cancer basics Flashcards

(55 cards)

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
leiomyosarcoma
malignant smooth muscle tumor
26
tumor with more than 1 cell type mature: mature tissues, no anaplastic cells (ovarian tumor) immature: MALIGNANT
teratoma
27
how much cellular differentiation and mitotic activity the tumor cells show
grade low grade: well-differentiated, cells resemble normal cells high grade: less differentiated
28
size of tumor | how much it has spread
stage
29
TNM staging system
Tumor size Nodal involvement Metastasis
30
prognostic value + treatment options depends on
stage
31
neoplastic progressoin
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
liver metastasis (more common than 1° liver cancer)
``` Cancer Sometimes Penetrates Benign Liver: Colon (drains to liver) Stomach (drains to liver) Pancreas Breast Lung ```
33
``` ↑ LFTs: ↑ alk phos liver tenderness ab pain hepatomegaly hepatic dysfunction: ascites, jaundice ```
liver mets S/S
34
brain metastasis (50% brain tumors are mets = most common brain tumor is mets)
``` Lots of Bad Stuff Kills Glia: Lung Breast Skin (melanoma) Kidney (renal cell carcinoma) GI tract (colon cancer) ```
35
headache - 50% cases focal neuro dysfunction: hemiparesis cognitive dysfunction: memory loss, personality changes seizures
brain mets S/S
36
bone metastasis (more common than 1° bone tumors)
``` Permanently Relocated Tumors Like Bone Prostate Renal cell cancer Thyroid Lung Breast ```
37
lytic: break down bone (lung, multiple myeloma, breast) blastic: build new bone - but disordered and weak (prostate, breast)
bone mets S/S
38
profound weight loss fat + lean muscle loss cause: tumor produces cytokines (TNF α) that raise BMR main cause of cancer death + disability
cachexia
39
``` histological finding in: papillary thyroid cancer Serous papillary cystadenocarcinoma of ovary Meningioma Malignant mesothelioma ```
psammoma body
40
laminated, concentric, calcified spherules
psammoma body
41
malignant tumors arise from clonal expansion of
single precursor cell daughter cells pass on mutated DNA
42
4 main targets of genetic damage:
proto-oncogenes tumor suppressor gene genes that regulate apoptosis DNA repair genes (susceptible to ionizing radiation, chemical carcinogens)
43
malignant transformation is due to
nonlethal genetic damage (no trigger for apoptosis) | multistep: multiple mutations (protooncogene + dna repair gene, etc)
44
normal genes that regulate cell proliferation and differentiation (code for GF, GF R, tyrosine kinase) but when mutated become called
proto-oncogenes: normal | oncogenes: mutated
45
regulate cell cycle
tumor suppressor genes: G1→ S: DNA repair, if can't repair: p53, Rb (stays bound to E2F TF) G2 →M: p53
46
cyclin D activates CDK4
cyclin D-CDK 4 phosphorylates Rb → Rb unbinds from E2F TF → allow G1 to S
47
how many mutations in tumor suppressor alleles to get cancer
two: | TWOmor suppressor alleles
48
p53
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
mutation in Rb
not bound to E2F: G1→S
50
mutation in p53
progress through cell cycle despite presence of DNA damage/mutations
51
cell growth in absence of normal mitotic signals
oncogenes: oncoproteins are missing important regulatory elements GOF mutation
52
how many mutations in proto-oncogene alleles to get cancer
ONE mutation
53
most common oncogene abnormality in human tumors: | 15% all human tumors have mutated RAS proteins
ras oncogene
54
most common mutations that cause cancer
``` p53 (50% human cancers) ras oncogene (20% human cancers) ```
55
RAS proto-oncogene protein product
part of G protein in GF receptor → when GF + RAS protein bind to GF R → activate MAP kinase → stimulate cell proliferation