Flashcards in Neoplasia IV Deck (25):
disordered growth, pleomorphism, mitoses, loss of polarization
leukoplakia can develop into what type of cancer?
squamous cell carcinoma (via dysplasia)
Barrett esophagus can transform into what type of cancer?
adenocarcinoma (via dysplasia / metaplasia)
chronic atrophic gastritis of pernicious anemia can transform into what type of cancer?
gastric adenocarcinoma (via dysplasia)
chronic UC can transform into what type of cancer?
adenocarcinoma of colon (via dysplasia)
hep B or C can transform into what type of cancer?
hepatocellular carcinoma (via macronodular cirrhosis)
what are the roles of proto-oncogenes?
regulation of growth and differentiation
what are the activation mechanisms for proto-oncogenes?
mutation, chromosomal translocation, amplification
what are the two main categories of cellular / molecular change following activation of an oncogene?
1. normal protein is overproduced 2. mutant protein is produced and has an aberrant function
ERBB2 / Her-2 / Neu is associated with what type of cancer? how?
breast / ovarian - amplification
RET is associated with what type of cancer? how?
MEN 2a / 2b, familial medullary thyroid carcinomas - point mutation
KRAS is associated with what type of cancer? how?
pancreas, colon, lung - point mutation
ABL is associated with what type of cancer? how?
chronic myeloid leukemia, acute lymphoblastic leukemia - translocation
B-catenin is associated with what type of cancer? how?
hepatoblastomas (point mutation), hepatocellular carcinoma (overexpression)
C-myc is associated with what type of cancer? how?
Burkitt lymphoma - translocation
N-myc is associated with what type of cancer? how?
neuroblastoma, small cell CA of lung - amplification
cyclin D is associated with what type of cancer? how?
mantle cell lymphoma (translocation), breast and esophageal (amplification)
what are the important clinical features of multiple endocrine neoplasia 2a / 2b?
1. mutation of RET 2. many endocrine organs can be involved 3. most are tumors, but can be hyperplasia
what is the pathogenesis of chronic myelogenous leukemia (CML)?
1. c-abl oncogene on chromosome 9 translocated to bcr on chromosome 22 2. increase in tyrosine kinase activity 3. proliferation of granulocytic precursors
what drug inhibits tyrosine kinase in CML?
Imatinib mesylate (Gleevec)
what is the pathogenesis of burkitt lymphoma?
1. translocation of c-myc proto-oncogene from chromosome 8 to Ig heavy chain on chromosome 14 2. overexpression of c-myc leads to excess transcription signals
what is the pathogenesis of B cell follicular lymphoma?
1. translocation 14-18 2. over expression of BCL-2 protein product 3. prevents apoptosis of B cells
what is the most common lymphoma?
follicular lymphoma (evasion of apoptosis)
what is the pathogenesis of neuroblastoma?
amplification of N-myc