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D&D > Exam 2 - Neoplasia > Flashcards

Exam 2 - Neoplasia Flashcards

1
Q

Benign macroscopic features

A

circumscribed, encapsulated
necrosis uncommon (slow growth)
more boundary

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2
Q

Metastatic macroscopic features

A 
invasive into adjacent tissues
necrosis common (fast growth)
less boundary
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3
Q

Benign microscopic features

A 
well differentiated (looks like origin tissue)
low turnover
less mitotic activity
no invasion
organized
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4
Q

Metastatic microscopic features

A 
poor differentiation
high turnover
more mitotic activity
invasion
poor organization
pleiomorphism
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5
Q

Hallmarks of Cancer

A 
Evading apoptosis
Self-sufficiency in growth signals
Insensitivity to anti-growth signals
Tissue invasion and metastasis
Limitless replicative potential
Sustained angiogenesis
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6
Q

Histologic Grade

A

Low = more differentiation, closer to normal
High = less differentiation, further from normal
Take into account mitotic activity/architectural features
Less reliable than disease stage

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7
Q

Tumor/Disease Stage

A

T: Tumor (is,1-4)
N: Regional LN (X, 0, 1, 2), where 1=1-3
M: Distant metastasis (X, 0, 1)
N,M relate more to prognosis

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8
Q

Three metastatic disseminations

A

Direct seeding (cavitary)
Lymphatic spread
Hematogenous spread

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9
Q

4 Steps of the metastatic cascade

A
  1. Invasion
  2. Intravasation
  3. Extravasation
  4. Colonization
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10
Q

Invasion (metastatic cascade)

A
  1. loss of E-cadherin, down regulated
  2. Degradation of BM/CT (cleaves/squeezes)
  3. De-attachment to ECM (should apoptose, don’t)
  4. Locomotion (protrusion, adhesion, translocation, retraction)
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11
Q

Epithelial to mesenchymal transition

A

Normal process used inappropriately by cancer cells
Ex: palate formation, neural crest fusion
EMT to undergo intravasation
MET to undergo extravasation
More M character = more aggressive

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12
Q

Metastatic organ preference
Prostatic carcinoma
Neuroblastomas

A

Prostatic= bone
Neuroblastoma= liver/bone
Seed and soil (environment)
Ewing’s mechanical arrest (stop in first capillary bed)

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13
Q

Cancer effects

A

Direct effects: invasive mass interference
Indirect effects: paraneoplastic syndrome (7-15%)
Paracrine/endocrine effects

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14
Q

Causes of death in cancer

A
  1. Infection (chemo)
  2. Organ Failure
  3. Hemorrhage
  4. Thromboembolism
  5. Emaciation
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15
Q

Emerging Hallmarks of Cancer

A

Deregulation cellular energetics
Avoiding immune destruction
Genome instability/mutation
Tumor-promoting inflammation

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16
Q

Environmental impact on cancer

A
  1. 80% caused by environmental factors
  2. Variation due to region/country
  3. Migrants/decendents adopt risk of new country
17
Q

Most common cancer incidence men/women

A
  1. Prostate/breast
  2. Lung
  3. Colorectal
18
Q

Most common cancer death men/women

A
  1. Lung
  2. Prostate/breast
  3. Colorectal
19
Q

Ames test

A

Measures ability of chemical to mutate salmonella
His- agar, biosynth reveals mutation
Clear zone = toxic, ring = low dose/mutagenic

20
Q

Animal testing conclusions on cancer

A

Effect is dose dependent
One carcinogen = one type cancer
Requires time/proliferation
Transmittable to daughter cells

21
Q

Two step model of carcinogensis

A

Initation (mutagen, irreversible)

Promotion (nonmutagen, reversible, often inflammation or proliferation stimulating)

22
Q

4 types of lung carcinoma

A
  1. Squamous
  2. Adenocarcinoma
  3. Large cell
  4. Small cell
23
Q

Squamous cell carcinoma (lung)

A

Strongly linked to smoking
Occur centrally
Large, necrotic, hemorrhagic
Keratin pearls

24
Q

Adenocarcinoma (lung)

A

Central or periphery (sometimes scarring)
Little stroma
Best prognosis

25
Q

Large cell lung carcinoma

A

Pleomorphic, aggresive

26
Q

Small cell lung carcinoma

A

Anywhere in lung
High grade cancer
Small, dark staining, + stain for neuroendocrine markers
Terrible prognosis

27
Q

Risk Factors Lung Carcinoma

A

Pack years
Family fx
Industrial vapors

28
Q

Risk Factors Pancreatic Carcinoma

A

Unknown!
Diabetes mellitus
Back pain, jaundice, cachexia

29
Q

Colon carcinoma

A

Most sporadic,

30
Q

Conditions that increase risk for colon carcinoma

A

FAP
Lynch Syndrome
MutY

31
Q

Risk Factors Prostate Cancer

A

Age
Race
Genetics
Sunlight via Vit D?

32
Q

PIN and Pca

A 
Non-invasive precursors in prostate cancer
Gleason grade (differentiation grade)
33
Q

Primary chemotherapy

A

on it’s own
often palliative (sometime curative)
primary cancer treatment

34
Q

Neoadjuvant therapy

A

before local therapy to make local more effective

easy to assess effects during local therapy

35
Q

Adjuvant therapy

A

after local therapy, targets micromets

harder to assess from research pov

36
Q

Classes of anti-tumor agents

A 
DNA damaging
Topoisomerase
Microtubule interacting
Hormonal
Antibodies
Kinase inhibitors
37
Q

Common resistance mechanisms

A 
Drug efflux (common)
Resistance to apoptosis (common)
Mutations in drug target (specific)
Activation of repair enzymes (specific)
Other ways to activate receptors (specific)

D&D (6 decks)

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