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605 Pathology > Neoplasia and Apoptosis > Flashcards

Neoplasia and Apoptosis Flashcards

1
Q

apoptosis

A

tightly regulated cell death

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2
Q

apoptotic bodies

A

cells with intact plasma membranes that will be phagocytized by macrophages

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3
Q

Does apoptosis have an inflammation component?

A

no

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4
Q

Can apoptosis be physiologic?

A

yes

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5
Q

Can apoptosis by pathologic?

A

yes

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6
Q

Physiologic Apoptosis

A

embryogenesis, involution due to hormone withdrawal, and self-reactive lymphocytes

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7
Q

Pathologic Apoptosis

A

most commonly due to DNA damage, but can also be accumulation of misfolded proteins, viral infections, or atrophy

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8
Q

2 Phases of Apoptosis

A
  1. Initiation Phase
  2. Execution Phase
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9
Q

2 Pathways in the Initiation Phase

A
  1. Intrinsic (Mitochondrial) Pathway
  2. Extrinsic (death receptor) Pathway
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10
Q

Which caspase is involved in the intrinsic pathway?

A

Caspase-9

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11
Q

Which caspase is involved in the extrinsic pathway?

A

Caspase-8

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12
Q

Intrinsic (Mitochondrial) Pathway

A

Bcl protein regulators activated by irreversible cell damage resulting in increased mitochondrial permeability (MOMP) and and release of cytochrome C into cytoplasm which promotes the formation of the apoptosome and caspase 9 activation

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13
Q

apoptosome

A

caspase-activating complex promoted by the release of cytochrome-C

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14
Q

MOMP

A

mitochondrial outer membrane permeabilization

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15
Q

Extrinsic (death receptor) pathway

A

activated by a “death ligand” (FasL) external to the cell [binding to the Fas receptor on cell membrane], then goes through a second messenger cascade via FADD which activates Caspase-8

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16
Q

FADD

A

Fas-Associated Death Domain

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17
Q

Are Bcl-2 genes pro or anti apoptotic proteins?

A

BOTH, mwahaha trick question

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18
Q

Main Caspases involved in the execution phase?

A

Caspase 3, 6, and 7

(MAINLY Caspase-3)

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19
Q

Execution Phase

A

cleaves DNA into small pieces, degrades structural components, and fragments to nucleus

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20
Q

Result of the Execution Phase of Apoptosis?

A

Apoptotic bodies

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21
Q

p53

A

tumor suppressor gene that will prevent propagation of genetically damaged cells when it is activated

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22
Q

When is p53 activated?

A

in response in cellular stress or damage, most often due to DNA damage, but also shortened telomeres and hypoxia

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23
Q

3 Ways p53 Prevents Neoplasms

A
  1. Quiescence
  2. Senescence
  3. Apoptosis
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24
Q

quiesence

A

temporary cell cycle arrest to allow for DNA repair

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25
Q

Senescence

A

permanent cell cycle arrest (if DNA repair fails) and cell continues to live on

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26
Q

The ultimate protective mechanism against neoplastic transformation?

A

APOPTOSIS (you know, the whole focus of this lecture)

27
Q

p53 mutation is present in what % of human cancers?

A

approximately 50%

28
Q

Factors that can help control apoptosis?

A

proto-oncogenes, tumor suppressor genes (like p53), and even mutations

29
Q

Without blood vessels, what’s the maximum size a tumor could be?

A

~2mm

30
Q

Mechanism of Angiogenesis

A

endothelial cells are recruited from pre-existing vessels, then proliferate and migrate through the ECM into tissues, before making their own “capillary bed”

31
Q

Angiogenic Factors (2)

A

involved in the upregulation of vessel formation
1. Vascular Endothelial Growth Factor (VEGF)
2. Fibroblast Growth Factor (FGF)

32
Q

Antiangiogenic Factors

A

involved in the downregulation of vessel formation
ex: thrombospondin

33
Q

Where do angiogenic and antiangiogenic factors come from?

A

extracellular matrix (ECM), where they are already present and ready to be used

34
Q

Function of Blood Vessels within Tumors

A

supply oxygen and nutrients, produce growth factors (PDFG and IL1), and allow for [continued] metastasis

35
Q

Can metastasis occur without VEGF (vascular endothelial growth factor)?

A

in experiments with mice, nope

36
Q

Morphology of “Capillary Beds” in Tumors

A

unstable, disorganized, and leaky with no meaningful distribution

37
Q

immunosurveillance

A

exists to identify and destroy tumor cells

38
Q

What are tumor antigens typically made of?

A

proteins, glycoproteins, glycolipids, and/or carbohydrates on the surface of tumor cells

39
Q

3 Types of Tumor Antigens

A
  1. Tumor-specific Antigens
  2. Tumor-specific SHARED Antigens
  3. Tissue-specific Antigens
40
Q

Tumor-Specific Antigens

A

present within a specific type of tumor and only that specific type

ex: proteins produced by papillomavirus

41
Q

Tumor-Specific Shared Antigens

A

on many different types of tumors (instead of just one), but still absent in normal tissue

ex: MAGE family proteins [in human med]

42
Q

Tissue-Specific Antigens

A

present in the tumors but also the tissue from which they arise from

43
Q

Most common antigen used in determining cell of origin in neoplasms?

A

tissue-specific

44
Q

First line of defense in the body?

A

Innate immune system

45
Q

Cells which make up the Innate Immune System

A
  1. NK Cells (Lymphocytes)
  2. Macrophages
46
Q

Most effective antitumor defense?

A

cytotoxic T lymphocytes (CTL, CD8)

47
Q

Cytotoxic T Lymphocytes

A

targets MHC Class I receptors on tumors and kills cell via cytolysis

48
Q

plasma cells

A

terminally differentiated B lymphocytes

49
Q

4 Ways in Which Tumors are able to Evade the Immune Response

A
  1. Altered MHC expression
  2. Antigen Masking
  3. Tolerance
  4. Immunosuppression
50
Q

NK cells are activated by what cytokine?

A

IL-2

51
Q

Antigen Masking

A

tumors hide the target antigen with other molecules, for example fibrin

52
Q

Tolerance

A

tumors can have antigens shared with normal tissues, also Tregs

53
Q

Immunosuppression

A

tumors can produce TGF-a/b to inhibit T lymphocyte activation; tumors can also express FAS ligand which will cause apoptosis of lymphocytes

54
Q

Can benign tumors metastasize?

A

NO, it is ONLY malignant

55
Q

What % of human cancer deaths are due to metastasis?

A

90%

56
Q

Is metastasis an efficient process?

A

no, it takes a lot of time and effort from the neoplastic cells

57
Q

The Steps of Metastasis (6)

A
  1. [Loss of] Adhesion
  2. Migration
  3. Stromal Invasion
  4. Intravasation
  5. Tumor Emboli Formation
  6. Extravasation
58
Q

Mechanism of Stromal Invasion

A

release of proteases (from either/both neoplastic and surrounding cells) degrades the basement membrane

59
Q

Intravasation

A

getting into the blood vessels

60
Q

3 Most Common Pathways of Metastasis

A
  1. Lymphatics
  2. Hematogenous
  3. Transcoelomic
61
Q

Lymphatic Metastasis

A

often carcinomas via regional lymph nodes, can be very widespread

62
Q

Hematogenous Metastasis

A

often sarcomas that travel through the venous system and will deposit themselves at the next capillary bed

63
Q

If you have metastatic hemangiosarcoma in the lung, where is its likely origin?

A

right atrium of the heart (follow veins backwards)

64
Q

Transcoelomic

A

often transabdominal, typically carcinomas within a body cavity; jumps between surface of organs

605 Pathology (14 decks)

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