Chapter 7 Neoplasia Flashcards
Definitions and identification
growth fraction
portion of tumor cells actively proliferating
metastasis
invasion of lymphatics, blood vessels or body cavities
tumor capsule
a surrounding rim of condensed connective tissue
3 routes of cancer dissemination
1) seeding of body cavities and surfaces - dispersion into another cavity eg. ovarian carcinoma to abdominal viscera
2) lymphatic spread - from metastasis or reactive hyperplasia
3) Hematogenous spread - typical of sarcomas, veins more than arteries
features of neoplasms
1) variation in shape and size of cells 2) approach a 1:1 nuclear to cytoplasmic ratio 3) abundant or atypical mitoses 4) loss of polarity 5) tumor giant cells, single polyploid nuclei or multiple nuclei 6) Ischemic necrosis
3 categories of genetic pre-disposition of cancer
1) Autosomal dominant inherited cancers 2) Defective DNA repair syndromes 3) Familial Cancers
Autosomal Dominant Inherited Cancers
characterized by single mutant gene, usually point mutation in one allele of a tumor suppressor gene usually develop in a specific kind of tissue
Defective DNA repair syndromes
typically autosomal recessive example of autosomal dominant is HNPCC hereditary nonpolyposis colon cancer, resulting from inactivation of DNA mismatch repair gene
Malignant characteristicss
lack differentiation erratic rate of growth invasive of surrounding tissue frequent metastasis
Li-Fraumeni Syndrome
mutation to p-53 gene
Regulatory genes that can result in cancer if damaged
proto-onco genes tumor suppressor genes apoptosis genes DNA repair genes
7 changes in cell physiology that determine malignancy
1) self sufficienct growth
2) lack of growth inhibition
3) Evasion of apoptosis
4) Limitless replication
5) Sustained angiogenesis
6) Ability to invade and metastasize
7) Defective DNA repair
C-myc
oncogene associated with Burkitt’s lymphoma
transcription factor, nuclear regulatory protein
bcl-2
oncogene associated with follicular and undifferentiated lymphomas
Inhibits apoptosis
RAS
oncogene associated with many cancers
point mutations here are most common abnormality of proto-oncogenes
Rb
tumor suppressor gene
associated with Retinoblastoma, and osteosarcoma
its product blocks G1—->S phase of cell cycle
p53
Tumor suppressor gene associated with most human cancers
its gene product blocks G1—>S phase of cell cycle (allows time for repair of DNA)
induces p21 (cell cycle inhibitor)
BRCA1
Tumpr suppressor gene associated with breast and ovarian cancer
its gene product is responsible for DNA repair protein
BRCA2
Tumor suppressor gene associated with breast cancer
Its gene product is responsible for DNA repair
ABL
Translocation btw 9 & 22
oncogene associated with Chronic Myeloid Leukemia
its gene product is tyrosine kinase (non-receptor)
senescence
permanent exit of cell cycle
quiescence
temporary exit of cell cycle
RB protein
Key component in cell cycle decision point (enter cell cycle, exit and differentiate, or die)
hypophosphorylated - remains on EG2F and blocks S phase genes, blocks transcription—> cell cycle stops
hyperphosphorylated - released E2F, S phase gene activated, transcription activated —> cell cycle continues
What are the key regulators of cell cycle control that are dysregulated in the vast majority of human cancers?
p16 / INK4a
cyclin D
CDK4
RB
