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Pathology > Neoplasia I > Flashcards

Neoplasia I Flashcards

1
Q

What are the 5 qualities of a neoplasm?

A
  1. autonmous
  2. irreversible
  3. clonal
  4. benign
  5. malignant
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2
Q

What are some characteristics of benign?

A

cohesive expansile local growth, commonly w/ fibrous capsule, more differentiated and grows slowly

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3
Q

What are some characteristics of malignant?

A

progressively infiltrative invasive local growth, commonly w/ destruction of surrounding tissue

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4
Q

What is malignancy?

A

when neoplasm has the ability to metastasize

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5
Q

What is metastasis?

A

secondary site of tumor discontinuous w/ the primary site.

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6
Q

What are the patterns of metastatic spread?

A
  1. lymphatics
  2. Hematogenous
  3. Seeding
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7
Q

What is lymphatic spread?

A

goes to regional lymph nodes, typical of carcinoma

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8
Q

What is hematogenous spread?

A

goes to lungs or liver, typical for sarcoma

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9
Q

What is seeding?

A

goes to body cavities or surfaces, typical of ovarian carcinoma

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10
Q

What is a carcinoma?

A

malignant neoplams of epithelial cells

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11
Q

What is a sarcoma?

A

malignant neoplasm of mesenchyme-derived tissue

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12
Q

What is teratoma?

A

mixed germ cell tumor, it can be benign or malignant neoplasm w/ components of more than one germ cell layer

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13
Q

What is a hamartoma?

A

mass of mature but disorganized tissue indigenous to its site, developmental anomaly

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14
Q

What is a choristoma?

A

ectopic rest = mass of normal tissue present outside its normal site, developmental anomaly

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15
Q

What is a polyp?

A

macroscopic projection above mucosal surface, a bump or a nodule on a stalk

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16
Q

What is a pedunculcated polyp?

A

one that is on a stalk

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17
Q

What is a sessile polyp?

A

one that flat, like a plateau

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18
Q

What is an adenoma?

A

benign epithelial neoplasm forming glands or derived from glands

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19
Q

What is anaplasia?

A

lack of visible differentiation of malignant tumor cells giving them the appearances of primitive unspecialized cells

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20
Q

What are some features of an anaplastic cell?

A
  1. larger
  2. higher nuclear/cytoplasmic ratio - bigger nucleus, less cytoplasm
  3. pleomorphic (vary in size and shape)
  4. nuclear abnormalities (angulated shape, hyperchromatism, clumped chromatin, mitoses, nucleoli)
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21
Q

What is dysplasia?

A

disordered growth

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22
Q

What are the 2 types of dysplasia?

A
  1. congenital embryonically abnormal organization of cells

2. acquired cellular atypia usually premalignant, can be reversible

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23
Q

What is desmoplasia?

A

formation of abundant fibrous stroma by some carcinomas

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24
Q

What is a carcinoma in situ?

A

tissue w/ all the cytologic (individual cell) features of malignancy w/out visible invasion

25
Q

What are the most common causes of cancer death?

A
  1. lung
  2. breast (women), prostate (men)
  3. colon
26
Q

What are some causes of cancer?

A

smoking, obesity, alcohol, diet, UV light, asbestos, HPV

27
Q

What cancers can smoking cause?

A

mouth, pharynx, larynx, esophagus, stomach, pancreas, kidneys, and bladder, lungs

28
Q

Obesity is a cause of 14% of cancers of men and 20% of cancers of women in the US

A

FUCK THIS SHIT, know all of the percentages and be able to quote them in your nightmares

29
Q

What are some genetically inherited cancers?

A

Retinoblastoma, FAP, Li-Fraumenit Syndrome, Multiple Endocrine neoplasia, Xeroderma pigmentosum, ataxia-telangiectasia, BRCA1 and BRCA2

30
Q

What is the definition of tumor suppressor genes?

A

they control cell proliferation so defects are like faulty brakes on proliferation

31
Q

What is the definition oncogenes?

A

genes that drive autonomous cell growth in cancer cells like an accelerator pedal stuck to the floor

32
Q

What are some examples of TSGs?

A

RB, p53, APC/beta-catenin

33
Q

When is normal state of RB and what does it do in that state?

A

-hypophosphorylated and prevents cell proliferation by binding up TF E2F

34
Q

What happens when RB gets phosphorylated?

A

it lets go of E2F and starts cell proliferation

35
Q

At what step does RB block the cell cycle?

A

G1 state

36
Q

What does the APC TSG do?

A

it controls intestinal stem cell proliferation by WNT signaling

37
Q

What is APC’s normal function?

A

it’s gene product breaks down Beta-catenin so it doesn’t bind to TF TCF that turns a bunch of genes on for cell signaling

38
Q

When are APC mutations prevalent?

A

in 100% of colon cancers w/ familal adenomatous polyposis, and 70% sporadic colon cancers

39
Q

What is the role of p53?

A

molecular policeman, prevents propagation of genetically damaged cells, binds to DNA, arrests cells cycle for DNA repair, initiates apoptosis if repair is impossible

40
Q

What is the short life of p53?

A

20 minutes, gets bound by MDM2 something is degraded

41
Q

What are some ways a cell can acquire resistance to p53?

A

increased MDM2, E6 protein of HPV – both degrade P53

42
Q

What are some things that p53 recruits when repairing the cell damage?

A

p21 – a CDK inhibitor
GADD45 – used for DNA repair
if no repair possible then Bax kills cell

43
Q

What are some more TSGs?

A 
Nf-1 and Nf-2
VHL
PTEN (endometrium, brain)
TGF-beta pathway (pancreas)
WT-1 (wilms tumor)
Cadherins (esophagus, colon, etc)
KLF6 (prostate)
Patched (PTCH, basal cell carcinoma)
44
Q

What is the NF-1 gene products role?

A

activates GTPase, creating GDP that binds to cell membrane RAS protein making it inactive — thus no transduction of signals

45
Q

What happens in an inherited mutation of NF-1?

A

neurofibromatosis type 1, numerous benign NFs due to 2nd hit mutation

46
Q

What is the role of VHL?

A

Serves as a TSG essentially.

Product causes ubquintation and degradation of HIF-1 in normal oxygenated areas. prevents angiogenesis

47
Q

What does HIF-1 do?

A

if induced to act, it would yield increased PDGF and VEGF and promotes angiogenesis

48
Q

What cancers occur when you have a germ line mutation in VHL?

A

kidney cancer, pheochromoctyoma (adrenal medulla tumor), retinal angioma, and other tumors

49
Q

What are oncogene examples?

A

HER2, K-RAS, L-MYC, C-MYC

50
Q

What is HER2?

A

an EGF receptor overexpressed in 20% of breast cancers, which often respond to blocking w/ antibody

51
Q

what drugs can be used to treat HER2 positive breast cancer?

A

trastuzumab, lapatinib, pertuzumab

52
Q

How is HER2 overexpression diagnosed?

A
  1. immunohistochemistry stains the gene product and is on a continuum.
  2. FISH used! count the dots!
53
Q

What do K-RAS oncogenes code for?

A

A GTPase in the cytoplasm on the inner side of the cell membranes bound to the EGFR

54
Q

What does K-RAS do?

A

carries out signal transduction from ctyoplasm to nucleus when EGFR binds growth factors, transducing signals for the cell to proliferate

55
Q

What happens when growth factors bind to EGFR?

A

causes K-RAS GTPase to make more GDP that generates proteins that ultimately enter the nucleus to deliver the signal

56
Q

Why can’t you give EGFR target therapy for K-RAS mutations?

A

b/c RAS is downstream from EGFR so upstream therapy won’t work when RAS is constitutively on

57
Q

A single mutation in RAS is found in how many colon carincomas?

A

40%

58
Q

An EGFR mutation is found in how many lunc cancers?

A

10-15% of primary adenomcarcinoms

59
Q

What drugs can be used for EGFR mutations?

A

gefitinib and erlotinib

Pathology (6 decks)

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