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44 Cards in this Set
- Front
- Back
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What are the 8 basic principles
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(1) Genetic damage
(2) Clonal expansion (3) unidirectional X-linked isoenzyme (4) Regulatory genes of 4 types (5) Accumulated mutations needed (6) Ongocgenes (mutants of protos) are Dominant single alleles (7) disabled Repair genes predispose only (8) Multistep process |
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6 hallmarks of cancer
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(1) Growth signals self sufficient (GF or GFR)
(2) insensitive to Anti-growth signals (3) can Invade and Metastasize (4) replicative potential is limitless (Telomerases) (5) Angiogenesis sustained (6) Apoptosis evaded |
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Etiology of glioblastomas
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excess production of PDGF
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Etiology of sarcomas
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excess production of TGF alpha and its receptor
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Etiology of squamous cell carcinomas of the lung
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80% are from ERBB1, an EGFR
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HER2/NEU
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An ERBB2 (EGFR) that favors cell grwoth in breast carcinoma
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anti-HER2/NEU
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herceptin; can be given in tx of breast carcinoma
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What's RAS and what's its significance
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most commonly mutated proto-oncogene in human tumors
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Where do RAS mutations normally happen?
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In its GTP-binding pocket or the enzymatic region necessary for GTP hydrolysis. There are 3 hotspots that make RAS trapped in activated state
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In what kind of cancers do we see RAS mutations
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majority of colon and pancreatic carcinomas
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What is ABL?
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signal transducing protein that figures in cML
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How is RAS normally kept inactive
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achored in inner leaflet of cell membrane by farnesyl membrane anchor, bound to GDP
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Why don't activated RAS always cause cancer?
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Because they revert to inactive by GTPase activity
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who discovered the elephant man disease and what is it called
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von Recklinghausen
neurofibromatosis 1 |
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characteristics of neurofibromatosis
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mjultiple cutaneous tumor masses and skin pigmentation
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What's the mutation driving Neurofibromatosis
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neurofibromin 1, which bears the GTPase activity that take Ras back to its inactive form
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Is neurofibromatosis benign?
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yes
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What can neurofibromas tansform into?
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malignant Schwannomas
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What chromosome is the Neurofibromin gene on?
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17 q11.2
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What are CDK's
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cyclin dependent kinase conmplexes
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What role do CDK inhibitors serve in carcinogenesis
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they are brakes to the cell cycle, so their mutation favors tumor growth
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how many doublings can normal cells do
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60-80
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What limits normal cell doublings
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telomeres, which get lost in each replication, leading to replicative senescence
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What happens when our DNA gets too short by losing telomeres
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DNAs are detected and eliminated via p53 and retinoblastoma checkpoints
OR they enter a crisis point and are eliminated |
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What is the significance of telomerase in carcinogenesis
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tumor cells can make a telomerase to add on TTAGGG groups and restore length, thus allowing survival
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What percentage of tumors express telomerase?
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90%
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What was Percival Pott's discovery
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chimney sweeps got scrotal skin cancer
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What cancer did Thorotrast give rise to
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angiosarcoma of the liver and squamous cell carcinomas of the nasal sinuses
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What's the problem with thorotrast
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alpha decay with half-life of 30 years
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What cancer develops from HPV
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squamous cell carcinoma of the cervix
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What cancer develops from HHV8
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kaposi sarcoma, a vascular neoplasm
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Which HPV's lead to squamous cell carcinoma of the cervix
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16 and 18
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What does Epstein-Barr virus lead to
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Burkitt lymphoma, other B cell tumors (lymphomas, some cases of mixed cellularity type Hodgkin lymphoma), and nasopharyngeal carcinoma
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What cancer develops from HBV
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hepatocellular carcinoma
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What kinds of viruses are most oncogenic viruses
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DNA
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Are there any RNA viruses
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HCV which also produces HCC (hepatocellular carcinoma)
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What is kaposi sarcoma
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a vascular neoplasm led to by HHV8
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What is LMP-1?
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an oncogene that activates signaling, cyclin D and (with a transolcation 8-14) MYC
this leads to several malignant B cell tumors and nasopharyngeal carcinoma |
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How can LMP-1 activate MYC
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if it has an 8-14 translocation
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What cancer has the starry sky
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Burkitt lymphoma. The normal dendritic cels and macrophages appear light, surrounded by malignant B lymphocytes
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what's the gene proeduct of HBV
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HBxAg
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What does hepatits B x antigen do?
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activates transcription factors and signal transduction
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What happens in chronic Hep B patients
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HBxAg expression favors outgrowth of malignant cells in hepatocellular carcinoma
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What is the long term problem with HBV DNA
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it can get incorporated into the host genome
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