucleus of a cell. Do not confuse with NUCLEOPROTEINS which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus.
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.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
Tumors or cancers of the KIDNEY.
Abnormal growths of tissue that follow a previous neoplasm but are not metastases of the latter. The second neoplasm may have the same or different histological type and can occur in the same or different organs as the previous neoplasm but in all cases arises from an independent oncogenic event. The development of the second neoplasm may or may not be related to the treatment for the previous neoplasm since genetic risk or predisposing factors may actually be the cause.
DNA-dependent DNA polymerases found in bacteria, animal and plant cells. During the replication process, these enzymes catalyze the addition of deoxyribonucleotide residues to the end of a DNA strand in the presence of DNA as template-primer. They also possess exonuclease activity and therefore function in DNA repair.
DNA present in neoplastic tissue.
Proteins obtained from ESCHERICHIA COLI.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
Proteins that control the CELL DIVISION CYCLE. This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS.
A species of the genus SACCHAROMYCES, family Saccharomycetaceae, order Saccharomycetales, known as "baker's" or "brewer's" yeast. The dried form is used as a dietary supplement.
A species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.
An abnormal balloon- or sac-like dilatation in the wall of the ABDOMINAL AORTA which gives rise to the visceral, the parietal, and the terminal (iliac) branches below the aortic hiatus at the diaphragm.
An adenocarcinoma producing mucin in significant amounts. (From Dorland, 27th ed)
Tumors or cancer of the THYROID GLAND.
Conditions which cause proliferation of hemopoietically active tissue or of tissue which has embryonic hemopoietic potential. They all involve dysregulation of multipotent MYELOID PROGENITOR CELLS, most often caused by a mutation in the JAK2 PROTEIN TYROSINE KINASE.
The first continuously cultured human malignant CELL LINE, derived from the cervical carcinoma of Henrietta Lacks. These cells are used for VIRUS CULTIVATION and antitumor drug screening assays.
Tumors or cancer of the LUNG.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
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.
Restoration of integrity to traumatized tissue.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Tumors or cancer of the PAROTID GLAND.
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 benign neoplasm derived from glandular epithelium, in which cystic accumulations of retained secretions are formed. In some instances, considerable portions of the neoplasm, or even the entire mass, may be cystic. (Stedman, 25th ed)
Tumors or cancer of the LIVER.
Surgical insertion of BLOOD VESSEL PROSTHESES to repair injured or diseased blood vessels.
Neoplasms developing from some structure of the connective and subcutaneous tissue. The concept does not refer to neoplasms located in connective or soft tissue.
Repair of DNA DAMAGE by exchange of DNA between matching sequences, usually between the allelic DNA (ALLELES) of sister chromatids.
Tumors or cancer of the APPENDIX.
The presence of an uncomplimentary base in double-stranded DNA caused by spontaneous deamination of cytosine or adenine, mismatching during homologous recombination, or errors in DNA replication. Multiple, sequential base pair mismatches lead to formation of heteroduplex DNA; (NUCLEIC ACID HETERODUPLEXES).
Neoplasms associated with a proliferation of a single clone of PLASMA CELLS and characterized by the secretion of PARAPROTEINS.
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 multilocular tumor with mucin secreting epithelium. They are most often found in the ovary, but are also found in the pancreas, appendix, and rarely, retroperitoneal and in the urinary bladder. They are considered to have low-grade malignant potential.
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.
Experimentally induced new abnormal growth of TISSUES in animals to provide models for studying human neoplasms.
A family of DNA repair enzymes that recognize damaged nucleotide bases and remove them by hydrolyzing the N-glycosidic bond that attaches them to the sugar backbone of the DNA molecule. The process called BASE EXCISION REPAIR can be completed by a DNA-(APURINIC OR APYRIMIDINIC SITE) LYASE which excises the remaining RIBOSE sugar from the DNA.
Tumors or cancer of the ENDOCRINE GLANDS.
Tumors or cancer of the GASTROINTESTINAL TRACT, from the MOUTH to the ANAL CANAL.
Carcinoma that arises from the PANCREATIC DUCTS. It accounts for the majority of cancers derived from the PANCREAS.
Tumors, cancer or other neoplasms produced by exposure to ionizing or non-ionizing radiation.
A DNA-binding protein that mediates DNA REPAIR of double strand breaks, and HOMOLOGOUS RECOMBINATION.
Proteins found in any species of bacterium.
Tumors or cancer of the EYE.
Neoplasms composed of vascular tissue. This concept does not refer to neoplasms located in blood vessels.
Tumors or cancer of the NOSE.
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.
Elements of limited time intervals, contributing to particular results or situations.
Tumors or cancer of the SALIVARY GLANDS.
Tomography using x-ray transmission and a computer algorithm to reconstruct the image.
Neoplasms composed of glandular tissue, an aggregation of epithelial cells that elaborate secretions, and of any type of epithelium itself. The concept does not refer to neoplasms located in the various glands or in epithelial tissue.
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 benign epithelial tumor with a glandular organization.
Tumors or cancer of the TESTIS. Germ cell tumors (GERMINOMA) of the testis constitute 95% of all testicular neoplasms.
A malignant neoplasm characterized by the formation of numerous, irregular, finger-like projections of fibrous stroma that is covered with a surface layer of neoplastic epithelial cells. (Stedman, 25th ed)
Tumors or cancer of the INTESTINES.
Neoplasms composed of muscle tissue: skeletal, cardiac, or smooth. The concept does not refer to neoplasms located in muscles.
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)
Methods which attempt to express in replicable terms the extent of the neoplasm in the patient.
A general term for various neoplastic diseases of the lymphoid tissue.
Tumors or cancer of the UTERUS.
Neoplasms located in the blood and blood-forming tissue (the bone marrow and lymphatic tissue). The commonest forms are the various types of LEUKEMIA, of LYMPHOMA, and of the progressive, life-threatening forms of the MYELODYSPLASTIC SYNDROMES.
Techniques for securing together the edges of a wound, with loops of thread or similar materials (SUTURES).
Neoplasms of whatever cell type or origin, occurring in the extraskeletal connective tissue framework of the body including the organs of locomotion and their various component structures, such as nerves, blood vessels, lymphatics, etc.
Neoplasms located in the vasculature system, such as ARTERIES and VEINS. They are differentiated from neoplasms of vascular tissue (NEOPLASMS, VASCULAR TISSUE), such as ANGIOFIBROMA or HEMANGIOMA.
A rare, pigmentary, and atrophic autosomal recessive disease. It is manifested as an extreme photosensitivity to ULTRAVIOLET RAYS as the result of a deficiency in the enzyme that permits excisional repair of ultraviolet-damaged DNA.
Neoplasms composed of sebaceous or sweat gland tissue or tissue of other skin appendages. The concept does not refer to neoplasms located in the sebaceous or sweat glands or in the other skin appendages.
An abdominal hernia with an external bulge in the GROIN region. It can be classified by the location of herniation. Indirect inguinal hernias occur through the internal inguinal ring. Direct inguinal hernias occur through defects in the ABDOMINAL WALL (transversalis fascia) in Hesselbach's triangle. The former type is commonly seen in children and young adults; the latter in adults.
Tumors or cancer of the COLON.
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 located in bone tissue or specific BONES.
A DNA repair enzyme that catalyses the excision of ribose residues at apurinic and apyrimidinic DNA sites that can result from the action of DNA GLYCOSYLASES. The enzyme catalyzes a beta-elimination reaction in which the C-O-P bond 3' to the apurinic or apyrimidinic site in DNA is broken, leaving a 3'-terminal unsaturated sugar and a product with a terminal 5'-phosphate. This enzyme was previously listed under EC
MutS homolog 2 protein is found throughout eukaryotes and is a homolog of the MUTS DNA MISMATCH-BINDING PROTEIN. It plays an essential role in meiotic RECOMBINATION and DNA REPAIR of mismatched NUCLEOTIDES.
Tumors or cancer of the PALATE, including those of the hard palate, soft palate and UVULA.
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.
Enzymes that catalyze the hydrolysis of the internal bonds and thereby the formation of polynucleotides or oligonucleotides from ribo- or deoxyribonucleotide chains. EC 3.1.-.
Tumors or cancer of the THYMUS GLAND.
Neoplasms composed of more than one type of neoplastic tissue.
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.
Ability of neoplasms to infiltrate and actively destroy surrounding tissue.
Tumors or cancer of the BILE DUCTS.
The tearing or bursting of the wall along any portion of the AORTA, such as thoracic or abdominal. It may result from the rupture of an aneurysm or it may be due to TRAUMA.
Tumors or cancer of the MANDIBLE.
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)
A ZINC FINGER MOTIF protein that recognizes and interacts with damaged DNA. It is a DNA-binding protein that plays an essential role in NUCLEOTIDE EXCISION REPAIR. Mutations in this protein are associated with the most severe form of XERODERMA PIGMENTOSUM.
Tumors in any part of the heart. They include primary cardiac tumors and metastatic tumors to the heart. Their interference with normal cardiac functions can cause a wide variety of symptoms including HEART FAILURE; CARDIAC ARRHYTHMIAS; or EMBOLISM.
Tumors or cancer of the SPLEEN.
Pathologic processes that affect patients after a surgical procedure. They may or may not be related to the disease for which the surgery was done, and they may or may not be direct results of the surgery.
An abnormal balloon- or sac-like dilatation in the wall of the THORACIC AORTA. This proximal descending portion of aorta gives rise to the visceral and the parietal branches above the aortic hiatus at the diaphragm.
A cystic tumor of the ovary, containing thin, clear, yellow serous fluid and varying amounts of solid tissue, with a malignant potential several times greater than that of mucinous cystadenoma (CYSTADENOMA, MUCINOUS). It can be unilocular, parvilocular, or multilocular. It is often bilateral and papillary. The cysts may vary greatly in size. (Dorland, 27th ed; from Hughes, Obstetric-Gynecologic Terminology, 1972)
Diseases of the domestic dog (Canis familiaris). This term does not include diseases of wild dogs, WOLVES; FOXES; and other Canidae for which the heading CARNIVORA is used.
Cancer or tumors of the MAXILLA or upper jaw.
Device constructed of either synthetic or biological material that is used for the repair of injured or diseased blood vessels.
Neoplasms composed of primordial GERM CELLS of embryonic GONADS or of elements of the germ layers of the EMBRYO, MAMMALIAN. The concept does not refer to neoplasms located in the gonads or present in an embryo or FETUS.
Tumors or cancer of the anal gland.
Neoplasms located in the bone marrow. They are differentiated from neoplasms composed of bone marrow cells, such as MULTIPLE MYELOMA. Most bone marrow neoplasms are metastatic.
Benign and malignant neoplastic processes that arise from or secondarily involve the meningeal coverings of the brain and spinal cord.
Neoplasms composed of fatty tissue or connective tissue made up of fat cells in a meshwork of areolar tissue. The concept does not refer to neoplasms located in adipose tissue.
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.
Tumors or cancer of the DUODENUM.
Radiographic visualization of the aorta and its branches by injection of contrast media, using percutaneous puncture or catheterization procedures.
Tumors or cancer of the URINARY BLADDER.
Surgical procedures undertaken to repair abnormal openings through which tissue or parts of organs can protrude or are already protruding.
Tumors or cancer of the MOUTH.
A malignant epithelial tumor with a glandular organization.
A class of enzymes involved in the hydrolysis of the N-glycosidic bond of nitrogen-linked sugars.
Operative procedures for the treatment of vascular disorders.
Tumors or cancer of the human BREAST.
Tumors or cancer of the STOMACH.
Minimally invasive procedures, diagnostic or therapeutic, performed within the BLOOD VESSELS. They may be perfomed via ANGIOSCOPY; INTERVENTIONAL MAGNETIC RESONANCE IMAGING; INTERVENTIONAL RADIOGRAPHY; or INTERVENTIONAL ULTRASONOGRAPHY.
Tumors or cancers of the ADRENAL CORTEX.
Tumors or cancer in the ILEUM region of the small intestine (INTESTINE, SMALL).
Tumors or cancer of the MEDIASTINUM.
Tumors or cancer of the TONGUE.
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 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.
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)
Benign and malignant neoplasms which occur within the substance of the spinal cord (intramedullary neoplasms) or in the space between the dura and spinal cord (intradural extramedullary neoplasms). The majority of intramedullary spinal tumors are primary CNS neoplasms including ASTROCYTOMA; EPENDYMOMA; and LIPOMA. Intramedullary neoplasms are often associated with SYRINGOMYELIA. The most frequent histologic types of intradural-extramedullary tumors are MENINGIOMA and NEUROFIBROMA.
Tumors or cancer of the VAGINA.
The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.
Experimentally induced tumors of the LIVER.
A methyl-directed mismatch DNA REPAIR protein that has weak ATPASE activity. MutS was originally described in ESCHERICHIA COLI.
An increased tendency of the GENOME to acquire MUTATIONS when various processes involved in maintaining and replicating the genome are dysfunctional.
A usually benign glandular tumor composed of oxyphil cells, large cells with small irregular nuclei and dense acidophilic granules due to the presence of abundant MITOCHONDRIA. Oxyphil cells, also known as oncocytes, are found in oncocytomas of the kidney, salivary glands, and endocrine glands. In the thyroid gland, oxyphil cells are known as Hurthle cells and Askanazy cells.
Benign and malignant neoplastic processes arising from or involving components of the central, peripheral, and autonomic nervous systems, cranial nerves, and meninges. Included in this category are primary and metastatic nervous system neoplasms.
A rare malignant neoplasm characterized by rapidly proliferating, extensively infiltrating, anaplastic cells derived from blood vessels and lining irregular blood-filled or lumpy spaces. (Stedman, 25th ed)
A Janus kinase subtype that is involved in signaling from GROWTH HORMONE RECEPTORS; PROLACTIN RECEPTORS; and a variety of CYTOKINE RECEPTORS such as ERYTHROPOIETIN RECEPTORS and INTERLEUKIN RECEPTORS. Dysregulation of Janus kinase 2 due to GENETIC TRANSLOCATIONS have been associated with a variety of MYELOPROLIFERATIVE DISORDERS.
Tumors or cancer located in muscle tissue or specific muscles. They are differentiated from NEOPLASMS, MUSCLE TISSUE which are neoplasms composed of skeletal, cardiac, or smooth muscle tissue, such as MYOSARCOMA or LEIOMYOMA.
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.
A genotoxicological technique for measuring DNA damage in an individual cell using single-cell gel electrophoresis. Cell DNA fragments assume a "comet with tail" formation on electrophoresis and are detected with an image analysis system. Alkaline assay conditions facilitate sensitive detection of single-strand damage.
Clonal myeloid disorders that possess both dysplastic and proliferative features but are not properly classified as either MYELODYSPLASTIC SYNDROMES or MYELOPROLIFERATIVE DISORDERS.
Surgical removal of the pancreas. (Dorland, 28th ed)
A repeat operation for the same condition in the same patient due to disease progression or recurrence, or as followup to failed previous surgery.
Neoplasms of the thin serous membrane that envelopes the lungs and lines the thoracic cavity. Pleural neoplasms are exceedingly rare and are usually not diagnosed until they are advanced because in the early stages they produce no symptoms.
A family of enzymes that catalyze the exonucleolytic cleavage of DNA. It includes members of the class EC 3.1.11 that produce 5'-phosphomonoesters as cleavage products.
Neoplasms which arise from peripheral nerve tissue. This includes NEUROFIBROMAS; SCHWANNOMAS; GRANULAR CELL TUMORS; and malignant peripheral NERVE SHEATH NEOPLASMS. (From DeVita Jr et al., Cancer: Principles and Practice of Oncology, 5th ed, pp1750-1)
A hernia caused by weakness of the anterior ABDOMINAL WALL due to midline defects, previous incisions, or increased intra-abdominal pressure. Ventral hernias include UMBILICAL HERNIA, incisional, epigastric, and spigelian hernias.
Highly reactive chemicals that introduce alkyl radicals into biologically active molecules and thereby prevent their proper functioning. Many are used as antineoplastic agents, but most are very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. They have also been used as components in poison gases.
Neoplasms located in the brain ventricles, including the two lateral, the third, and the fourth ventricle. Ventricular tumors may be primary (e.g., CHOROID PLEXUS NEOPLASMS and GLIOMA, SUBEPENDYMAL), metastasize from distant organs, or occur as extensions of locally invasive tumors from adjacent brain structures.
Tumors or cancer of the PARANASAL SINUSES.
Proteins obtained from the species SACCHAROMYCES CEREVISIAE. The function of specific proteins from this organism are the subject of intense scientific interest and have been used to derive basic understanding of the functioning similar proteins in higher eukaryotes.
The products of chemical reactions that result in the addition of extraneous chemical groups to DNA.
Primary or metastatic neoplasms of the CEREBELLUM. Tumors in this location frequently present with ATAXIA or signs of INTRACRANIAL HYPERTENSION due to obstruction of the fourth ventricle. Common primary cerebellar tumors include fibrillary ASTROCYTOMA and cerebellar HEMANGIOBLASTOMA. The cerebellum is a relatively common site for tumor metastases from the lung, breast, and other distant organs. (From Okazaki & Scheithauer, Atlas of Neuropathology, 1988, p86 and p141)
A benign tumor composed of fat cells (ADIPOCYTES). It can be surrounded by a thin layer of connective tissue (encapsulated), or diffuse without the capsule.
Tumor or cancer of the COMMON BILE DUCT including the AMPULLA OF VATER and the SPHINCTER OF ODDI.
Nuclear antigen with a role in DNA synthesis, DNA repair, and cell cycle progression. PCNA is required for the coordinated synthesis of both leading and lagging strands at the replication fork during DNA replication. PCNA expression correlates with the proliferation activity of several malignant and non-malignant cell types.
The physiological renewal, repair, or replacement of tissue.
Neoplasms of the bony orbit and contents except the eyeball.
Tumors or cancer of the BRONCHI.
Tumors or cancer of the PERITONEUM.
A collective term for precoordinated organ/neoplasm headings locating neoplasms by organ, as BRAIN NEOPLASMS; DUODENAL NEOPLASMS; LIVER NEOPLASMS; etc.
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.
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.
A DNA helicase that is a component of TRANSCRIPTION FACTOR TFIIH. It plays an essential role in NUCLEOTIDE EXCISION REPAIR, and mutations in this protein are associated with XERODERMA PIGMENTOSUM.
Distinctive neoplastic disorders of histiocytes. Included are malignant neoplasms of MACROPHAGES and DENDRITIC CELLS.
Tumors or cancer of the UROGENITAL SYSTEM in either the male or the female.
An exchange of DNA between matching or similar sequences.
Experimental transplantation of neoplasms in laboratory animals for research purposes.
Double-stranded nucleic acid molecules (DNA-DNA or DNA-RNA) which contain regions of nucleotide mismatches (non-complementary). In vivo, these heteroduplexes can result from mutation or genetic recombination; in vitro, they are formed by nucleic acid hybridization. Electron microscopic analysis of the resulting heteroduplexes facilitates the mapping of regions of base sequence homology of nucleic acids.
A cell line derived from cultured tumor cells.
An enzyme that transfers methyl groups from O(6)-methylguanine, and other methylated moieties of DNA, to a cysteine residue in itself, thus repairing alkylated DNA in a single-step reaction. EC
Malignant neoplasms[edit]. DNA damage[edit]. The central role of DNA damage and epigenetic defects in DNA repair genes in ... Deficiencies in DNA repair cause increased mutation rates.[34][35][36] A deficiency in DNA repair, itself, can allow DNA ... During repair of DNA double strand breaks, or repair of other DNA damages, incompletely cleared sites of repair can cause ... ICD-10 classifies neoplasms into four main groups: benign neoplasms, in situ neoplasms, malignant neoplasms, and neoplasms of ...
If accurate DNA repair is deficient, DNA damages tend to accumulate. Unrepaired DNA damage can increase mutational errors ... Such mutations and epigenetic alterations can give rise to cancer (see malignant neoplasms). Thus, epigenetic downregulation or ... DNA Repair and Cancer". In Chen, Clark (ed.). New Research Directions in DNA Repair. p. 413. ISBN 978-953-51-1114-6. O'Hagan HM ... July 2007). "DNA damage, homology-directed repair, and DNA methylation". PLOS Genetics. 3 (7): e110. doi:10.1371/journal.pgen. ...
This occurs through multiple mutations that affect the DNA-mismatch-repair pathways. As a consequence, DNA mutations during ... Paris classification of colorectal neoplasms. In colonoscopy, colorectal polyps can be classified by NICE (Narrow-band imaging ... The increased risk of cancer seen in patients with by the syndrome is associated with dysfunction of DNA repair mechanism. ... A neoplasm is a tissue whose cells have lost normal differentiation. They can be either benign growths or malignant growths. ...
DNA damage appears to be the primary underlying cause of cancer. If accurate DNA repair is deficient, DNA damages tend to ... Such mutations and epigenetic alterations can give rise to cancer (see malignant neoplasms). Thus, CpG island hyper/hypo- ... DNA Repair and Cancer". In Chen, Clark (ed.). New Research Directions in DNA Repair. p. 413. ISBN 978-953-51-1114-6. O'Hagan HM ... July 2007). "DNA damage, homology-directed repair, and DNA methylation". PLOS Genetics. 3 (7): e110. doi:10.1371/journal.pgen. ...
Such mutations and epigenetic alterations can give rise to cancer (see malignant neoplasms). Germ line mutations in DNA repair ... a DNA repair gene; APC, a cell cycle regulator; MLH1, a DNA-repair gene; and BRCA1, another DNA-repair gene. Indeed, cancer ... If DNA repair is deficient, DNA damage tends to accumulate. Such excess DNA damage can increase mutational errors during DNA ... Epigenetic repression of DNA repair genes in accurate DNA repair pathways appear to be central to carcinogenesis. The two gray- ...
Another component of the DNA repair machinery in the cell is the protein MLH1. Ablation of MLH1 in mice causes development of ... 1996). "Spontaneous intestinal carcinomas and skin neoplasms in Msh2-deficient mice". Cancer Res. 56 (16): 3842-9. PMID 8706033 ... Thus, 8-OH-dG was increased, DNA repair protein ERCC1 was decreased, autophagy protein beclin-1 was increased and, in the stem ... Another gene involved in DNA mismatch repair is Msh6. Both the Msh6 and Msh2 mutant mice develop gastrointestinal cancer but ...
... expression of DNA repair enzymes due to epigenetic methylation of DNA repair genes or altered microRNAs that control DNA repair ... Malignancy, malignant neoplasm and malignant tumor are synonymous with cancer. *Malignant ascites ...
2009). "Towards identification of hereditary DNA mismatch repair deficiency: sebaceous neoplasm warrants routine ... Routine immunohistochemical detection of DNA mismatch repair proteins help identify hereditary DNA mismatch repair deficiency. ... The genes affected are MLH1, MSH2, and more recently, MSH6, and are involved in DNA mismatch repair. Muir-Torre syndrome is ... These genes code for DNA mismatch repair genes, and mutations increase the risk of developing cancerous qualities.[citation ...
The absence of staining for DNA mismatch repair MSH2, MSH6, and MLH1 may suggest a diagnosis of MTS and identify patients for ... The incidence of MTS in patients with sebaceous neoplasms as high as 14 to 50%. Besides mutations in mismatch repair genes, Wnt ... MTS results from defects in DNA mismatch repair genes, MLH1, MSH2, and MSH6, leading to a buildup of unstable microsatellite ... SGc accounts for approximately 0.7% of all skin cancers and 0.2 to 4.6% of all malignant cutaneous neoplasms. Notable risk ...
In addition, MBD4 has protein sequence similarity to bacterial DNA repair enzymes and thus may have some function in DNA repair ... MBD4 mRNA expression is reduced in colorectal neoplasms due to methylation of the promoter region of MBD4. A majority of ... "The base excision repair enzyme MED1 mediates DNA damage response to antitumor drugs and is associated with mismatch repair ... "Biphasic kinetics of the human DNA repair protein MED1 (MBD4), a mismatch-specific DNA N-glycosylase". J. Biol. Chem. 275 (42 ...
These authors strongly suggest a link between the increase in the MGMT DNA repair pathway and a delay in the aging process in ... "A novel gene which is up-regulated during colon epithelial cell differentiation and down-regulated in colorectal neoplasms". ... a DNA repair protein. Thus, higher expression of NDRG1 can promote MGMT protein stability and activity. Dominick et al. showed ... DNA repair and cell adhesion among other functions. NDRG1 is localised in the cytoplasm, nucleus and mitochondrion, at ...
As summarized in the articles Carcinogenesis and Neoplasm, for sporadic cancers in general, a deficiency in DNA repair is ... Epigenetic reductions of DNA repair enzyme expression may likely lead to the genomic and epigenomic instability characteristic ... Lahtz C, Pfeifer GP (February 2011). "Epigenetic changes of DNA repair genes in cancer". Journal of Molecular Cell Biology. 3 ( ... Stool DNA screening test looks for biomarkers associated with colorectal cancer and precancerous lesions, including altered DNA ...
This pathology results from persistently thwarted attempts at normal DNA replication, DNA repair, and cell division, and ... Folate deficiency hinders DNA synthesis and cell division, affecting hematopoietic cells and neoplasms the most because of ... DNA production[edit]. Folate derivatives participate in the biosynthesis of both purines and pyrimidines. Formyl folate is ... Folic acid is essential for the body to make DNA, RNA, and metabolise amino acids, which are required for cell division. Not ...
This pathology results from persistently thwarted attempts at normal DNA replication, DNA repair, and cell division, and ... Folate deficiency hinders DNA synthesis and cell division, affecting hematopoietic cells and neoplasms the most because of ... DNA production[edit]. Folate derivatives participate in the biosynthesis of both purines and pyridines. Formyl folate is ... Folate is necessary for the production and maintenance of new cells, for DNA synthesis and RNA synthesis through methylation, ...
Deficiencies in DNA repair cause increased mutation rates. A deficiency in DNA repair, itself, can allow DNA damages to ... ICD-10 classifies neoplasms into four main groups: benign neoplasms, in situ neoplasms, malignant neoplasms, and neoplasms of ... and the consequent DNA repair deficiency is shown at the fourth level. When expression of DNA repair genes is reduced, DNA ... During repair of DNA double strand breaks, or repair of other DNA damages, incompletely cleared sites of repair can cause ...
During repair of DNA double strand breaks, or repair of other DNA damage, incompletely cleared repair sites can cause ... They form a subset of neoplasms. A neoplasm or tumor is a group of cells that have undergone unregulated growth and will often ... red wording indicates the central role of DNA damage and defects in DNA repair in progression to cancer.) When DNA repair is ... "DNA Damage, DNA Repair and Cancer". In Chen C. New Research Directions in DNA Repair. InTech. doi:10.5772/53919. ISBN 978-953- ...
... ... which may be benign neoplasms) or else a malignant neoplasm (cancer). These neoplasms are also indicated, in the diagram below ... Bernstein C, Prasad AR, Nfonsam V, Bernstein H. (2013). DNA Damage, DNA Repair and Cancer, New Research Directions in DNA ... Epigeneticically deficient DNA repair proteins include BRCA1, WRN, MGMT, MLH1, MSH2, ERCC1, PMS2, XPF, P53, PCNA and OGG1, and ...
The import of DNA repair proteins aprataxin and DNA ligase I is selectively decreased, and this may increase the vulnerability ... is commonly found in precancerous dysplasias and malignant neoplasms. Nucleoporin protein aladin is a component of the nuclear ... of the cell's DNA to oxidative stress induced damages that trigger cell death. Each individual nucleoporin is named according ...
... homozygous null mutation in BLM DNA repair enzyme. similar mechanism and etiology to ataxia telangiectasia) Naevus flammeus ( ... Some telangiectasias are due to developmental abnormalities that can closely mimic the behaviour of benign vascular neoplasms. ...
Mutations in DNA mismatch repair systems can lead to difficulty transmitting regions within the DNA which contain repeating ... and sebaceous neoplasms. Increased risk of prostate cancer and breast cancer has also been associated with Lynch syndrome, ... which coordinates the binding of other proteins involved with mismatch repair like DNA helicase, single-stranded-DNA binding- ... The increased risk for these cancers is due to inherited mutations that impair DNA mismatch repair. It is a type of cancer ...
The relationship of DNA and proteins to genes was still uncertain. Nothing was known about the existence of DNA repair ... induction of neoplasms, and lethality of cells and organisms-would require a detailed knowledge of the intervening chemical ...
A nose prosthesis is only required if the nose cannot be repaired, and there are a variety of reasons this may occur. A benign ... Also, something can go wrong during development with the nose inside the womb, even if the DNA is correct. Developing a nose ... tumor or a malignant neoplasm forms within the nasal cavity. Threatening or not, it's too dangerous to leave cancerous tissue ... A congenital anomaly causes DNA for the formation of the nose to be damaged. ...
... would reflect the earliest event in formation of a malignant neoplasm. In experimental evaluation of specific DNA repair ... In sporadic cancers, a deficiency in DNA repair is occasionally due to a mutation in a DNA repair gene; much more frequently, ... For example, individuals with an inherited impairment in any of 34 DNA repair genes (see article DNA repair-deficiency disorder ... Faster rates of mitosis increasingly leave fewer opportunities for repair enzymes to repair damaged DNA during DNA replication ...
... of DNA repair termed homologous recombinational repair that is the only known cellular process that can accurately repair DNA ... Ovarian neoplasms Germ cell tumor Seen most often in young women or adolescent girls. Other germ cell tumors are: Endodermal ... Meiosis as an Evolutionary Adaptation for DNA Repair. Chapter 19 in DNA Repair. Inna Kruman editor. InTech Open Publisher. DOI ... ...
The c-Abl gene in wild-type cells is implicated in DNA binding, which affects such processes as DNA transcription, repair, ... JAK2 mutations have been shown to be central to myeloproliferative neoplasms and JAK kinases play a central role in driving ... Moreover, it inhibits DNA repair, causing genomic instability and potentially causing the feared blast crisis in CML. The BCR- ... The BCR-ABL fusion, in contrast, has been shown to inhibit apoptosis, but its effect on DNA binding in particular is unclear. ...
... recruited to DNA damage and is sufficient to accelerate the repair oxidative DNA damage and mono-alkylated bases in genomic DNA ... "Genome integrity of myeloproliferative neoplasms in chronic phase and during disease progression". Blood 2011, 118:167-76. ... In agreement with results from in vitro DNA repair assays, a p200 CUX1-GFP fusion protein is rapidly recruited to DNA damage ... CUX1 knockdown delays DNA repair in multiple cell lines. Mouse embryo fibroblasts (MEFs) derived from a Cux1-/- knockout mouse ...
... see malignant neoplasms). Thus, CpG island hyper/hypo-methylation in the promoters of DNA repair genes are likely central to ... DNA damage appears to be the primary underlying cause of cancer.[39][40] If accurate DNA repair is deficient, DNA damages tend ... DNA repair genes with hyper/hypo-methylated promoters in cancers[edit]. DNA repair genes are frequently repressed in cancers ... DNA Repair and Cancer". In Chen, Clark. New Research Directions in DNA Repair,. p. 413. ISBN 978-953-51-1114-6.. ...
This blockage ultimately contributes to an increase in DNA damage by reducing repair activity.[citation needed] Due to these ... Neoplasms occurring in epithelial tissue such as the liver, gastrointestinal tract, and the pancreas have been linked to ... A biological target, also known as the site of action, can be binding proteins, ion channels, DNA, or a variety of other ... These diol-epoxides covalently bind with DNA base pairs, most often with guanine and adenine to form stable adducts within the ...
Lindahl, T. (1986). "DNA Glycosylases in DNA Repair". Mechanisms of DNA Damage and Repair. 38: 335-340. doi:10.1007/978-1-4615- ... MBD4 expression is reduced in almost all colorectal neoplasms due to methylation of the promoter region of MBD4. Also MBD4 is ... This was the most frequent DNA repair abnormality found among the 8 DNA repair genes tested. NEIL1 was also one of six DNA ... Uracil-DNA glycosylases are DNA repair enzymes that excise uracil residues from DNA by cleaving the N-glycosydic bond, ...
Among the 27 DNA repair genes evaluated, 13 DNA repair genes, MLH1, MLH3, MGMT, NTHL1, OGG1, SMUG1, ERCC1, ERCC2, ERCC3, ERCC4 ... "Clinicopathological relevance of the association between gastrointestinal and sebaceous neoplasms: the Muir-Torre syndrome". ... Only a minority of sporadic cancers with a DNA repair deficiency have a mutation in a DNA repair gene. However, a majority of ... In addition, there are Exo1-dependent and Exo1-independent DNA mismatch repair subpathways. DNA mismatches occur where one base ...
A non-viral PDGF "bio patch" can regenerate missing or damaged bone by delivering DNA in a nano-sized particle directly into ... Repairing bone fractures, fixing craniofacial defects and improving dental implants are among potential uses. The patch employs ... Neoplasm: Tumor suppressor genes/proteins and Oncogenes/Proto-oncogenes. Ligand. Growth factors. ... in orthopaedic bone repair and regeneration". Current Pharmaceutical Design. 19 (19): 3384-90. doi:10.2174/1381612811319190005 ...
Cells have mechanisms for repairing single-strand DNA damage and double-stranded DNA damage. However, double-stranded DNA ... Hypopituitarism commonly develops after radiation therapy for sellar and parasellar neoplasms, extrasellar brain tumours, head ... Single-strand DNA damage is then passed on through cell division; damage to the cancer cells' DNA accumulates, causing them to ... Radiation therapy works by damaging the DNA of cancerous cells. This DNA damage is caused by one of two types of energy, photon ...
... and plays a regulatory role in S phase DNA replication and DNA damage repair.[17][18][19] Specifically, p21 has a high affinity ... Neoplasm: Tumor suppressor genes/proteins and Oncogenes/Proto-oncogenes. Ligand. Growth factors. ... but not PCNA dependent nucleotide excision repair (NER).[21] As such, p21 acts as an effective inhibitor of DNA S-phase DNA ... Xiong Y, Zhang H, Beach D (1992). "D type cyclins associate with multiple protein kinases and the DNA replication and repair ...
DNA repair deficiency in NSCLC[edit]. Deficiencies in DNA repair underlie many forms of cancer.[21] If DNA repair is deficient ... Large cell lung carcinoma (LCLC) is a heterogeneous group of undifferentiated malignant neoplasms originating from transformed ... In addition, during repair of DNA double-strand breaks, or repair of other DNA damages, incompletely cleared sites of repair ... Epigenetic promoter methylation in DNA repair genes in NSCLC Gene Frequency of hyper- (or hypo-) methylation DNA repair pathway ...
Many chemotherapy drugs also cause DNA damage, which can be repaired by enzymes in the cell that carry out DNA repair. ... Secondary neoplasm[edit]. Development of secondary neoplasia after successful chemotherapy or radiotherapy treatment can occur ... When the DNA double-strand helix is unwound, during DNA replication or transcription, for example, the adjacent unopened DNA ... If the cell tries to replicate crosslinked DNA during cell division, or tries to repair it, the DNA strands can break. This ...
The most studied chemotheraputic agent in PCNSL is methotrexate (a folate analogue that interferes with DNA repair). ... Nervous tissue tumors/NS neoplasm/Neuroectodermal tumor (ICD-O 9350-9589) (C70-C72, D32-D33, 191-192/225) ... DNA virus. HBV (B). RNA virus. CBV. HAV (A). HCV (C). HDV (D). HEV (E). HGV (G). ... DNA virus. HBV Hepatocellular carcinoma. HPV Cervical cancer. Anal cancer. Penile cancer. Vulvar cancer. Vaginal cancer. ...
Template:DNA and protein biosynthesis navs(edit talk links history)- Genetics ({{Protein biosynthesis navs}}, R) ... "Neoplasms and cancer" has been chosen to reflect the fact that not all tumours are benign. The word "cancer" has been included ...
DNA repair[edit]. In somatic cells, deficiencies in DNA repair sometimes arise by mutations in DNA repair genes, but much more ... 8560-8580) Complex epithelial neoplasms. Carcinoma In situ[edit]. The term carcinoma in situ (or CIS) is a term for cells that ... a b Bernstein C, Prasad AR, Nfonsam V, Bernstein H. (2013). DNA Damage, DNA Repair and Cancer, New Research Directions in DNA ... ...
Several different repair processes can remove DNA damages (see chart in DNA repair). However, those DNA damages that remain un- ... Carcinogenesis and Neoplasm) and reference[24]). Furthermore, the ability of HRR to accurately and efficiently repair double- ... DNA damage and repair[edit]. DNA damage[edit]. DNA damage (or RNA damage in the case of some virus genomes) appears to be a ... Repair of DNA damages[edit]. Five major pathways are employed in repairing different types of DNA damages. These five pathways ...
"Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications". Genes Dev. 25 (5): 409-33. doi: ... more specifically in the transcatheter repair and replacement of heart valves.[29][30][31] ... superior information as compared to CT scans when seeking information about headache to confirm a diagnosis of neoplasm, ... The radiation used in CT scans can damage body cells, including DNA molecules, which can lead to cancer.[10] According to the ...
positive regulation of transcription, DNA-templated. • cellular response to lithium ion. • cell adhesion. • extracellular ... Neoplasm: Tumor suppressor genes/proteins and Oncogenes/Proto-oncogenes. Ligand. Growth factors. ...
Attachment of alkyl groups to DNA bases, resulting in the DNA being fragmented by repair enzymes in their attempts to replace ... trophoblastic neoplasms, and ovarian carcinoma. Moreover, it also has been used as an immunosuppressive drug for various ... Chlorambucil produces its anti-cancer effects by interfering with DNA replication and damaging the DNA in a cell. The DNA ... DNA damage via the formation of cross-links which prevents DNA from being separated for synthesis or transcription. ...
... and DNA repair. As more damage accumulates, the risk of cancer increases.[23] ... Horn, L; Lovly, CM; Johnson, DH (2015). "Chapter 107: Neoplasms of the lung". In Kasper, DL; Hauser, SL; Jameson, JL; Fauci, AS ... DNA methyltransferase inhibitors in development include decitabine, azacytidine, and hydralazine.[59]. The TRACERx project is ... Epigenetic changes-such as alteration of DNA methylation, histone tail modification, or microRNA regulation-may lead to ...
細胞的癌變與DNA及表觀遺傳等遺傳信息的突變有關,这些变化会影响细胞的正常功能,包括细胞增殖、程序性细胞死亡(细胞凋亡)和DNA修复。损伤累积的越多,癌症发生的风险就越高[23]。 ... Chapter 107: Neoplasms of the lung. (编) Kasper DL, Hauser SL, Jameson JL, Fauci AS, Longo DL, Loscalzo J. Harrison's Principles ... Mulvihill MS, Kratz JR, Pham P, Jablons DM, He B. The role of stem
As summarized in the articles Carcinogenesis and Neoplasm, for sporadic cancers in general, a deficiency in DNA repair is ... "DNA Damage, DNA Repair and Cancer". In Chen C. New Research Directions in DNA Repair. InTech. ISBN 978-953-51-1114-6 ... Epigenetic reductions of DNA repair enzyme expression may likely lead to the genomic and epigenomic instability characteristic ... Other options include virtual colonoscopy and stool DNA screening testing (FIT-DNA). Virtual colonoscopy via a CT scan appears ...
It also contains DNA repair enzymes that help reverse UV damage, such that people lacking the genes for these enzymes suffer ... Diseases of the skin include skin infections and skin neoplasms (including skin cancer). ... Skin repair. References[edit]. *^ a b c d e f "Skin care" (analysis),, 2007, webpage: HCcare Archived 12 ... while in the older population the skin becomes thinner and the epidermis turnover rate for cell repair is lower, which may ...
... effects of immunosuppressive medications on DNA repair". Experimental Dermatology. 21 (1): 2-6. doi:10.1111/j.1600-0625.2011. ... Tumors: Skin neoplasm, skin appendages / Adnexal and skin appendage (C44.L40-L68/D23.L15-49, 173/216) ... When skin defects are small in size, most can be repaired with simple repair where skin edges are approximated and closed with ... However malignant melanoma is predominantly caused by UVA radiation via indirect DNA damage. The indirect DNA damage is caused ...
RET is an abbreviation for "rearranged during transfection", as the DNA sequence of this gene was originally found to be ... Neoplasm: Tumor suppressor genes/proteins and Oncogenes/Proto-oncogenes. Ligand. Growth factors. ... Takahashi M, Ritz J, Cooper GM (1985). "Activation of a novel human transforming gene, ret, by DNA rearrangement". Cell. 42 (2 ... positive regulation of transcription, DNA-templated. • regulation of axonogenesis. • protein phosphorylation. • enteric nervous ...
DNA replication and repair-deficiency disorder ... World Health Organization classification of myeloid neoplasms ...
DNA Increased reports of cancers Increased urine mutagenicity and induction of tumors Binucleated cells with micronuclei, ... found no consistent evidence of excess risks of neoplasms that could have some link to DU, and that "[t]he overall incidence of ... and are repainted and repaired as necessary. ... "Depleted uranium-catalyzed oxidative DNA damage: absence of ...
... overexpression was shown to inhibit DNA double-strand break repair mediated through a novel, direct interaction between ... Neoplasm: Tumor suppressor genes/proteins and Oncogenes/Proto-oncogenes. Ligand. Growth factors. ... caused delays in DNA break repair, chromosomal abnormalities, and genome instability. These data demonstrated Mdm2-induced ... negative regulation of DNA damage response, signal transduction by p53 class mediator. • response to ether. • blood vessel ...
The gene that codes for the SDHB protein is nuclear, not mitchondrial DNA. However, the expressed protein is located in the ... Neoplasm: Tumor suppressor genes/proteins and Oncogenes/Proto-oncogenes. Ligand. Growth factors. ...
Ruxolitinib-induced defects in DNA repair cause sensitivity to PARP inhibitors in myeloproliferative neoplasms. Download Prime ... AnimalsCalreticulinCell LineDNA RepairDrug SynergismHeterograftsHumansJanus Kinase 2MiceMyeloproliferative DisordersNeoplasms ... Ruxolitinib-induced Defects in DNA Repair Cause Sensitivity to PARP Inhibitors in Myeloproliferative Neoplasms. Blood. 2017 12 ... Ruxolitinib-induced defects in DNA repair cause sensitivity to PARP inhibitors in myeloproliferative neoplasms.. Blood. 2017 12 ...
DNA Damage Signalling and Repair Inhibitors 2019 Base WP designed by Iografica Themes. ... Ewing sarcoma is an intense neoplasm predominantly occurring in adolescents and. Posted on February 19, 2018. by Dale Miles ... Ewing sarcoma is an intense neoplasm predominantly occurring in adolescents and has a poor prognosis when metastasized. without ...
DNA, Neoplasm. Grant support. *P01 CA129186/CA/NCI NIH HHS/United States ... The tumor microenvironment and DNA repair.. Klein TJ1, Glazer PM.. Author information. 1. Department of Therapeutic Radiology, ... they downregulate a number of DNA repair pathways, thus leading to genetic instability. Understanding the mechanisms involved ...
Genital Neoplasms, Male. Urogenital Neoplasms. Neoplasms by Site. Neoplasms. Genital Diseases, Male. Niraparib. Poly(ADP-ribose ... A Phase 2 Efficacy and Safety Study of Niraparib in Men With Metastatic Castration-Resistant Prostate Cancer and DNA-Repair ... An Efficacy and Safety Study of Niraparib in Men With Metastatic Castration-Resistant Prostate Cancer and DNA-Repair Anomalies ... Biomarker-positive by at least one of the following criteria: (a) Biallelic deoxyribonucleic acid (DNA)-repair anomaly based on ...
Prostatic Neoplasms. Congenital Abnormalities. Genital Neoplasms, Male. Urogenital Neoplasms. Neoplasms by Site. Neoplasms. ... A Phase 2 Efficacy and Safety Study of Niraparib in Men With Metastatic Castration-Resistant Prostate Cancer and DNA-Repair ... An Efficacy and Safety Study of Niraparib in Men With Metastatic Castration-Resistant Prostate Cancer and DNA-Repair Anomalies ... ORR in participants with measurable metastatic castration-resistant prostate cancer (mCRPC) and DNA-repair anomalies. ORR of ...
Keywords: BRCA1 and BRCA2 mutations; PD-1 and PD-L1; high grade serous ovarian cancer; homologous recombination DNA repair; ... Ovarian Neoplasms / genetics * Ovarian Neoplasms / immunology* * Ovarian Neoplasms / metabolism * Ovarian Neoplasms / pathology ... 5 Division of Genomic Stability and DNA Repair, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA. ...
Colorectal Neoplasms, Hereditary Nonpolyposis / genetics* * DNA Repair / genetics* * DNA, Neoplasm / analysis * DNA-Binding ...
Genetic polymorphisms in genes related to PAH metabolism, cell cycle control, and DNA repair associated with the risk of lung ... Whether polymorphisms in genes related to PAH metabolism, cell cycle control, and DNA repair modify the PAHs-lung cancer ... 442 Studies found for: lung neoplasms AND (woman OR women OR female) ...
Assess activity of novel DNA repair inhibitors as a function of DNA repair mutations detected in CTC samples ... Circulating Tumor DNA in Surgical Lung Cancer Patients. *Lung Neoplasms. Observational. *Shenzhen Gene Health Bio Tech Co., Ltd ... Irreversible Electroporation(IRE) For Lung Neoplasms Accompanied by Respiratory Function Insufficiency. *Lung Neoplasms ... Studying Tumor Tissue Samples and Blood Samples to Learn More About DNA Changes in Patients With Lung Cancer. *Lung Cancer ...
DNA Damage • DNA Methylation • DNA Modification Methylases • DNA RepairDNA, NeoplasmDNA-Binding Proteins • Dopamine • ... Ulrich, CM; Reed, MC; Nijhout, HF, Modeling folate, one-carbon metabolism, and DNA methylation., Nutrition Reviews, vol. 66 ... official journal of the DNA Methylation Society, vol. 1 no. 2 (April, 2006), pp. 81-87, ISSN 1559-2294 [17998813] [abs] * ... Neoplasms • Neural Tube Defects • Neurons • Neuropeptides • Neurosecretory Systems • Nonlinear Dynamics • Nutrition • Nutrition ...
Malignant neoplasms[edit]. DNA damage[edit]. The central role of DNA damage and epigenetic defects in DNA repair genes in ... Deficiencies in DNA repair cause increased mutation rates.[34][35][36] A deficiency in DNA repair, itself, can allow DNA ... During repair of DNA double strand breaks, or repair of other DNA damages, incompletely cleared sites of repair can cause ... ICD-10 classifies neoplasms into four main groups: benign neoplasms, in situ neoplasms, malignant neoplasms, and neoplasms of ...
abnormal DNA repair*cells from the small intestine exhibit an increase in gamma-H2AX foci, indicative of DNA damage, compared ... neoplasm. *decreased incidence of induced tumors*fifth generation mutants show decreased tumor growth rate and lower tumor ... abnormal DNA repair*cells from the small intestine exhibit an increase in gamma-H2AX foci, indicative of DNA damage, compared ... neoplasm. *increased lymphoma incidence*the incidence of lymphomas decreases in successive generation ...
DNA Mismatch Repair Status Predicts Need for Future Colorectal Surgery for Metachronous Neoplasms in Young Individuals ... This study aims to assess the prognostic role of DNA mismatch repair deficiency and extended colorectal resection for ... Mismatch repair deficiency was identified in biospecimens from 44% of patients and was significantly associated with an ... Using univariate and multivariate analysis, we assessed the prognostic role of mismatch repair deficiency and standard ...
... a necessary component of DNA mismatch repair (MMR), in G2-M cell cycle checkpoint arrest after 6-thioguanine (6-TG) exposure ... Colonic Neoplasms / genetics*. DNA Repair. Fibroblasts. Humans. Mice. Mice, Knockout. Neoplasm Proteins / genetics, physiology* ... A role for the Mut L homologue-1 (MLH1) protein, a necessary component of DNA mismatch repair (MMR), in G2-M cell cycle ... Defective expression of the DNA mismatch repair protein, MLH1, alters G2-M cell cycle checkpoint arrest following ionizing ...
DNA repair, cell-cycle checkpoints, and transcriptional regulation. BRCA1 germline mutations confer a high risk of early-onset ... DNA Mutational Analysis. DNA Repair-Deficiency Disorders. DNA, Neoplasm / analysis. Death-Associated Protein Kinases. Female. ... BRCA1 breast cancers displayed a mutational signature consistent with that caused by lack of HR DNA repair in both ER-positive ... BRCA1 encodes a tumour suppressor protein that plays pivotal roles in homologous recombination (HR) DNA repair, cell-cycle ...
Mutations in DNA repair genes implicated in cellular mechanisms of familial MDS/acute leukemia ... Although the mechanistic underpinnings of this observation are unknown, the RUNX1 link to DNA repair pathways (e.g., RUNX1 ... Disruption of Runx1 and Runx3 leads to bone marrow failure and leukemia predisposition due to transcriptional and DNA repair ... The C/EBPα basic region contains DNA-binding specificity and affinity determinants (159). Since C/EBPα binds DNA as a homo- or ...
Influence of DNA repair gene polymorphisms on the initial repair of MMS-induced DNA damage in human lymphocytes as measured by ... Second Malignant Neoplasms and Cardiovascular Disease Following Radiotherapy. Journal of the National Cancer Institute 2012, ... DNA mismatch repair status affects cellular response to Ara-C and other anti-leukemic nucleoside analogs. Leukemia 2011, 25(6 ... Meeting Abstract] DNA repair dysfunction and genomic instability in therapy-related malignancy. Mutagenesis 2009, 24(6), 530. ...
2.8 DNA Repair-Associated Genes; 2.9 RNA Processing Genes; 2.10 Wnt Pathway Genes."@en ;. schema:description "This book ... Pancreatic Neoplasms a schema:Intangible ;. schema:name "Pancreatic Neoplasms"@en ;. . ... 2.8 DNA Repair-Associated Genes; 2.9 RNA Processing Genes; 2.10 Wnt Pathway Genes. 2.11 Phosphatidylinositol 3-Kinase (PI3K) ... 3.1.8 Acinar Neoplasms; 3.1.9 Solid Pseudopapillary Neoplasm; 3.1.10 Pancreatoblastoma; 3.1.11 Miscellaneous Cystic Pancreatic ...
Hereditary Nonpolyposis Colorectal Neoplasms * Colorectal Neoplasms * Frameshift Mutation * DNA Mismatch Repair * Nonsense ... Cancer risks by gene, age, and gender in 6350 carriers of pathogenic mismatch repair variants: findings from the Prospective ... Risk-reducing hysterectomy and bilateral salpingo-oophorectomy in female heterozygotes of pathogenic mismatch repair variants: ... and a Subset With Retained Mismatch Repair Function. Klarskov, L. L., Holck, S., Bernstein, I. T., Okkels, H., Rambech, E., ...
Cancer risks by gene, age, and gender in 6350 carriers of pathogenic mismatch repair variants: findings from the Prospective ... Correction: Cancer risks by gene, age, and gender in 6350 carriers of pathogenic mismatch repair variants: findings from the ... Diskrepans mellem immunhistokemisk ekspression af mismatch repair proteiner i colorectale carcinomer og gentest. Lindberg, L. J ... Diskrepans mellem immunhistokemisk ekspression af mismatch repair proteiner i colorectale carcinomer og gentest. Lindberg, L. J ...
They also function in DNA REPAIR; transcriptional reactivation of latent HIV-1; and pre-mRNA processing and nuclear export of ... Colorectal Neoplasms. Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ... Heat and cold stress-inducible, transcription factors that bind to inverted 5-NGAAN-3 pentamer DNA sequences and are ...
Adding to the diagnostic difficulty is the plethora of melanocytic neoplasms that are common in the... ... Cancer and neurologic degeneration in xeroderma pigmentosum: long term follow-up characterises the role of DNA repair. J Med ... DNA extraction from formalin-fixed, paraffin-embedded tissue. Cold Spring Harb Protoc. 2009;2009(2):pdb.prot5138.PubMedCrossRef ... Pediatric melanoma and atypical melanocytic neoplasms. Cancer Treat Res. 2016;167:331-69.PubMedCrossRefGoogle Scholar ...
Colorectal neoplasms hereditary Nonpolyposis DNA repair gene Mutation DNA diagnosis Abbreviations. HNPCC. Hereditary ... Mutation in the DNA mismatch repair gene homologue hMLH1 is associated with hereditary non-polyposis colon cancer. Nature 368: ... Orita M, Suzuki Y, Sekiya T, Hayashi K (1989) Rapid and sensitive detection of point mutations and DNA polymorphisms using the ... These results indicate the value of DNA analysis in the screening and diagnosis of HNPCC patients and families. ...
DNA REPAIR DISEASES HNPCC, Xeroderma pigmentosum (excision repair defect-unusaully sensitive to sunlight because cant repair T ... w what neoplasm: Xeroderma pigmentosum; albinism melanoma, basal cell carcinoma, squamous cell carcinomas of skin ...
Ferguson on neoplasm malignant genitourinary: Carcinoids are carcinomas, usually more slow growing than adenocarcinomas. For ... such as programmed cell death or by preventing repair of DNA damage. ...Read more ... Neoplasms (Definition) "tumor" literally translates as "mass", so even a fresh bruise could be called a "tumor". Doctors use ... Not necessary: Hurtel cell neoplasm can be adenoma (not cancer) or carcinoma (cancer). There is not much difference between the ...
DNA Adducts; DNA Damage; DNA Repair; Melanoma, Experimental; Molecular Biology; Mutagenesis; Photobiology; Skin Neoplasms; ... Kidney Neoplasms; Penile Neoplasms; Prostatic Neoplasms; Testicular Neoplasms; Urinary Bladder Neoplasms; Urologic Neoplasms; ... Biophysics; Cell Hypoxia; DNA Damage; Heavy Ion Radiotherapy; Lung Neoplasms; Physics; Prostatic Neoplasms; Radiation Oncology ...
Neo Neoplasms. Translation:HumansCells * Beltran H. DNA mismatch repair in prostate cancer. J Clin Oncol. 2013 May 10; 31(14): ... Inherited DNA-Repair Gene Mutations in Men with Metastatic Prostate Cancer. N Engl J Med. 2016 Aug 04; 375(5):443-53. PMID: ... Biallelic tumour suppressor loss and DNA repair defects in de novo small-cell prostate carcinoma. J Pathol. 2018 10; 246(2):244 ... Clinical Outcome of Prostate Cancer Patients with Germline DNA Repair Mutations: Retrospective Analysis from an International ...
... Malignant neoplasm of prostate , Prostate Disorders , Prostatic disorder , Recurrent , ... An Efficacy and Safety Study of Niraparib in Men With Metastatic Castration-Resistant Prostate Cancer and DNA-Repair Anomalies ...
... An Efficacy and Safety Study of Niraparib in Men With Metastatic Castration-Resistant Prostate Cancer and DNA-Repair Anomalies ... Clinical trial for Malignant neoplasm of prostate , ...
DNA Repair; DNA Replication; Genes, Tumor Suppressor; Head and Neck Neoplasms; Human papillomavirus 11; Oncogenes; ... DNA Virus Infections; Membrane Lipids; Neoplasms; Papillomaviridae; Peptides; Polyomaviridae; Proteins; Tumor Virus Infections ... DNA Replication; Epstein-Barr Virus Infections; Infectious Disease Medicine; Oncogenic Viruses; Pediatrics; Phosphorylation; ... Arboviruses; Autophagy; Central Nervous System Viral Diseases; DNA Viruses; Encephalitis, Viral; Herpes Simplex; Immune System ...
  • We compared the DNA repair gene expression in cultivated untreated primary fibroblasts of both patients groups using customized cDNA microarrays (800 genes). (
  • 3 Both Muir-Torre and Lynch syndromes are linked to germline mutations in the DNA mismatch repair genes MLH1 , MLH3 , MSH2 and MSH6 . (
  • [3] They also frequently have reduced expression of DNA repair enzymes due to epigenetic methylation of DNA repair genes or altered microRNAs that control DNA repair gene expression. (
  • HNPCC has been associated with germline mutations in mismatch repair (MMR) genes. (
  • It is known that the expression of DSB repair genes is increased in tumors, which is one of the main reasons for radioresistance. (
  • Muir-Torre syndrome is most frequently caused by mutational inactivation of mismatch repair genes MSH2 and MLH1 with resultant microsatellite instability. (
  • Another involves mutations of DNA mismatch repair genes. (
  • Reduced activity of double-strand break repair genes in prostate cancer patients with late normal tissue radiation toxicity. (
  • Overall, the prevalence of MSI-H colorectal tumor was 2-3-fold higher, while the defect in the percentage expression of mismatch repair (MMR) genes (hMLH1 and hMSH2) was similar in AA patients compared to the U.S. Caucasian population. (
  • Mjelle R, Hegre SA, Aas PA et al (2015) Cell cycle regulation of human DNA repair and chromatin remodeling genes. (
  • Determine PAR levels in tumor biopsies, evaluate in archival tissue whether patients' tumors have mutations in genes involved in DNA damage repair (e.g. (
  • When DNA structural integrity is compromised, specific genes and proteins are activated. (
  • Inherited predisposition to breast cancer is known to be caused by loss-of-function mutations in BRCA1, BRCA2, PALB2, CHEK2, and other genes involved in DNA repair. (
  • p53, known as the "guardian of the genome," is a sequence-specific transcription factor that binds DNA and transactivates cellular proteins involved in growth and cell cycle regulation ( 1 - 6 ). (
  • Other mismatch repair proteins can be involved, such as MSH6 and PMS2. (
  • By antibody microarrays, we screened primary fibroblasts of matched patients for differences in the amount of representative DNA repair-associated proteins. (
  • We found constitutively decreased levels of RAD9A and several other DNA repair proteins in two-cancer patients, compared to one-cancer patients. (
  • Conclusions/Significance: Collectively, our results support the idea that modulation of RAD9A and other cell cycle arrest and DNA repair proteins contribute to the risk of developing a second malignancy in childhood cancer patients. (
  • We found constitutively decreased levels of RAD9A and several other DNA repair proteins in two-cancer patients, compared to onecancer patients. (
  • MSH proteins recognize errors in the genome sequence during replication, preventing the duplication of the damaged strand and repairing single strand breaks [ 11 , 12 ]. (
  • ROS are involved in inflammation-induced oxidative damage to cellular components including regulatory proteins and DNA. (
  • The term neoplasm refers to an abnormal growth of tissue caused by the rapid division of cells that have undergone some form of mutation. (
  • DNA mismatch repair corrects replication errors, thus reducing mutation rates and microsatellite instability. (
  • In this second part of our two-part review, we discuss the use of mutation profiling in the diagnosis, prognosis, and treatment of patients with myeloproliferative neoplasms and other myeloid diseases. (
  • Myeloproliferative neoplasms (MPNs) often carry JAK2(V617F), MPL(W515L), or CALR(del52) mutations. (
  • In addition to these 11 families already diagnosed with HNPCC, 3 new families with germ line mutations of hMSH2 gene and hMLH1 gene were found through analysis of DNA from patients who had multiple cancers with alteration in microsatellite DNA. (
  • In families in which germ line mutations were identified presymptomatic examination was then carried out using polymerase chain reaction single-strand conformation polymorphism analysis of DNA from peripheral blood, and the result was the detection of family members predisposed to HNPCC who did not yet show signs of cancer. (
  • This defect is caused by mutations in the (pol)eta polymerase, which initiates translesion synthesis of UV-damaged DNA in an error-free manner. (
  • In 2013, two seminal studies identified gain-of-function mutations in the Calreticulin ( CALR ) gene in a subset of JAK2 / MPL -negative myeloproliferative neoplasm (MPN) patients. (
  • Molecular characterization of myeloproliferative neoplasms (MPN), a group of hematologic neoplasms, has greatly evolved since the discovery of JAK2 V617F in 2005 ( 1-3 ), and subsequent gene discovery studies which identified additional driver mutations present in patients with MPN, namely activating JAK exon 12 mutations ( 4 ), MPL W515L ( 5 ), and most recently a spectrum of mutations in CALR . (
  • The great majority of these missense mutations have been mapped to the central DNA-binding region of the protein. (
  • We have recently found that transition metals such as nickel and chromium and oxidative stress induced lipid peroxidation metabolites such as aldehydes can greatly inhibit nucleotide excision repair (NER) and enhance carcinogen-induced mutations. (
  • This phase II trial studies how well olaparib works in treating patients with biliary tract cancer that has spread to other places in the body (metastatic) and with aberrant DNA repair gene mutations. (
  • So far, a reliable spectrum of mitochondrial DNA mutations in colorectal cancer cells is still unknown, and neither is their significance in carcinogenesis. (
  • We have analyzed both genetic (mutations of BRAF, KRAS, and p53 and microsatellite instability) and epigenetic alterations (DNA methylation of 27 CpG island promoter regions) in 97 primary colorectal cancer patients. (
  • Thus, the process of DNA replication associates with many errors that expose growing cells to a risk of acquiring mutations. (
  • APC gene mutations, seen in most colon neoplasms, are not found in pancreatic cancer. (
  • In addition, mutational analyses were performed using constitutional DNA from index patients, and deleterious heterozygous germline mutations were assessed for loss of heterozygosity in sorted leukaemic cells by single nucleotide polymorphism array. (
  • These results indicate that DGGE provides a reliable method for the detection of the presence of point mutations in the LDLR gene of FH patients, thereby facilitating the introduction of rapid DNA diagnosis for this common and genetically heterogeneous disorder. (
  • The influence of p53 status on the efficiency of the principal steps of this repair pathway was investigated after UV-C irradiation in the human ovarian carcinoma cell line IGROV-1 (expressing wild-type p53) and in the derived clone IGROV-1/Pt1 (with p53 mutations at codons 270 and 282). (
  • Results With a median latency of 79 months, 18 patients developed therapy-related acute myeloid leukemia and 21 presented with therapy-related myelodysplastic syndromes (8 refractory anemia with excess blasts I/II, 6 refractory anemia with multilineage dysplasia, 3 myelodysplastic syndromes with del(5q), 1 refractory anemia, 1 refractory anemia with ring sideroblasts, 1 chronic myelomonocytic leukemia II, 1 myelodysplastic/myeloproliferative neoplasm unclassifiable). (
  • Therapy related myeloid neoplasms (t-MNs) constitute a distinct clinical syndrome including therapy related acute myeloid leukaemia (t-AML), myelodysplastic syndrome (t-MDS), and myelodysplastic/myeloproliferative neoplasm (t-MDS/MPN). (
  • 1] As an example, for patients with a suspected myeloproliferative neoplasm (MPN), the presence of mutated CALR and/or absence of mutated JAK2 virtually excludes polycythemia vera as a potential diagnosis, with only rare exceptions. (
  • Potentially-malignant neoplasms include carcinoma in situ . (
  • Hurtel cell neoplasm can be adenoma (not cancer ) or carcinoma (cancer). (
  • As the study subjects were very heterogeneous regarding their first and second neoplasms, we performed two subgroup analyses in the most common groups: Subjects with lymphoid leukaemia as a fist neoplasm (n=10) and subjects with thyroid carcinoma as second neoplasm (n=6). (
  • The potentially aggressive course of sebaceous carcinoma necessitates accurate differentiation from benign sebaceous neoplasms. (
  • Trials with DNA mismatch repair protein Msh3 Expression Negative in the inclusion eligibility criteria most commonly target colorectal carcinoma, malignant solid tumor, gastric carcinoma, breast carcinoma, and endometrial carcinoma [ 5 ]. (
  • Atr kinase inhibitor bay1895344, anti-pd-1 monoclonal antibody jnj-63723283, and anti-pd1/ctla4 bispecific antibody xmab20717 are the most frequent therapies in trials for colorectal carcinoma that contain DNA mismatch repair protein Msh3 Expression Negative [ 5 ]. (
  • Anti-pd1/ctla4 bispecific antibody xmab20717, parp inhibitor bgb-290, and pi3k-delta inhibitor incb050465 are the most frequent therapies in trials for breast carcinoma that contain DNA mismatch repair protein Msh3 Expression Negative [ 5 ]. (
  • Renal cell carcinoma (RCC) is a highly immunogenic neoplasm, and cytokine-based immunotherapies have been used for decades with limited success. (
  • In the present study, we investigated the effect of trifluoperazine on (a) survival of bleomycin-treated human non-small cell lung carcinoma U1810 cells, (b) induction and repair of bleomycin-induced DNA strand breaks, and (c) nonhomologous end-joining (NHEJ), the major DNA double-strand break (DSB) repair pathway in mammalian cells. (
  • Basal cell carcinoma - BCC is considered a multifactorial neoplasm involving genetic, epigenetic and environmental factors. (
  • Thus, repair defects in p53-mutant ovarian carcinoma cells may be attributed to late events, possibly related to a reduced removal/recycling of PCNA at repair sites. (
  • DNA Mismatch Repair Status Predicts Need for Future Colorectal Surgery for Metachronous Neoplasms in Young Individuals Undergoing Colorectal Cancer. (
  • This study aims to assess the prognostic role of DNA mismatch repair deficiency and extended colorectal resection for metachronous colorectal neoplasia risk in young patients with colorectal cancer. (
  • Also, a DNA mismatch repair defect, seen in 15% of colorectal cancer, is uncommon in pancreatic cancer. (
  • For lymphoid neoplasms, e.g. lymphoma and leukemia , clonality is proven by the amplification of a single rearrangement of their immunoglobulin gene (for B cell lesions) or T cell receptor gene (for T cell lesions). (
  • We investigated the association between gene expression involved in DNA-repair and the development of SNs after childhood cancer. (
  • The DNA-repair gene results showed small differences in the basal gene expression of FTH1 and CDKN1A. (
  • To our knowledge, this is the first study using gene expression arrays in untreated primary fibroblasts regarding second neoplasms after a childhood neoplasm. (
  • The biological importance of the differences in the DNA-repair gene expression has to be elucidated yet. (
  • p53 is the most frequently mutated gene in human neoplasms ( 7 ). (
  • This gene encodes a DNA polymerase. (
  • Along the length of each gene, the DNA base at most positions is the same for everyone. (
  • It is thought that the protein encoded by this gene confers specificity to the SNF/SWI complex and may recruit the complex to its targets through either protein-DNA or protein-protein interactions. (
  • The tumour suppressor gene TP53 plays an important role in the regulation of DNA repair, and particularly of nucleotide excision repair. (
  • The diverse and damaging stimuli that affect DNA integrity, such as changes in the genetic sequence and modifications in gene expression, can disrupt the steady state of the cell and have serious repercussions to pathways that regulate apoptosis, senescence, and cancer. (
  • MSI is a common marker of an underlying functional inactivation of a human DNA mismatch repair (MMR) gene (Jeong et al. (
  • as tumors are exposed to repeated cycles of hypoxia and reoxygenation, they downregulate a number of DNA repair pathways, thus leading to genetic instability. (
  • A predisposition for the occurrence of a SN might be a pre-existing somatic genetic defect associated with DNA repair. (
  • We and others ( 11 - 16 ) have reported that genetic predisposition involved in several molecular pathways, such as carcinogen metabolism, DNA repair, and cell cycle control, is associated with the risk for SPM after primary SCCHN. (
  • A stepwise progression model involving two distinct genetic pathways has been proposed to explain the etiology of colon cancer from benign neoplasm to adenocarcinoma ( 2 ). (
  • It is plausible to assume that genetic differences, i.e. in the pathways responsible for cell cycle control and DNA repair, play a critical role in the development of secondary cancer. (
  • The cell continuously counteracts these processes and has developed a complex network to repair genetic alterations. (
  • 5 , 6 t-MNs are regarded as complex diseases and previously published data on genetic predisposition to t-MNs pointed to an interactive effect of different single nucleotide polymorphisms (SNPs) in pathways that mediate carcinogen detoxification, proliferation, DNA repair, and apoptosis. (
  • 7 , 8 The demonstration of increased familial tumour risk in patients with AML following a primary neoplasm further supported the concept of genetic susceptibility to t-MNs. (
  • Although researchers have learned much from the study of this diverse group of tumors over the years, the diagnosis and treatment of salivary gland neoplasms remain complex and challenging problems for the head and neck surgeon. (
  • Salivary gland neoplasms make up 6% of all head and neck tumors. (
  • Benign neoplasms occur more frequently in women than in men, but malignant tumors are distributed equally between the sexes. (
  • Almost half of all submandibular gland neoplasms and most sublingual and minor salivary gland tumors are malignant. (
  • Primary brain tumors, in particular, glioblastoma multiforme (GBM), continue to have dismal survivability despite advances in treating other neoplasms. (
  • In humans this defense can contribute to the ability of some tumors to resist the effects of chemotherapeutic agents that act through DNA alkylation. (
  • We anticipate that APLF could be exploited as a biomarker for breast tumors and additionally could be targeted in sensitizing cancer cells towards DNA damaging agents. (
  • Lipomas - These growths arise from fat cells and are the most common type of benign neoplasm found in adults, often occurring in the back, arms, neck or shoulders. (
  • Muir-Torre syndrome is an autosomal dominant cancer syndrome expressed clinically as cutaneous tumours (sebaceous neoplasms or multiple keratoacanthomas) and visceral malignant disease. (
  • 2 , 3 Sebaceous neoplasms occur in 9% of patients with Lynch syndrome. (
  • 2 In patients with Muir-Torre syndrome, sebaceous neoplasms appear as pink-to-yellowish papules or nodules, 1 which may precede visceral malignant disease in 22%-60% of patients. (
  • Sebaceous neoplasms should prompt clinicians to consider Muir-Torre syndrome: biopsy and cancer screening should be considered in the setting of multiple, especially eruptive, facial papules and a patient or family history of cancer. (
  • 2 Retinoids given orally have been used to treat sebaceous neoplasms. (
  • Caution is necessary when using adipophilin to distinguish sebaceous neoplasms from other cutaneous lesions with clear cell histology. (
  • 5,6) Xanthomatous lesions, including xanthelasma and xanthogranuloma, reportedly show adipophilin reactivity, but in contrast to the membranous vesicular pattern in sebaceous neoplasms, xanthomatous lesions show a more granular pattern. (
  • 158320 ]. Rare autosomal dominant disorder characterized by sebaceous neoplasms and visceral malignancy. (
  • benign neoplasms , in situ neoplasms , malignant neoplasms , and neoplasms of uncertain or unknown behavior. (
  • [5] Malignant neoplasms are also simply known as cancers and are the focus of oncology . (
  • Malignant neoplasms are commonly called cancer. (
  • [ 1 ] The incidence of salivary gland neoplasms as a whole is approximately 5.5 cases per 100,000 individuals in the United States, with malignant neoplasms accounting for 0.9 cases per 100,000. (
  • DNA damage is considered to be the primary underlying cause of malignant neoplasms known as cancers. (
  • Cleaver's seminal work in 1968 elucidated the pathophysiology of xeroderma pigmentosum by demonstrating defective DNA repair. (
  • This repair process, known as unscheduled DNA synthesis, is deficient in xeroderma pigmentosum. (
  • Cell complementation analysis of cultured cells from patients with xeroderma pigmentosum demonstrated that xeroderma pigmentosum was genetically heterogeneous for the ability to repair UV-induced thymine dimers. (
  • Fibroblasts from different patients with xeroderma pigmentosum were fused, and DNA repair after UV exposure was assayed. (
  • The xeroderma pigmentosum variant complementation group (XP-V) has normal unscheduled DNA synthesis after UV exposure. (
  • The purpose of this study is to assess the efficacy, safety, and pharmacokinetics of niraparib in men with metastatic castration resistant prostate cancer (mCRPC) and deoxyribonucleic acid (DNA) repair anomalies. (
  • ORR in participants with measurable metastatic castration-resistant prostate cancer (mCRPC) and DNA-repair anomalies. (
  • A neoplasm can be benign , potentially malignant, or malignant ( cancer ). (
  • Secondary neoplasm refers to any of a class of cancerous tumor that is either a metastatic offshoot of a primary tumor, or an apparently unrelated tumor that increases in frequency following certain cancer treatments such as chemotherapy or radiotherapy . (
  • Is hurtle cell neoplasm defined as cancer? (
  • Cutaneous photosensitivity and early development of skin cancer is caused by defective DNA repair. (
  • Treatment of the primary neoplasm with radiotherapy or chemotherapy is an established risk factor for second neoplasms (SNs) after childhood cancer. (
  • The central features of DNA damage, epigenetic alterations and deficient DNA repair in progression to cancer are shown in red. (
  • Tobacco smoke causes increased exogenous DNA damage, and these DNA damages are the likely cause of lung cancer due to smoking. (
  • Helicobacter pylori infection produces high levels of reactive oxygen species that damage DNA and contributes to gastric cancer. (
  • Bile acids, at high levels in the colons of humans eating a high fat diet, also cause DNA damage and contribute to colon cancer. (
  • Inflammation-induced ROS that cause DNA damage can trigger apoptosis, but may also cause cancer if repair and apoptotic processes are insufficiently protective. (
  • I would add that the argument that non-ionizing radiation cannot cause cancer because it cannot break DNA double bonds, has been disproven by the acceptance that the lower energy ultra-violet light can, with time, cause skin cancer. (
  • DNMT (DNA methyltransferase) inhibitors radiosensitize human cancer cells by suppressing DNA repair activity. (
  • The increased risk of cancer seen in patients with by the syndrome is associated with dysfunction of DNA repair mechanism. (
  • The inhibition of DSB repair pathways may be useful to increase tumor cell radiosensitivity and may target stem cell-like cancer cells, known to be the most radioresistant tumor components. (
  • Improperly repaired DSBs increase genomic instability, chromosomal translocation, and cancer risk ( 1 ). (
  • Thus, the ability to repair DSBs in cancer cells confers radioresistance, while RT reaching normal cells induces, among other side effects, the development of secondary malignancies. (
  • Second, cancer cells often have intrinsic dis-regulations of DNA repair. (
  • It is possible to specifically target a particular repair pathway for cancer therapy with a comprehensive understanding of how each of the DNA repair pathways interfaces with others. (
  • This, in turn, will allow a more fruitful understanding of how cancer cells specifically rely on each repair mechanism to maintain growth advantage. (
  • As expected, the anticancer activity of conventional genotoxic drugs is significantly augmented by combined treatment with RECQL1- or WRN-siRNAs that prevents DNA repair in cancer cells. (
  • Repair of ionizing radiation-induced DNA damage and risk of second cancer in childhood cancer survivors. (
  • Long-term risks of subsequent primary neoplasms among survivors of childhood cancer. (
  • Subsequent neoplasms in 5-year survivors of childhood cancer: the Childhood Cancer Survivor Study. (
  • Large-scale genomic analyses link reproductive aging to hypothalamic signaling, breast cancer susceptibility and BRCA1-mediated DNA repair. (
  • The RAD9A protein level increased in response to DNA damage, however to a lesser extent in the two-cancer patients. (
  • Targeting DNA Damage Response in Prostate Cancer by Inhibiting Androgen Receptor-CDC6-ATR-Chk1 Signaling. (
  • Ipilimumab plus nivolumab and DNA-repair defects in AR-V7-expressing metastatic prostate cancer. (
  • However, six pedigrees were suggestive for a hereditary breast and ovarian cancer syndrome, three of a Li-Fraumeni like syndrome, and three index patients showed multiple primary neoplasms. (
  • We propose that TFP might be capable of inhibiting one or more elements of the DNA DSB repair machinery, thereby increasing the cytotoxicity of bleomycin in lung cancer cells. (
  • Dizdaroglu M (2015) Oxidatively induced DNA damage and its repair in cancer. (
  • So, based on the involvement of APLF in MET and DNA repair, we studied the role of APLF in breast cancer. (
  • To this end, we carried out exome sequencing of constitutional genomic DNA from 24 breast cancer patients from 11 Finnish breast cancer families. (
  • From all rare damaging variants, 22 variants in 21 DNA repair geneswere genotyped in 3,166 breast cancer patients, 569 ovarian cancer patients, and 2,090 controls, all from the Helsinki or Tampere regions of Finland. (
  • Defective expression of the DNA mismatch repair protein, MLH1, alters G2-M cell cycle checkpoint arrest following ionizing radiation. (
  • A role for the Mut L homologue-1 (MLH1) protein, a necessary component of DNA mismatch repair (MMR), in G2-M cell cycle checkpoint arrest after 6-thioguanine (6-TG) exposure was suggested previously. (
  • MMR-deficient HCT116 cells or embryonic fibroblasts from MLH1 knockout mice also demonstrated classic DNA damage tolerance responses after 6-TG exposure. (
  • MLH1-mediated G2-M cell cycle delay (caused by either MMR proofreading of DNA lesions or by a direct function of the MLH1 protein in cell cycle arrest) may be important for DNA damage detection and repair prior to chromosome segregation to eliminate carcinogenic lesions (possibly brought on by misrepair) in daughter cells. (
  • Unlike FAMILIAL POLYPOSIS COLI with hundreds of polyps, hereditary nonpolyposis colorectal neoplasms occur much later, in the fourth and fifth decades. (
  • Ruxolitinib inhibited 2 major DSB repair mechanisms, BRCA-mediated homologous recombination and DNA-dependent protein kinase-mediated nonhomologous end-joining, and, when combined with olaparib, caused abundant accumulation of toxic DSBs resulting in enhanced elimination of MPN primary cells, including the disease-initiating cells from the majority of patients. (
  • BRCA1 encodes a tumour suppressor protein that plays pivotal roles in homologous recombination (HR) DNA repair, cell-cycle checkpoints, and transcriptional regulation. (
  • Eukaryotic homolog of the bacterial MutL DNA MISMATCH REPAIR protein. (
  • It heterodimerizes with MISMATCH REPAIR ENDONUCLEASE PMS2 to form MutL alpha, which is recruited to DNA mismatch sites by the MUTS DNA MISMATCH-BINDING PROTEIN. (
  • Strongly stimulates the DNA strand-invasion activity of RAD51, stabilizes the nucleoprotein filament against a disruptive BRC3-BRC4 polypeptide and helps RAD51 to overcome the suppressive effect of replication protein A (RPA). (
  • DNA mismatch repair protein Msh3 Expression Negative serves as an inclusion eligibility criterion in 16 clinical trials, of which 16 are open and 0 are closed. (
  • Of the trials that contain DNA mismatch repair protein Msh3 Expression Negative as an inclusion criterion, 5 are phase 1 (5 open), 5 are phase 1/phase 2 (5 open), and 6 are phase 2 (6 open). (
  • Nivolumab, pembrolizumab, atr kinase inhibitor bay1895344, anti-pd-1 monoclonal antibody jnj-63723283, and anti-pd1/ctla4 bispecific antibody xmab20717 are the most frequent therapies in trials with DNA mismatch repair protein Msh3 Expression Negative as an inclusion criteria [ 5 ]. (
  • Loss of ARID1A expression is associated with DNA mismatch repair protein deficiency and favorable prognosis in advanced stage surgically resected esophageal adenocarcinoma. (
  • The identification of O 6 -alkylguanine-DNA alkyltransferase (AGAT) as a major determinant of nitrosourea resistance has resulted in the development of several agents to inactivate this repair protein and counteract tumor cell resistance. (
  • This epimutation was associated with reduced basal protein levels and a higher induction of BRCA1 after DNA damage. (
  • E3 ubiquitin-protein ligase that specifically mediates the formation of 'Lys-6'-linked polyubiquitin chains and plays a central role in DNA repair by facilitating cellular responses to DNA damage. (
  • These results indicate that the presence of mutant p53 protein and its persistent interaction with RPA do not affect the early steps of nucleotide excision repair in IGROV-1/Pt1 cells. (
  • This is accomplished through the interaction of protein heterodimers with the DNA sequence containing the mismatch. (
  • Design and Methods We retrospectively analyzed 39 patients with myeloid neoplasms following radioiodine treatment, whose data were reported to the Duesseldorf Myelodysplastic Syndromes Register (8 of 3814 patients) and five other German Myelodysplastic Syndromes centers (n=31) between 1982 and 2011. (
  • These data were compared with those from 165 patients from our Myelodysplastic Syndromes Register with therapy-related myeloid neoplasms following chemotherapy (n=90), radiation (n=30), or radiochemotherapy (n=45). (
  • Myelodysplastic syndromes (MDS), acute myeloid leukemia (AML) and myelodysplastic/myeloproliferative neoplasms (MDS/MPN) arising as late complications following cytotoxic treatment are summarized as 'therapy-related myeloid neoplasms' within the current World Health Organization (WHO) classification. (
  • Conclusions Patients developing a therapy-related myeloid neoplasm after radioiodine treatment usually present with biological characteristics similar to those seen in patients with therapy-related myeloid neoplasms following other cytotoxic treatment modalities, associated with a low response rate to induction chemotherapy and poor prognosis. (
  • Recent progress in chemotherapy for malignant gliomas was led by DNA-methylating agent temozolomide (TMZ). (
  • Exposure of normal somatic cells to radiation and/or chemotherapy can damage DNA and if not all DNA lesions are properly fixed, the mis-repair may lead to pathological consequences. (
  • Half of the asxl1 +/ − zebrafish had myeloproliferative neoplasms (MPNs) by 5 months of age. (
  • Furthermore, ROS have a major role in carcinogenesis and disease progression in the myeloproliferative neoplasms (MPNs), where the malignant clone itself produces excess of ROS thereby creating a vicious self-perpetuating circle in which ROS activate proinflammatory pathways (NF- κ B) which in turn create more ROS. (
  • The Philadelphia negative chronic myeloproliferative neoplasms (MPNs) encompass essential thrombocythemia (ET), polycythemia vera (PV), and myelofibrosis (MF). (
  • No differences in the distribution of gender, World Health Organization subtype, acute myeloid leukemia progression, International Prognostic Scoring System score, and cytogenetic risk were observed between patients with therapy-related myeloid neoplasms following radioiodine or other treatment modalities. (
  • The median overall survival in the entire group was 21.7 months (95%-CI 10.5-33 months) and did not differ significantly in comparison to the survival of patients with therapy-related myeloid neoplasms following other cytotoxic treatments. (
  • Background Therapy related myeloid neoplasms (t-MNs) are complex diseases originating from an interplay between exogenous toxicities and a susceptible organism. (
  • This chapter focuses on the diagnosis and classification of atypical melanocytic neoplasms and melanoma in pediatric patients. (
  • UV light from solar radiation causes DNA damage that is important in melanoma. (
  • Histone modifications and DNA methylation are two major factors in epigenetic phenomenon. (
  • Genomic instability may result in numerous defects like replication errors, telomere dysfunction, epigenetic changes or defective DNA repair as a few examples. (
  • In conclusion, we postulate that ruxolitinib-induced deficiencies in DSB repair pathways sensitized MPN cells to synthetic lethality triggered by PARP inhibitors. (
  • Two overlapping pathways for NER have been proposed: the rapid transcription-coupled repair directed at the transcribed strand and slower global genome repair, which also includes the nontranscribed strand. (
  • Ataxia-telangiectasia-mutated (ATM)-dependent DNA-damage response, non-homologous end joining, and homologous recombination pathways coordinately contribute to repairing DSBs in higher eukaryotes. (
  • Recently, the capabilities of these cytokines to support DNA repair pathways and the ATM-dependent DNA response have been demonstrated. (
  • RECQL1 and WRN helicases in the human RecQ helicase family participate in maintaining genome stability, DNA repair, replication, and recombination pathways in the cell cycle. (
  • The DNA repair system contains various reactions, such as nucleotide excision repair, base excision repair, homologous recombination (HR), and non-homologous end joining (NHEJ) recombination pathways, mismatch repair pathways, and telomere maintenance for genomic integrity, in all of which RecQ helicases are considered to participate. (
  • DNA repair pathways are critical to repair the plethora of DNA lesions that occur in MM, and deregulation of these pathways is implicated in disease onset and survival. (
  • Defective DNA repair pathways are implicated in the pathogenesis and survival of MM cells. (
  • The importance of post-translational modification with ubiquitin in the regulation of DNA repair pathways is being increasingly recognized. (
  • The ubiquitin proteasome system is an important therapeutic target in MM. This chapter provides an overview of ubiquitin signaling, describes genomic instability in MM cells and defects in ubiquitin-mediated regulation of DNA repair pathways in MM, and discusses the impact of current and potentially novel therapeutic approaches in targeting these aberrations. (
  • The BRCA1-BARD1 heterodimer coordinates a diverse range of cellular pathways such as DNA damage repair, ubiquitination and transcriptional regulation to maintain genomic stability. (
  • its role is paramount in the preservation of DNA integrity, placing it as a necessary focal point in the study of pathways that prolong lifespan, aging, and disease. (
  • Plays a critical role in homologous recombination repair (HRR) through its ability to recruit BRCA2 and RAD51 to DNA breaks. (
  • MutS alpha may also play a role in DNA homologous recombination repair. (
  • Contributes to homologous recombination repair (HRR) via its direct interaction with PALB2, fine-tunes recombinational repair partly through its modulatory role in the PALB2-dependent loading of BRCA2-RAD51 repair machinery at DNA breaks. (
  • Cells in the process of replication have various endogenous DNA damage in the chromosomes resulting from base-mismatch, deletion, DNA double-strand break (DSB) or from replication errors caused by stalled replication forks and other anomalous DNA structures, such as G-quadruplex (G4) DNA. (
  • However, the stability of the genome is constantly threatened by DNA replication errors and by DNA damage due to a multitude of exogenous and endogenous factors, e.g., oxidative stress. (
  • The mismatch repair - MMR is important DNA repair mechanisms to maintain replication fidelity. (
  • DNA MMR is an evolutionarily conserved process that corrects base mismatches generated during DNA replication that have escaped the proofreading process [ 9 ]. (
  • Microsatellite instability (MSI), or replication error (RER), is an example of genomic instability that occurs in certain human neoplasms in which tumor cells have diminished abilities to accurately replicate their DNA. (
  • Although mice deficient in these helicases are indistinguishable from wild-type mice, their embryonic fibroblasts are sensitive to DNA damage. (
  • Current English, however, both medical and non-medical, uses tumor as a synonym for a neoplasm (a solid or fluid-filled cystic lesion that may or may not be formed by an abnormal growth of neoplastic cells) that appears enlarged in size. (
  • After exposure to UV light, normal cultured cells identify and excise the UV-induced thymine dimers and insert undamaged nucleotides after DNA synthesis and ligation. (
  • Correction of DNA repair deficiency in the fused cells indicates that each cell line has a unique abnormality of DNA repair. (
  • However, the ability to repair DNA is reduced after adding caffeine to cultured cells. (
  • FACS analysis revealed low concentration FP induced accumulation of TMZ-treated cells, but not untreated cells, exclusively at G2 (4N DNA content). (
  • H2AX, a DNA double strand break marker, but also with increased release of cytochrome C in cytoplasm, which suggests that FP promoted apoptotic cell death signal in TMZ-treated glioma cells. (
  • FP also enhanced cytotoxity of TMZ to the cells with over-activated Akt, which has been previously shown to associate with TMZ resistance, and re-sensitized TR clones to TMZ Our results suggest that TMZ resistance could be promoted by enhanced DNA repair activity in G2-M transition following G2 checkpoint activation, and that cdk inhibitor enhanced TMZ cytotoxicity by suppression of this activity. (
  • Because PM is rich in metal and aldehyde content and can induce oxidative stress, we tested the effect of PM on DNA repair capacity in cultured human lung cells using in vitro DNA repair synthesis and host cell reactivation assays. (
  • We found that PM greatly inhibits NER for ultraviolet (UV) light and benzo(a)pyrene diol epoxide (BPDE) induced DNA damage in human lung cells. (
  • In proliferating cells, however, cellular DNA damage checkpoints coordinate an arrest at G1, intra-S, and G2 of the cell-cycle to allow the DNA repair process to eventually avoid mitotic catastrophe or mitosis of cells having unrepaired DNA damage. (
  • Multiple myeloma (MM) is a hematological neoplasm characterized by the clonal proliferation of malignant plasma cells in the bone marrow. (
  • During their maturation, plasma cells undergo physiological DNA rearrangements to generate a diverse range of antibodies. (
  • When a person is growing up, the cells of the body rapidly divide, but once adulthood is reached, cells generally only divide to replace worn-out, dying cells or to repair injured cells. (
  • Nonetheless, a small number of cells may not succeed in repairing damaged DNA. (
  • Moreover, trifluoperazine also increases the longevity of bleomycin-induced DNA strand breaks in U1810 cells, as shown by both comet assay and fraction of activity released (FAR)-assay. (
  • Functionally, APLF downregulation inhibited proliferative capacity, altered cell cycle behavior, induced apoptosis and impaired DNA repair ability of MDAMB-231 cells. (
  • Clonogenic survival after UV-C irradiation showed that IGROV-1/Pt1 cells were ∼2-fold more resistant to DNA damage than parental cells. (
  • In fact, both UV-induced DNA incision and the recruitment of proliferating cell nuclear antigen (PCNA) to DNA repair sites occurred to a comparable extent in p53-wild type and -mutant cell lines, although PCNA remained associated with chromatin for a longer period of time in IGROV-1/Pt1 cells. (
  • In contrast, lesion removal at 24 h was markedly reduced in IGROV-1/Pt1 cells, being ∼25% of the initial amount of damage, as compared with ∼50% repair in parental cells. (
  • However, cells have different mechanisms to maintain DNA biochemical integrity and stability. (
  • Circulating tumor cells are captured to predict the prognosis of patients in many types of cancers, but reports are rare on clinical utility and tumor cell shedding in neuroendocrine neoplasms (NENs). (
  • BRCA1 breast cancers displayed a mutational signature consistent with that caused by lack of HR DNA repair in both ER-positive and ER-negative cases. (
  • Unsupervised hierarchical clustering of the DNA methylation data identified three distinct groups of colon cancers named CpG island methylator phenotype (CIMP) 1, CIMP2, and CIMP negative. (
  • P16 and hMLH1 promoter methylation status was determined following bisulfite modification of DNA and using methylation specific PCR, while immunohistochemistry (IHC) was used to examine expression of hMLH1 and hMSH2. (
  • Several studies link chromosome rearrangements and aberrant DNA and histone methylation. (
  • Further studies of this defect led to significant progress in the understanding of nucleotide excision repair (NER) mechanisms under normal and pathologic conditions. (
  • Nucleotide excision repair (NER) is another DNA repair mechanism which differs from BER. (
  • Registered SN were confirmed to be no relapses or alternative manifestations of the primary neoplasm. (
  • We show here that cell lines expressing JAK2(V617F), MPL(W515L), or CALR(del52) accumulated reactive oxygen species-induced DNA double-strand breaks (DSBs) and were modestly sensitive to poly-ADP-ribose polymerase (PARP) inhibitors olaparib and BMN673. (
  • Unlike the histone deacetylase inhibitors, which are known to exert radiosensitizing effects, there have only been a few studies thus far concerning the role of DNA methyltransferase (DNMT) inhibitors as radiosensitizers. (
  • Immunocytochemical analysis using the anti-γH2AX antibodies was conducted in order to determine the effects of DNMT inhibitors on DNA repair. (
  • PARP-1 inhibition may therefore prevent efficient repair of DNA damage induced by topoisomerase 1 inhibitors. (
  • these individuals have an increased susceptibility to DNA-damaging agents and PARP inhibitors. (
  • γH2AX as a marker of DNA double strand breaks and genomic instability in human population studies. (
  • In certain embodiments, for example, these approaches and reagents can be used to detect instability in regions of genomic DNA that include. (
  • For example, certain aspects of the invention relate to the detection of instability in regions of genomic DNA that include tandem repeats, such as microsatellite markers. (
  • MSH2_HUMAN ] Component of the post-replicative DNA mismatch repair system (MMR). (
  • Forms two different heterodimers: MutS alpha (MSH2-MSH6 heterodimer) and MutS beta (MSH2-MSH3 heterodimer) which binds to DNA mismatches thereby initiating DNA repair. (
  • The C-terminal dimerization domains form an integral part of the MutS structure and coordinate asymmetrical ATP hydrolysis by Msh2 and Msh3 with mismatch binding to signal for repair. (
  • Heterodimerizes with MSH2 to form MutS alpha, which binds to DNA mismatches thereby initiating DNA repair. (
  • Radiation sensitivity is influenced by neoplastic cell proliferation or quiescence status, resistance to apoptosis, levels of free-radical scavengers, and the ability to repair highly cytotoxic DNA double strand breaks (DSBs) caused by radiation therapy (RT) ( 2 - 4 ). (
  • P16 and hMLH1 can be inactivated by hypermethylation of their respective promoter regions, abrogating the ability to regulate cell proliferation and repair processes. (
  • Benign neoplasms are non-cancerous forms of tissue proliferation such as skin moles, lipomas or uterine fibroids. (
  • We hypothesize that the slow proliferation of NENs provides sufficient time for the repair of beta-particle induced-DNA damage. (
  • repair of DNA damage. (
  • Taken together with previous studies, it has been suggested that G2 checkpoint system might suppress the linkage between DNA damage and cell death. (
  • DNA damage is very common. (
  • Some sources of DNA damage are indicated in the boxes at the top of the figure in this section. (
  • Also look up Naturally Occurring DNA Damage in Wikipedia. (
  • Such inflammation causes oxidative DNA damage. (
  • Although RT induces DNA damage, it also upregulates the expression of various interleukins (IL), including IL-1, IL-6, IL-8, transforming growth factor-beta (TGF-β), and tumor necrosis factor (TNF) ( 6 ), which, through the activity of the transcription factor nuclear factor κB (NF- κB), further increases the expression of IL-6 and IL-8 ( 7 ). (
  • DNA damage also includes damages generated exogenously by environmental mutagens, such as ionic radiation, reactive oxygen, and genotoxic compounds. (
  • Determine the effects of the study treatment on the level of PARP inhibition and DNA damage in PBMCs and tumor samples. (
  • The ubiquitin proteasome system has emerged as a central player in the regulation of DNA damage response (DDR). (
  • In this chapter, we review defects within the ubiquitin proteasome system that are associated with abnormal DNA damage response in MM and discuss current and potential novel ways of targeting these aberrations in the clinic. (
  • Indeed, c-myc is well known to be both an important regulator of cell growth and apoptosis through its action on cell cycle progression, cell metabolism, cell differentiation, cell death receptor signaling and DNA damage recovery [ 3 ]. (
  • Multiple reports support the concept that metals like nickel, chromium, cobalt, and arsenic can interfere with key steps in repairing DNA damage ( 14 - 18 ). (
  • The roles of JAK2 in DNA damage and repair in the myeloproliferative neoplasms: Opportunities for targeted therapy. (
  • Involved in transcriptional regulation of P21 in response to DNA damage. (
  • Required for FANCD2 targeting to sites of DNA damage. (
  • DNA damage-specific histone chaperone Aprataxin PNK-like factor (APLF) regulates mesenchymal-to-epithelial transition (MET) during cellular reprogramming. (
  • Inhibition of PARP inhibits the repair of DNA damage caused by alkylating agents such as cyclophosphamide. (
  • When oxidative damage occurs, in particular DNA damage, it creates a cascade of events that may contribute to aging and disease [ 5 ]. (
  • While BER repairs individual damaged bases, the NER system corrects larger portions of DNA damage by removing the strand section that contains a major nucleotide lesion [ 6 - 8 ]. (
  • Both BER and NER systems are constantly active in the cell death, repairing DNA damage as it is detected. (
  • The inhibition of DNA damage repair during PRRT may be an option to improve therapy response in NEN. (
  • We have recently demonstrated the damage repair inhibitory and pro-apoptotic effect of bortezomib in NEN in vitro (Briest et al. (
  • It is tempting to define neoplasms as clonal cellular proliferations but the demonstration of clonality is not always possible. (
  • This review details the clinical and pathologic features of these nonductal neoplasms, highlighting diagnostic criteria including the use of specific immunohistochemical stains to define the cellular differentiation of the neoplasms. (
  • O 6 -Alkylguanine-DNA alkyltransferase (AGT) is an important cellular defense against the mutagenic effects of DNA alkylating agents. (
  • This action seems to be related to suppression of cellular DNA DSB repair activities because NHEJ-mediated rejoining of DSBs occurs with significantly lower efficiency in the presence of trifluoperazine. (
  • The mechanisms that concern DNA repair have been studied in the last years due to their consequences in cellular homeostasis. (
  • Here, we review different insights concerning the malfunction or absence of the DNA-MMR and its impact on cellular homeostasis. (
  • One of them is the base excision repair (BER) system, a cellular mechanism that repairs damaged bases in the DNA sequence originating from deamination, oxidation, and alkylation. (
  • However, there are other mechanisms that are activated during specific cellular stages, such as DNA mismatch repair system (MMR). (
  • This review summarizes the current approach to the diagnosis, classification, grading, and therapeutic stratification of neuroendocrine neoplasms, with a focus on those arising in the lung and thymus, pancreas, and intestines. (
  • Peptide radioreceptor therapy (PRRT) is a promising therapy option for SSTR2-positive pancreatic neuroendocrine neoplasms (NEN). (
  • The study's purpose was to assess whether individuals who developed a second malignant neoplasm (SMN) after treatment for a first malignant neoplasm (FMN) had a lower ability to repair DNA double-strand breaks (DSBs) using a bioassay with γH2AX intensity as a surrogate endpoint. (
  • The repair and signaling responses to DNA double-strand breaks. (
  • The resulting Rag-induced DNA double-strand breaks are ideal sites for oncogene translocation. (
  • Recently, the detection by immunofluorescence of the phosphorylation of the histone variant H2AX (γ‐H2AX) has been established as a reliable and sensitive technique to monitor DNA double-strand breaks (DSBs) in blood lymphocytes. (
  • Expression of ARID1A in ovarian seromucinous neoplasms and its clinicopathological significance]. (