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DWT Exam 4 > Pathology: Neoplasia > Flashcards

Pathology: Neoplasia Flashcards

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1
Q

What is the molecular basis of cancer?

A

a tumor is initiated by the clonal expansion of a single precursor cell that has incurred genetic damage

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2
Q

What does “hallmarks of cancer” mean?

A

carcinogenesis results from the accumulation of complementary mutations in a stepwise fashion over time

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3
Q

What are the 4 classes of normal regulatory gene that are the principle targets of cancer causing mutations?

A

1) Proto-oncogenes
2) DNA repair genes
3) Tumor suppressor genes
4) Genes regulating cell death

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4
Q

How does a cell proliferate?

A

Using the growth signal pathway GF binds to receptor thus activating that receptor. Production/activation of numerous cytoplasmic signal transducing proteins in the nucleus. This activates transcription factors in the DNA. This leads to transcription of growth promotors & regulators

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5
Q

What is Growth Factor (GF) used for?

A

Normal cells require GF to proliferate

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6
Q

How does growth factor work?

A

Most soluble GF are made by a cell to act on a neighboring cell.

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7
Q

True/False: tumor cells can synthesize their on GF to which they respond to?

A

True

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8
Q

What can lead from common mutations in GF receptors?

A

Constitutive signaling that is independent of the presence of GF

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9
Q

What are examples of constitutive signaling ?

A

C-kit & HER2

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10
Q

What are the 2 signaling transducing proteins?

A

RAs and P13 kinase

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11
Q

What is Ras and what does it encode for?

A

Is a normal protooncogene that is activated by tyrosine kinase receptor activity & it encodes for a protein that binds to GDP & GTP

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12
Q

What does active & inactive Ras bind to?

A

Inactive Ras binds to GDP and when surface receptor binding facilitates swapping of bond GDP for GTP is active RAs

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13
Q

What are P13 kinase?

A

Normal proto-oncogenes in AKT signaling (another growth signaling pathway)

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14
Q

How is p13 kinase activated?

A

like Ras it is activated by GF binding & initiating receptor tyrosine kinase activity

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15
Q

What is transcription factor?

A

Are the proteins that actually bind to the DNA & turn it on/off

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16
Q

What does Myc do that we know of?

A

Very broad activities
activates the expression of many genes involved in cell growth
Can upregulate expression of telomerase
Can reprogram somatic cells to pluripotential stem cells

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17
Q

What is the importance of telomerase in neoplasia?

A

It is an important mechanism of cell aging
“Tumors up regulate this & have “cell replicate immortality”

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18
Q

What do Rb (retinoblastoma proteins) do?

A

They normally inhibit cell proliferation and lives in an active form that binds to E2F (transcription factor that goes to DNA & says lets grow)

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19
Q

What does the active form of Rb do?

A

The active form binds to & inhibits transcription factors thus preventing from advancing from G1 phase to S phase in replication.

20
Q

What is the importance of mutated Rb?

A

It is inactive and is the brake failure of cell division

21
Q

What are the examples of mutated Rb neoplasias?

A

Canine hemangiosarcoma & Osteosarcoma & retinoblastoma

22
Q

What is P53?

A

It is a tumor suppressor that regulates cell cycle progression, DNA, repair, cellular senescence & apoptosis. It is also the “guardian of the genome”. It also prevents propagation of genetically damaged cells

23
Q

What level of P53 is normal in normal cells?

A

Normal cells have low levels of P53

24
Q

What holds P53 in check?

A

MDM2

25
Q

What are the normal biochemical pathways that lead to intrinsic apoptosis?

A

Bcl-2 protein

26
Q

What is the most commonly affected pathway affected in cancer

A

Intrinsic apoptosis pathway

27
Q

What does Bcl-2 protein normally do?

A

Normally inhibits release of cytochrome C which would otherwise inhibit the intrinsic pathway & encodes a protein that inhibits apoptosis

28
Q

What does failure of Bcl-2 protein cause?

A

Prolongs cell lifespan by preventing apoptosis

28
Q

What does failure of Bcl-2 protein cause?

A

Prolongs cell lifespan by preventing apoptosis

29
Q

What are the normal biochemical pathways that lead to extrinsic apoptosis?

A

FLIP

30
Q

What does FLIP normally do

A

blocks the extrinsic pathway by binding procaspase-8 without activating it

31
Q

What does failure of FLIP do?

A

Prolongs cell life span and prevents apoptosis

32
Q

What must tumor cells successfully do to produce a metastatic leasion?

A

invade the extracellular matrix
disseminate through the vessel unharmed
locate a suitable distant site/tissue to live
successfully grow/proliferate there

33
Q

What do tumor cells tend to aggregate with?

A

Each other and Platelets and coagulation factors

34
Q

What is important to keep in mind about tumor metastasis?

A

Where the tumor leaves capillaries is related to anatomic location & vascular drainage of the primary rumor

35
Q

What places are “good” for matastisis and why?

A

Lungs and liver because they have high blood circulating

36
Q

What are the tumor antigens?

A

products of mutated genes-oncoproteins
overexpressed or aberrantly expressed cellular proteins
tumor antigens produced by oncogenic viruses
oncofetal antigens
altered cell surface glycolipids & glycoproteins
cell type specific differentiation antigens

37
Q

Why are cytotoxic T lymphocytes important?

A

Can respond to new antigens
many tumors produce proteins to decrease T cell response
their presence can be marker for better prognosis

38
Q

Why are NK cells important?

A

recognize absence of MHC1 or stress-induced proteins expressed on cell surface

39
Q

Why are M1 and M2 important.

A

M1 are pro-inflammatory which is important anti-tumor effector mechanism

M2 is associated with wound healing anti-inflammatory

40
Q

True/False: Immunodeficiency is not skewed toward infectious agents?

A

False

41
Q

How does cancer evade an intact immune system?

A

Antigen negative variants
loss or reduction of MHC expression
weakly immunogenic until tumor burden is to large to control
Immunosuppression
TH1 suppression
convert T-cell to Treg
upregulation of T cell suppresion
Myeloid derived suppressor cells

42
Q

What does TGFB & IL-10 do?

A

suppress Th1 response
convert effector T cells to Treg- immunosupressive

43
Q

What upregulates T cell suppression?

A

CTLA-4
PD-1

44
Q

What promotes tumor inflammation?

A

release of factors that promote proliferation
reactive oxygen species production
removal of growth supressors
enhanced resistance to cell death
inducing angiogenesis
activating invasion & metastasis
evading immune destruction

45
Q

What helps tumor cells evade the immune system?

A

TAMs
MDSCs

DWT Exam 4 (5 decks)

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