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Disease and Defense > Cell Growth and Neoplasia > Flashcards

Cell Growth and Neoplasia Flashcards

1
Q

different tissue have different homeostatic states (3)

A

continously dividing

quiescent

non-dividing

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2
Q

continuously dividing tissues?

A

e.g. skin, gut, epithelium, hematopoietic system

constant cell turnover

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3
Q

quiescent tissues?

A

e.g. hepatocytes

normally little to no turnover

capacity for proliferation if needed

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4
Q

non-dividing tissues?

A

e.g. CNS neurons

little to no capacity for proliferation

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5
Q

4 levels involved in homeostatic balance?

A

external environment interaction (physical environment / infectious agents / inhaled and ingested substances)

cell-extrinsic - macroenvironment (circulating factors e.g. cytokines / hormones)

cell extrinsic - microenvironment (ECM / stroma / GF and inflammatory milieu)

cell instrinsic (e.g. differentiation program / age of cell)

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6
Q

Physiological and pathological examples of hypertrophy?

A

physiological - uterus in pregnancy (actually combo of hypertrophy and hyperplasia)

pathological - heart in hypertension (high bp)

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7
Q

Physiological and pathological examples of hyperplasia?

A

physiologic - mammary gland during puberty / pregnancy

pathologic - endometrium - known risk factor for endometrial neoplasia (epithelial shifts to outnumbering stroma)

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8
Q

metaplasia?

A

change from one benign, differentiated cell type to another - usually in response to injury (e.g. inflammation)

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9
Q

bronchus and esophagus example of metaplasia

A

bronchus - columnar to squamous metaplasia - due to smoking - known risk for bronchopulmonary neoplasia

esophagus - squamous to columnar (Barrett) - due to acid reflux - risk factor for esophageal neoplasia

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10
Q

neoplasia =

A

new formation
progressive increase in cell number
clonal
irreversible

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11
Q

global mechanistic hallmarks of neoplasia

cell autonomous

A

diruption of normal homeostatic mechanisms
- altered cell autonomous mechanisms - activation of oncogenes / inactivation of tumor suppressor
-

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12
Q

global mechanistic hallmarks of neoplasia (cell-nonautonomous)

A

altered microenvironment - surrounding tissue, including stroma, blood vessels, and immune cells
altered macroenvironment -
circulating cells (immune cells) and factors (hormones / cytokines)

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13
Q

benign neoplasms vs malignant
gross features
sequestration and necrosis

A

benign - circumscribed / encapsulated - necrosis uncommon

malignant - invasive into adjacent tissue - necrosis common

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14
Q

benign vs malignant neoplasms
microscopic pathological features

differentiation?
turnover?
uniformity?
boundary?

A

benign

  • well differentiated
  • low rate of turnover
  • cytologic uniformity (cells similar to each other)
  • boundary maintained

malignant

  • variable differentiation
  • higher rate turnover
  • cytologic pleomorphism - cells different from each other
  • lose boundary
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15
Q

neoplasias are generally classified by?

A

tissue of origin

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16
Q

benign epithelial neoplasia?

A

adenoma

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17
Q

osteoma / chondroma / fibroma are examples of

A

benign mesenchymal neoplasia

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18
Q

malignant epithelial neoplasia

A

carcinoma

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19
Q

malignant mesenchymal neoplasia

A

sarcoma

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20
Q

malignant hematopoietic neoplasia -

A

lymphoma / leukemia

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21
Q

what is adenocarcinoma

A

malignant carcinoma with formation of glandular structures

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22
Q

clinical correlates of benign neoplasia
treatment?
recurrence?
malignancy progression?

A 
treated by surgical resection alone
may recur (especially if incompletely excised)
generally do not progress to malignant - important exception - benign, but premalignant neoplasms (e.g. colonic adenoma)
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23
Q

what molecular pathways are involved in benign neoplasms?

A

don’t know - no funding

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24
Q

malignant neoplasia =

A

cancer

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25
ratio americans get cancer
1/2
26
ratio american die cancer
1/5
27
6 hallmarks of cancer pathobiology
1. sustained angiogenesis 2. limitless replicative potential 3. tissue invasion / metastasis 4. insensitivity to anti-growth signaling 5. self sufficiency in growth signaling 6. evading apoptosis
28
what are the most common cancers?
carcinomas (cancer of epithelia)
29
what is dysplasia?
disordered growth
30
dyplasia in epithelia is hallmark of?
early premalignant neoplasia
31
characteristic histological features of dysplasia? (3)
loss of cytologic uniformity loss of normal histologic maturation loss of architectural orientation
32
marked / extensive dysplasia =
carcinoma in-situ
33
non-genetic factors influencing cancer etiology (6)
``` age lifestyle (etoh / tobacco) occupation (carcinogens) radiation infection (oncogenic) inflammation (IBD / UC) ```
34
Type of heritable cancers (3)
dominant tend to be oncogene recessive tend to be tumor suppressor there are also familial clustering familial cancers
35
Histological grade
degree of tumor histologic differentiation (i.e. resemblance of normal tissue counterpart)
36
grade vs stage?
grade is less reliable than stage
37
Tumor Stage TNM T = N = M =
Tumor - invasion extent N - lymph node involvement M - distance of metastasis
38
T1 or T2 N0 M0
Stage 1 (93)
39
T3 N0 M0
Stage 2A (85)
40
T4 N0 M0
Stage 2B (72)
41
T1 or T2 N1 M0
Stage 3A (83)
42
T3 or T4 N1 M0
Stage 3B (64)
43
Any T N2 M0
Stage 3C (44)
44
Any T Any N M1
Stage 4 (8)
45
Tis
tumor in situ
46
T1
tumor invades submucosa
47
T2
Tumor invades into, but not through, muscularis propria
48
T3
Tumor invades through muscularis propria
49
T4
Tumor invades adjancent organs
50
NX
Lymph nodes cannot be assessed
51
N0
No lymph node
52
N1
Metastasis to 1-3 regional lymphnodes
53
N2
Metastasis to >3 regional lymph nodes
54
M0
No distant metastasis
55
M1
Distant metastasis / seeding or abdominal organs
56
what makes sarcoma unique from carcinoma in initial presentation?
no pre-malignant lesion and no in-situ state
57
what makes CNS neoplasms unique from carcinoma in initial presentation?
no pre-malignant nor in-situ phase
58
does the carcinoma cancer progression paradigm apply to other cancer? (sarcoma / heme / cns?)
no
59
what makes cns neoplasms metastasis unique?
rare outside neuraxis
60
where do pediatric neoplasms tend to originate?
developmental precursors
61
what behavior do pediatric neoplasms tend to recapitulate?
aspects of developmental program of tissue of origin
62
latency and metastasis in pediatric cancer
short latency | early metastasis
63
mutations in pediatric neopalsms?
fewer mutations | prominent role for oncogenic fusions and epigenetic dysregulation

Disease and Defense (12 decks)

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