Chapter 7 Flashcards
desmoplasia
abundant collagenous stroma
benign
scirrhous
benign stony hard tumors (breast)
sarcomas
arise from mesenchyme and have little CT
carcinomas
arise from epithelium
squamous cell carcinoma
tumor cells resemble stratified squamous epithelium
mixed tumors
divergent differentiation of single neoplastic clone along 2 lineages, but only one germ layer involved
pleomorphic adenoma
arise from mixed tumors
most common in parotid gland
malignant tumors that sound benign
lymphoma
melanoma
mesothelioma
seminoma
hematomas
disorganized, benign cells
choristoma
congenital anomaly
heterotopic rest of cells
anaplasia
lack of differentiation
major components of anaplasia
pleomorphism
abnormal nuclear morphology
mitoses
loss of polarity
minor components of anaplasia
tumor giant cells (don’t confuse w/langhans cells)
central necrosis
autosomal dominant cancers
childhood retinoblastoma familial adenomatous polyposis Li-Fraumen syndrome multiple endocrein neoplaia 1 and 2 HNPCC
childhood retinoblastoma
RB tumor supressor gene
familial adenomatous polyposis
APC tumor supressor gene
multiple endocrine neoplasia type 1 and 2
MENI TF
RET tyrosine kinase genes
HNPCC
hereditary non-polyposis colon cancer
inactivation of DNA mismatch repair gene
defective DNA syndrome
usually autosomal recessive
xeroderma pigmentosum, ataxia-telangiectasia, bloom syndrome
HPNCC most common
glioblastomas often secrete what GF
PDGF
sarcomas often secrete what GF
TGF alpha
RET gene
MEN2a and 2b and medullary thyroid cancer
RAS
point mutations in this family is single most common abnormality of proto-oncogenes in humans
KRAS
carcinomas of colon and pancreas
HRAS
carcinomas of bladder
NRAS
hematopoietic cancer
Blocking RAS
blocks proliferative response to EGF, PDGF, CSF-1
BRAF
member of RAS family
60% of cancers
80% of benign growths
BCR-ABL
mutated tyrosine kinase due to translocation
designer drug imatinib mesylate blocks BCR-ABL kinase
MYC
most commonly implicated TF
modulates histones methylation, decreases cell adhesion, increased cell mortality, increased telomerase activity, increased protein synthesis, decreased proteinase, and modulated cell metabolism, possibly interacts with DNA repair mechanism
CIP/WAF family
CDKI
broadly block CDKs
p21, p27,p57
INK4 family
block specifically cyclin D/CDK4A and cyclin D/CDK6
p15, p18, p19
RB
13q14
active hypophosphorylated state in quiescent cells
inactive hyperphosphorylated state in G1/S transition
controls cell cycle and stability of p27 and involved w/differentiation
early G1
RB active and bound to E2F family of TF inhibiting cyclin E
also recruits chromatin remodeling proteins which bind E2F responsive genes (cyclin E) making them insensative to TFs
mitogenic signals
activate cyclin D expression -> cyclin D-CDK4/6 complexes-> complexes phosphorylate RB -> inactive -> progress thru cell cycle
M phase
phosphates removed -> RB active
mir34
critical for p53 function
activators of p53
ATM and ATR
MDM2
blocks p53
released from p53 if DNA damage repair successful
p53 collaborators
p63, p73