Neoplasia I Flashcards

(59 cards)

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
What are the most common causes of cancer death?
1. lung 2. breast (women), prostate (men) 3. colon
26
What are some causes of cancer?
smoking, obesity, alcohol, diet, UV light, asbestos, HPV
27
What cancers can smoking cause?
mouth, pharynx, larynx, esophagus, stomach, pancreas, kidneys, and bladder, lungs
28
Obesity is a cause of 14% of cancers of men and 20% of cancers of women in the US
FUCK THIS SHIT, know all of the percentages and be able to quote them in your nightmares
29
What are some genetically inherited cancers?
Retinoblastoma, FAP, Li-Fraumenit Syndrome, Multiple Endocrine neoplasia, Xeroderma pigmentosum, ataxia-telangiectasia, BRCA1 and BRCA2
30
What is the definition of tumor suppressor genes?
they control cell proliferation so defects are like faulty brakes on proliferation
31
What is the definition oncogenes?
genes that drive autonomous cell growth in cancer cells like an accelerator pedal stuck to the floor
32
What are some examples of TSGs?
RB, p53, APC/beta-catenin
33
When is normal state of RB and what does it do in that state?
-hypophosphorylated and prevents cell proliferation by binding up TF E2F
34
What happens when RB gets phosphorylated?
it lets go of E2F and starts cell proliferation
35
At what step does RB block the cell cycle?
G1 state
36
What does the APC TSG do?
it controls intestinal stem cell proliferation by WNT signaling
37
What is APC's normal function?
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
When are APC mutations prevalent?
in 100% of colon cancers w/ familal adenomatous polyposis, and 70% sporadic colon cancers
39
What is the role of p53?
molecular policeman, prevents propagation of genetically damaged cells, binds to DNA, arrests cells cycle for DNA repair, initiates apoptosis if repair is impossible
40
What is the short life of p53?
20 minutes, gets bound by MDM2 something is degraded
41
What are some ways a cell can acquire resistance to p53?
increased MDM2, E6 protein of HPV -- both degrade P53
42
What are some things that p53 recruits when repairing the cell damage?
p21 -- a CDK inhibitor GADD45 -- used for DNA repair if no repair possible then Bax kills cell
43
What are some more TSGs?
``` 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
What is the NF-1 gene products role?
activates GTPase, creating GDP that binds to cell membrane RAS protein making it inactive --- thus no transduction of signals
45
What happens in an inherited mutation of NF-1?
neurofibromatosis type 1, numerous benign NFs due to 2nd hit mutation
46
What is the role of VHL?
Serves as a TSG essentially. | Product causes ubquintation and degradation of HIF-1 in normal oxygenated areas. prevents angiogenesis
47
What does HIF-1 do?
if induced to act, it would yield increased PDGF and VEGF and promotes angiogenesis
48
What cancers occur when you have a germ line mutation in VHL?
kidney cancer, pheochromoctyoma (adrenal medulla tumor), retinal angioma, and other tumors
49
What are oncogene examples?
HER2, K-RAS, L-MYC, C-MYC
50
What is HER2?
an EGF receptor overexpressed in 20% of breast cancers, which often respond to blocking w/ antibody
51
what drugs can be used to treat HER2 positive breast cancer?
trastuzumab, lapatinib, pertuzumab
52
How is HER2 overexpression diagnosed?
1. immunohistochemistry stains the gene product and is on a continuum. 2. FISH used! count the dots!
53
What do K-RAS oncogenes code for?
A GTPase in the cytoplasm on the inner side of the cell membranes bound to the EGFR
54
What does K-RAS do?
carries out signal transduction from ctyoplasm to nucleus when EGFR binds growth factors, transducing signals for the cell to proliferate
55
What happens when growth factors bind to EGFR?
causes K-RAS GTPase to make more GDP that generates proteins that ultimately enter the nucleus to deliver the signal
56
Why can't you give EGFR target therapy for K-RAS mutations?
b/c RAS is downstream from EGFR so upstream therapy won't work when RAS is constitutively on
57
A single mutation in RAS is found in how many colon carincomas?
40%
58
An EGFR mutation is found in how many lunc cancers?
10-15% of primary adenomcarcinoms
59
What drugs can be used for EGFR mutations?
gefitinib and erlotinib