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
Large cell lung carcinoma
Pleomorphic, aggresive
26
Small cell lung carcinoma
Anywhere in lung High grade cancer Small, dark staining, + stain for neuroendocrine markers Terrible prognosis
27
Risk Factors Lung Carcinoma
Pack years Family fx Industrial vapors
28
Risk Factors Pancreatic Carcinoma
Unknown! Diabetes mellitus Back pain, jaundice, cachexia
29
Colon carcinoma
Most sporadic,
30
Conditions that increase risk for colon carcinoma
FAP Lynch Syndrome MutY
31
Risk Factors Prostate Cancer
Age Race Genetics Sunlight via Vit D?
32
PIN and Pca
``` Non-invasive precursors in prostate cancer Gleason grade (differentiation grade) ```
33
Primary chemotherapy
on it's own often palliative (sometime curative) primary cancer treatment
34
Neoadjuvant therapy
before local therapy to make local more effective | easy to assess effects during local therapy
35
Adjuvant therapy
after local therapy, targets micromets | harder to assess from research pov
36
Classes of anti-tumor agents
``` DNA damaging Topoisomerase Microtubule interacting Hormonal Antibodies Kinase inhibitors ```
37
Common resistance mechanisms
``` Drug efflux (common) Resistance to apoptosis (common) Mutations in drug target (specific) Activation of repair enzymes (specific) Other ways to activate receptors (specific) ```