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DIT topics > cancer basics > Flashcards

cancer basics Flashcards

1
Q

normal cell type replaced by another

A

metaplasia

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2
Q

barrett’s esophagus

A

metaplasia:

squamous epithelium → columnar epithelium (intestinal)

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3
Q

abnormal growth

loss of normal size, shape, orientation

A

dysplasia

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4
Q

REVERISBLE changes in histoogy

A

hyperplasia
metaplasia
dysplasia

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5
Q

cells regressing
less differentiated
less like mature cells, more like primitive cells

A

anaplasia

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6
Q

high nucleus to cytoplasmic ratio
prominent nucleoli
clumping of nuclear chromatin
mitotic figures

A

anaplastic characteristics

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7
Q

cells growing in uncontrolled fashion

benign OR malignant

A

neoplasia

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8
Q

IRREVERISBLE changes in histology

A

anaplasia

neoplasia

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9
Q

adenoma: glandular architecture (colon polyp)
papilloma: finger-like architecture

A

benign tumor arising from epithelium

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10
Q

carcinoma:
adenocarcinoma
papillary carcinoma
use cytokeratin stain

A

malignant tumor arising from epithelium

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11
Q

tumors that spread via lymphatics

A

epithelial tumors

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12
Q

tumors that spread hematogenously

A

mesenchymal tumors

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13
Q

malignant blood cell tumors

A

leukemia
lymphoma
multiple myeloma

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14
Q

hemangioma (cherry)

A

benign blood vessel tumor

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15
Q

angiosarcoma (usually liver)

A

malignant blood vessel tumor

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16
Q

osteoma

A

benign bone tumor

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17
Q

osteosarcoma

A

malignant bone tumor

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18
Q

lipoma

A

benign fat tumor

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19
Q

liposarcoma

A

malignant fat tumor

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20
Q

benign mesynchymal tumors rarely progress to

A

sarcoma (vs epithelial tumors: adenoma → carcinoma)

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21
Q

sarcomas (mesenchymal) are more aggressive than

A

carcinomas

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22
Q

rhabdomyoma

A

benign skeletal muscle tumor

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23
Q

rhabdomyosarcoma

A

malignant skeletal muscle tumor

24
Q

leiomyoma

A

benign smooth muscle tumor

25
Q

leiomyosarcoma

A

malignant smooth muscle tumor

26
Q

tumor with more than 1 cell type

mature: mature tissues, no anaplastic cells (ovarian tumor)
immature: MALIGNANT

A

teratoma

27
Q

how much cellular differentiation and mitotic activity the tumor cells show

A

grade

low grade: well-differentiated, cells resemble normal cells
high grade: less differentiated

28
Q

size of tumor

how much it has spread

A

stage

29
Q

TNM staging system

A

Tumor size
Nodal involvement
Metastasis

30
Q

prognostic value + treatment options depends on

A

stage

31
Q

neoplastic progressoin

A

normal → hyperplasia → dysplasia (lose normal size, shape, orientation) → carcinoma in situ (malignant cells haven’t invaded BM yet) → invasive carcinoma (malignant cells break thru BM: locally invasive)→ metastasis (invade lymphatic or blood vessel)

32
Q

liver metastasis (more common than 1° liver cancer)

A 
Cancer Sometimes Penetrates Benign Liver:
Colon (drains to liver)
Stomach (drains to liver)
Pancreas
Breast
Lung
33
Q 
↑ LFTs: ↑ alk phos
liver tenderness
ab pain
hepatomegaly
hepatic dysfunction: ascites, jaundice
A

liver mets S/S

34
Q

brain metastasis (50% brain tumors are mets = most common brain tumor is mets)

A 
Lots of Bad Stuff Kills Glia:
Lung 
Breast
Skin (melanoma)
Kidney (renal cell carcinoma)
GI tract (colon cancer)
35
Q

headache - 50% cases
focal neuro dysfunction: hemiparesis
cognitive dysfunction: memory loss, personality changes
seizures

A

brain mets S/S

36
Q

bone metastasis (more common than 1° bone tumors)

A 
Permanently Relocated Tumors Like Bone
Prostate
Renal cell cancer
Thyroid
Lung 
Breast
37
Q

lytic: break down bone (lung, multiple myeloma, breast)
blastic: build new bone - but disordered and weak (prostate, breast)

A

bone mets S/S

38
Q

profound weight loss
fat + lean muscle loss
cause: tumor produces cytokines (TNF α) that raise BMR
main cause of cancer death + disability

A

cachexia

39
Q 
histological finding in:
papillary thyroid cancer
Serous papillary cystadenocarcinoma of ovary
Meningioma
Malignant mesothelioma
A

psammoma body

40
Q

laminated, concentric, calcified spherules

A

psammoma body

41
Q

malignant tumors arise from clonal expansion of

A

single precursor cell

daughter cells pass on mutated DNA

42
Q

4 main targets of genetic damage:

A

proto-oncogenes
tumor suppressor gene
genes that regulate apoptosis
DNA repair genes (susceptible to ionizing radiation, chemical carcinogens)

43
Q

malignant transformation is due to

A

nonlethal genetic damage (no trigger for apoptosis)

multistep: multiple mutations (protooncogene + dna repair gene, etc)

44
Q

normal genes that regulate cell proliferation and differentiation (code for GF, GF R, tyrosine kinase) but when mutated become called

A

proto-oncogenes: normal

oncogenes: mutated

45
Q

regulate cell cycle

A

tumor suppressor genes:
G1→ S: DNA repair, if can’t repair: p53, Rb (stays bound to E2F TF)
G2 →M: p53

46
Q

cyclin D activates CDK4

A

cyclin D-CDK 4 phosphorylates Rb → Rb unbinds from E2F TF → allow G1 to S

47
Q

how many mutations in tumor suppressor alleles to get cancer

A

two:

TWOmor suppressor alleles

48
Q

p53

A

acts through p21 to cause cell cycle arrest
works at G1/S and G2/M checkpoints
causes apoptosis by inducing TF of pro-apoptotic genes (BAX)
p53 binds to damaged DNA → stop cell cycle → either repair DNA or trigger apoptosis

49
Q

mutation in Rb

A

not bound to E2F: G1→S

50
Q

mutation in p53

A

progress through cell cycle despite presence of DNA damage/mutations

51
Q

cell growth in absence of normal mitotic signals

A

oncogenes: oncoproteins are missing important regulatory elements
GOF mutation

52
Q

how many mutations in proto-oncogene alleles to get cancer

A

ONE mutation

53
Q

most common oncogene abnormality in human tumors:

15% all human tumors have mutated RAS proteins

A

ras oncogene

54
Q

most common mutations that cause cancer

A 
p53 (50% human cancers)
ras oncogene (20% human cancers)
55
Q

RAS proto-oncogene protein product

A

part of G protein in GF receptor → when GF + RAS protein bind to GF R → activate MAP kinase → stimulate cell proliferation

DIT topics (115 decks)

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