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
Q

ratio americans get cancer

A

1/2

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26
Q

ratio american die cancer

A

1/5

27
Q

6 hallmarks of cancer pathobiology

A
  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
Q

what are the most common cancers?

A

carcinomas (cancer of epithelia)

29
Q

what is dysplasia?

A

disordered growth

30
Q

dyplasia in epithelia is hallmark of?

A

early premalignant neoplasia

31
Q

characteristic histological features of dysplasia? (3)

A

loss of cytologic uniformity
loss of normal histologic maturation
loss of architectural orientation

32
Q

marked / extensive dysplasia =

A

carcinoma in-situ

33
Q

non-genetic factors influencing cancer etiology (6)

A
age
lifestyle (etoh / tobacco)
occupation (carcinogens)
radiation 
infection (oncogenic)
inflammation (IBD / UC)
34
Q

Type of heritable cancers (3)

A

dominant tend to be oncogene
recessive tend to be tumor suppressor
there are also familial clustering familial cancers

35
Q

Histological grade

A

degree of tumor histologic differentiation (i.e. resemblance of normal tissue counterpart)

36
Q

grade vs stage?

A

grade is less reliable than stage

37
Q

Tumor Stage TNM
T =
N =
M =

A

Tumor - invasion extent

N - lymph node involvement

M - distance of metastasis

38
Q

T1 or T2 N0 M0

A

Stage 1 (93)

39
Q

T3 N0 M0

A

Stage 2A (85)

40
Q

T4 N0 M0

A

Stage 2B (72)

41
Q

T1 or T2 N1 M0

A

Stage 3A (83)

42
Q

T3 or T4 N1 M0

A

Stage 3B (64)

43
Q

Any T N2 M0

A

Stage 3C (44)

44
Q

Any T Any N M1

A

Stage 4 (8)

45
Q

Tis

A

tumor in situ

46
Q

T1

A

tumor invades submucosa

47
Q

T2

A

Tumor invades into, but not through, muscularis propria

48
Q

T3

A

Tumor invades through muscularis propria

49
Q

T4

A

Tumor invades adjancent organs

50
Q

NX

A

Lymph nodes cannot be assessed

51
Q

N0

A

No lymph node

52
Q

N1

A

Metastasis to 1-3 regional lymphnodes

53
Q

N2

A

Metastasis to >3 regional lymph nodes

54
Q

M0

A

No distant metastasis

55
Q

M1

A

Distant metastasis / seeding or abdominal organs

56
Q

what makes sarcoma unique from carcinoma in initial presentation?

A

no pre-malignant lesion and no in-situ state

57
Q

what makes CNS neoplasms unique from carcinoma in initial presentation?

A

no pre-malignant nor in-situ phase

58
Q

does the carcinoma cancer progression paradigm apply to other cancer? (sarcoma / heme / cns?)

A

no

59
Q

what makes cns neoplasms metastasis unique?

A

rare outside neuraxis

60
Q

where do pediatric neoplasms tend to originate?

A

developmental precursors

61
Q

what behavior do pediatric neoplasms tend to recapitulate?

A

aspects of developmental program of tissue of origin

62
Q

latency and metastasis in pediatric cancer

A

short latency

early metastasis

63
Q

mutations in pediatric neopalsms?

A

fewer mutations

prominent role for oncogenic fusions and epigenetic dysregulation