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
Q

parneoplastic syndrome

A

symptoms stemming from humoral factors from tumor cells, rather than local effects

26
Q

carcinoma in situ

A

dysplastic changes that do not extend beyond basement membrane

27
Q

carcinoma

A

malignant growth of epithelial origin invades surrounding tissue beyond basement membrane, most common solid tumor

28
Q

sarcoma

A

malignant growth of mesenchymal origin, more common in kids/adolescents

29
Q

osteogenic sarcoma

A

bone sarcoma

30
Q

chondrosarcoma

A

cartilage sarcoma

31
Q

rhabdosarcoma

A

skeletal muscle

32
Q

adenocarcinoma

A

gladular epithelium neoplasm

33
Q

teratoma

A

mixed cellular origin

34
Q

histologic grade

A

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
Q

anatomic stage

A

extent of the spread: TMN= Tumor size, Node involvement, and Metastasis