Cancer intro Flashcards

1
Q

epistatic

A

only one lesion per pathway required to acquire cancer

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2
Q

4 ways to dysregulate cellular process in cancer

A

inappropriate proliferation, resist differentiation and apoptosis, genomic instability, grow where it shouldnt

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3
Q

viral oncogene

A

viral genes capable of altering cells

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4
Q

cellular oncogene

A

genes involved in development or maintenance of malignant phenotype

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5
Q

protooncogene

A

conserved eurkaryotic genes, can become oncogenes with changes in expression or mutation

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6
Q

what are 4 oncogenic mechanisms

A

growth factors, signal transduction, cell cycle control, regulation of gene xpression

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7
Q

2 common growth factors related to cancer

A

TGF-alpha w/ ras mutation and PDGF, PDGF-R w/ sis viral oncogene

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8
Q

2 important tumor suppressor genes

A

p53 and p16(INK4a)

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9
Q

Li-fraumeni syndrome

A

hereditary predisposition to cancer from p53 mutation, affected pts born w/ one abnormal copy- tumors will have mutations at both alleles

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10
Q

Cdk4 (cyclin D) effect on cell proliferation

A

blocks retinoblastoma, which inhibits cell cycle-high in lymphomas and breast cancer

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11
Q

p53 mutation effect on cell proliferation

A

p53 stimulates retinoblastoma which in turn inhibits cell cycle- losing p53 loses inhibition

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12
Q

pRB mutation effect on cell cycle

A

pRB is inhibitor, loss causes loss of inhibition and greater cell proliferation

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13
Q

p16 mutation effect on cell cycle

A

p16 blocks cyclin D which in turn blocks pRB which inhibits cell cycle- long chain but w/o p16= more cyclin d= less pRB=more cell division

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14
Q

p53 role in apoptosis

A

promotes this process, when mutated cells become resistant to apoptosis

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15
Q

what are some things a tumor must to do metastasize and cause harm

A
  • locally invade
  • grow into lymphatics/ blood vessels
  • spread to other sites
  • attach to endothelium
  • grow and destroy normal stroma in new home
  • induce new blood vessels
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16
Q

what are some mutations involved in colon cancer progression?

A

FAP- familial adenomatous polyposis, RAS- protooncogene, DCC- tumor suppressor deleted in colon cancer

17
Q

mutations involved in pancreatic cancer

A

K-ras, p16, p53

18
Q

hyperplasia

A

increase in cell number can be physiologic (hormonal) or pathologic

19
Q

hypertrophy

A

increase in cell size with production of more subcellular components, physiologic (skeletal muscle) or pathologic (cardiomyocytes)

20
Q

metaplasia

A

change from one differentiated cell type to another, commonly see in lung epithelium in smoking

21
Q

dysplasia

A

atypical proliferation of cells: weird size/nuclei, disorderly arrangement and maturation

22
Q

neoplasia

A

abnormal growth of tissue, can be well or poorly differentiated, autonomous

23
Q

benign neoplasms

A

growth without invasion or spread, resembles normal cells and well differentiated with low mitotic rate

24
Q

causes of morbitiy with benign neoplasms

A

size, location, production of cell products

25
parneoplastic syndrome
symptoms stemming from humoral factors from tumor cells, rather than local effects
26
carcinoma in situ
dysplastic changes that do not extend beyond basement membrane
27
carcinoma
malignant growth of epithelial origin invades surrounding tissue beyond basement membrane, most common solid tumor
28
sarcoma
malignant growth of mesenchymal origin, more common in kids/adolescents
29
osteogenic sarcoma
bone sarcoma
30
chondrosarcoma
cartilage sarcoma
31
rhabdosarcoma
skeletal muscle
32
adenocarcinoma
gladular epithelium neoplasm
33
teratoma
mixed cellular origin
34
histologic grade
3 levels of differentiation: well, moderate, and poor; in well you can tell where it came from and in poor it is a mess of cells
35
anatomic stage
extent of the spread: TMN= Tumor size, Node involvement, and Metastasis