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Pathology > Robbins chp 5 > Flashcards

Robbins chp 5 Flashcards

1
Q

T/F Pancreatic cancers are almost always fatal

A

True

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2
Q

What does it mean to say that all tumors are clonal?

A

-all cells are derived from a single progenitor cell

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3
Q

what are the hallmarks of cancer?

A
  1. Self sufficiency in growth signals
  2. Lack of response to growth inhibitory signals
  3. Evasion of apoptosis
  4. Limitless replicative potential
  5. Angiogenesis
  6. Ability to invade local tissues and metastasize
  7. Reprogramming of metabolic pathways
  8. Evasion of the immune system
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4
Q

What are the two basic components of all tumors?

A

Parenchyma: neoplastic cells
Stroma: connective tissue, blood vessels, host-derived inflammatory cells

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5
Q

What would we call a benign tumor arising in fibrous tissue?

A

Fibroma

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6
Q

What’s a benign tumor growing in cartilage called?

A

Chondroma

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7
Q

What is a benign epithelial neoplasm growing on any surface and produces finger-fronds?

A

Papilloma

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8
Q

T/F all polyps are benign tumors

A

False,
Though polyp is the term commonly used for benign tumors, some polyps are malignant and others are not neoplastic at all (nasal polyps)

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9
Q

Where are Cystadenomas found?

A

Cystadenomas are hollow cystic masses arising in the ovary

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10
Q

What is the term for a malignant tumor arising in “solid” mesenchymal tissue?

A

Sarcoma

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11
Q

What is the term for a malignant neoplasm originating from the mesenchymal cells of the blood?

A

Leukemias or lymphomas

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12
Q

What’s a cancer of fibrous tissue called?

A

Fibrosarcoma

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13
Q

what are malignant neoplasms of epithelial cells called?

A

Carcinomas

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14
Q

what are carcinomas that grow in a glandular pattern called?

A

adenocarcinomas

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15
Q

The term “oma” is generally used for benign neoplasms. Do the terms, mesothelioma, lymphoma, melanoma and siminoma refer to benign or malignant cells?

A

These are actually malignant terms that are exceptions to the “oma” rule

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16
Q

Hamartoma?

A

mass of disorganized tissue localized to it’s site of origin

Not neoplastic, developmental anomaly

17
Q

Choristoma?

A

Mass of disorganized tissue localized to a site different than it’s origin
Not neoplastic, developmental anomaly

18
Q

What is anaplasia?

A

lack of differentiated cells
literally means “backward formation”
-loss of structural and functional differentiation of normal cells

19
Q

T/F Poorly differentiated tumors generally grow more rapidly than well-differentiated tumors

A

True

20
Q

What proteins primarily regulate the cell cycle?

A

Cyclins

21
Q

What do cyclins form complexes with to phosphorylate targets in the regulation of the cell cycle?

A

Cyclin Dependent Kinase (CDK)

22
Q

Why is there a G1-S checkpoint?

A

this checkpoint allows for DNA damage repair before entering the synthesis phase.

23
Q

What do CDKI’s do?

A

Regulate the CDK-cyclin complex. In doing so they enforce cell cycle checkpoints

24
Q

What is true of all cancer cells in reference to the G1-S phase?

A

All cancers have genetic lesions that disable the G1-S checkpoint. This causes cells to continually re-enter the S phase.

25
Q

T/F if one tumor suppressor gene is dysfunctional, tumor development will occur

A

False, both copies of the gene must be knocked out for tumor development to occur

26
Q

What do tumor suppressor genes do?

A

Encode proteins that inhibit cellular proliferation by regulating the cell cycle

27
Q

What is the function of the RB protein?

A

RB has antiproliferative effects by controlling the G1-S transition in the cell cycle

28
Q

What does Rb bind in it’s hypophosphorylated form and what is the significance?

A

Rb binds the transcription factor E2F in its non-phosphorylated form. E2F This interaction prevents transcription of genes like cyclin E that are needed for DNA replication. Thus cells are arrested in G1 phase

29
Q

What happens when Rb is phosphorylated?

A

When Rb is phosphorylated by cyclin D, it releases the E2F it had stored up. E2F then goes on to cause cell proliferation

30
Q

T/F almost all cancers have a disabled G1 checkpoint due to mutation of the RB gene or genes that affect Rb function

A

True

31
Q

What is the “ultimate protective mechanism against neoplastic transformation”?

A

p53 induced apoptosis

32
Q

How does p53 work?

A

p53 is activated by stresses such as DNA damage and assists in DNA repair by causing G1 arrest and inducing DNA repair genes. a cell with irreparable DNA is directed by p53 to enter senescence or undergo apoptosis

33
Q

What is Li-Fraumeni syndrome?

A

Familial disorder where patients inherit a mutant Tp53 gene. Only one hit is required to knock out the p53 gene. These patients are prone to develop malignant tumors at a young age

34
Q

What type of pathogen can inactivate both p53 and Rb?

A

DNA viruses

Pathology (4 decks)

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