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5 Cards in this Set
- Front
- Back
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Benign tumors? |
do not develop subsequent mutations-> retain well-controlled growth, benign histologic features. |
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Malignant tumors? |
develop subsequent multiple mutations, overexpressions acqured enzyme pathways (telomerases), loss of cell adhesion markers. devleop capacity for invasion and metastasis. acquire gross microscopic features of malignancy. |
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Evolution of malignant melanoma? |
benign nevus(benign limited growth, BRAF mutation)-> dysplastic nevus(premalignant, lesions may regress, random atypia, CDKN2A loss, PTEN loss)-> radial-growth phase(dec differentiation, unlimited hyperplasia, connot grow in soft agar, clonal proliferation, inc CD1)-> vertical-growth phase(crosses BM, grows in soft agar, forms tumor, Ecad loss, Ncad expression, alphaVbeta3 integrin expression, MMP2 expression, survivin, reduced TRPM1)-> metastatic melanoma(dissociates fr primary tumor, grows at distant sites, absent TRPM1). |
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RAS activation pathway? |
GAPs (GTPase-activating proteins). Active RAS->PI3K-AKT-mTOR-activation of transcription-MYC protein-cell cycle progression. or RAF-MAPK. |
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GFR's? ERBB1? HER2/NEU (ERBB2)? |
GFR's-overexpression (amplification)->cancer cells hyperrespond to levels of GF's.
ERBB1 (EGF receptor) -overexpressed in 80% sq. cell ca's lung.
HER2/NEY (ERBB2)-amplified in 25-30% breast cancers-> bad prognosis.
rx: role of anti-HER2/NEU |
