Neoplasia Flashcards

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FlashCards sobre Neoplasia Flashcards, criado por Pooja Acharya em 24-02-2020.
Pooja Acharya
FlashCards por Pooja Acharya, atualizado more than 1 year ago
Pooja Acharya
Criado por Pooja Acharya mais de 4 anos atrás
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Neoplasia New growth; the formation of clonal tumors by the uncontrolled proliferation of cells triggered by a series of genomic alterations and independent of physiological growth signals
Metaplasia Differentiated cell type is replaced by a different mature cell type Found in association with tissue damage/ repair/ regeneration (ex: smokers bronchi - ciliated columnar epithelium replaced by squamous metaplasia)
Pleomorphism variable size and shape of cells/nuclei histologic feature of malignant cells
Dysplasia Precursor to cancer confined to epithelium by basement membrane
Carcinoma in situ dysplastic cells involving full thickness of epithelium but still confined by basement membrane; patient can still be cured by complete surgical excision
Teratoma rare benign tumor containing cells/tissues from more than one germ layer
Hamartoma benign proliferation of cells indigenous to involved site (ie odontoma - toothlets) Hamartoma of lung
Choristoma benign proliferation of cells in non-native site (ie small nodule of pancreatic tissue in submucosa of stomach)
What four classes of normal regulatory genes are the principal targets of cancer-causing mutations? 1. Proto-oncogenes (growth promoting) 2. Tumor suppressor genes (growth-inhibiting) 3. Genes that regulate programmed cell death/apoptosis 4. Genes involved in DNA repair
Oncoproteins Mutant proteins that have gained function to promote cell growth independently of normal extracellular growth-promoting signals (traffic light is always green)
Most commonly mutated proto-oncogene RAS
Most common mitogen activated protein kinase (MAPK) pathway alteration present in 78-88% of ameloblastomas BRAF (BRAFV600E mutation - valine is substituted for glutamine at codon 600)
MYC mutation Oncogene that activates expression of many genes involved in cell growth Can reprogram banal somatic cells into pluripotent stem cells Upregulates telomerase in some contexts (Contributes to stem-cell like immortalization of tumor cells)
Abnormalities in tumor suppressor genes are characterized by __________-of-function mutations Loss Encode proteins that have lost function to regulate signal transduction pathways and other critical cellular functions
Restinoblastoma gene (RB) Governor of the cell. Regulates expression of genes necessary for dividing cells to pass through G1/S cell cycle checkpoint
Knudson "two-hit" hypothesis With tumor suppressor genes, both alleles must be mutated for all loss of function to occur (one allele can pick up the slack for its mutated counterpart) explains why retinoblastoma has a hereditary pattern
Most frequently mutated gene in human cancers TP53 (guardian of the genome) Central monitor of DNA damage and cell stress Regulates cell cycle progression, DNA repair, cellular senescence, apoptosis
APC Gatekeeper of colonic neoplasia (APC mutations present in 70-80% of colorectal carcinoma) Tumor suppressor that downregulates Wnt/β-catenin signaling pathway
Familial adenomatous polyposis (FAP) Cancer predisposition syndrome characterized by polyps caused by germline APC mutations Risk of colorectal cancer approaches 100%
Enzyme whose activation causes apoptosis caspase activated either by mitochondrial or death receptor pathways
Follicular lymphoma a neoplasm that evades cell death Characterized by overexpression of Bcl-2 via a specific chromosomal translocation
Result of translocation of the philadelphia chromosome t(9;22): Chronic myelogenous leukemia
Xeroderma pigmentosum Cancer predisposition syndrome characterized by impaired ability to repair UV-induced DNA damage Abnormal cross-linking of pyrimidine bases prevents error-free DNA replication
Lynch Syndrome (HNPCC) Hereditary nonpolyposis colon cancer syndrome characterized by loss of DNA proof-reading microsatellite instability-high (MSh2/mlh1)
Aflatoxin B1 Fungal food contaminant that results in increased risk of hepatocellular carcinoma in Africa and the Far East
Warburg effect Cancer cells use aerobic glycolysis generating just 2 ATP = inefficient pathway for energy production, but generates metabolic intermediates necessary for frequent cell division / synthesis
Neoangiogenesis development of new blood vessels from previously existing capillaries; allow malignancies to enlarge (create its own blood supply) accomplished by VEGF - Vascular endothelial growth factor
8 hallmarks of cancer Self-sufficiency in growth signals (Oncogenes - gain of function - green light) Insensitivity to growth-inhibition (tumor suppressor loss of function) Evasion of apoptosis (follicular lymphoma) Ability to evade the host immune response (immune surveillance; immunoediting; downregulate T-cells) Limitless replicative potential (immortality; upregulate telomerase ) Altered cellular metabolism (Warburg effect) Sustained angiogenesis (blood vessel formation) Ability to invade and metastasize (spread)
Cancer cachexia progressive loss of body fat and lean body mass, accompanied by profound weakness, anorexia and anemia (TNF-A)
Eaton-Lambert syndrome SCLC, myasthenia-gravis-like symptoms but gets better with exercise and doesn't respond to Ach-esterase inhibitors, antibodies against presynaptic Ca channels
Nephrotic syndrome Lung, breast, stomach cancer. Diffuse membranous glomerulopathy
Cushing syndrome SCLC, secretes ACTH, moon face, weight gain
Hypercalcemia SCC lung, ectopic production of parathrelated peptide
Polycythemia Renal and liver cancer, erythropoietin
Loss of function of E-cadherin Binds to B-Catenin / growth inhibition of epithelial cells Familial Gastric Cancer (AD) -- (CDH1)
mechanism for tumor invasion invade ECM detach from E-cadherin and N-CAM attach to matrix degrade ECM (metalloproteinases and cathepsin D) migrate vascular dissemination attach to another organ
tumor viruses acute transforming retrovirus = contains active oncogene slow transforming retrovirus = inserts itself, does not have own oncogene
human T-cell leukemia virus (HTLV) has TAX protein, which increases survival and growth of infected cells, increases genomic instability adult T-cell leukemia (ATL)
high risk HPV types 16, 18 can cause invasive cancers proteins E6 and E7 promote growth and proliferation of cancer
HPV E6 blocks p53 stimulates temolerase expression increased tumor proliferation
HPV E7 blocks p21 blocks RB-E2F increased tumor proliferation
EBV associated cancers Burkitt's & Hodgkin's lymphoma nasopharyngeal cancers CNS-Lymphoma in HIV
LMP-1 EBV oncogenes Activates signaling pathways for B-cell via CD40 Activates BCL-2
Helobacter pylori and cancer lymphoma (MALT) due to chronic gastritis = polyclonal/monoclonal b cell proliferation monoclonal cured by eradicating HP carcinoma due to chronic gastritis = intestinal metaplasia, dysplasia, takes decades, not seen w ulcers
CA-125 Surface epithelial ovarian cancers
PSA Prostatic cancer
AFP HCC, GERM CELL TUMORS OF TESTIS
CEA Colon cancer
CA19-9 Pancreatic cancer
NMYC oncogene amplication Neuroblastoma
t(8:14) Burkitt lymphoma
t(11:22) Ewing sarcoma
IHC: Cytokeratin Epithelial cancers
Vimentin sarcomas: Mesenchymal cancers
Desmin Rhabdomyosarcoma: striated muscle

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