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SFM Exam 2 > 24: Cell Cycle, Cell Death, And Cancer > Flashcards

24: Cell Cycle, Cell Death, And Cancer Flashcards

1
Q

Five phases of the cell cycle and what occurs in each

A
  1. G0: quiescent
  2. G1: first gap phase
  3. S: DNA replication
  4. G2: second gap phase for growth
  5. Mitosis

(First four = interphase)

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2
Q

Four phases of mitosis

A

Prophase: chromosomes condense into sister chromatids, attach to the mitotic spindle
Metaphase: sister chromatids line up at the equator attached to opposite poles of spindle
Anaphase: sister chromatids become daughter chromosomes and are pulled to opposite poles of the spindle
Telophase: spindle disassembles, chromosomes packaged into separate nuclei, cytokinesis

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3
Q

Three checkpoints in cell division and what happens in them

A
  1. START: G1 to S: cell commits to cell cycle entry
  2. G2/M: chromosome alignment on spindle
  3. M: triggers anaphase and cytokinesis
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4
Q

What tumor suppressor plays a role in checkpoint 1 of cell cycle?

A

P16

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5
Q

What CKI plays a role in G1 phase of interphase?

A

p21

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6
Q

Four examples of CKI

A

P16, p21, p27, CDC25

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7
Q

Five examples of oncogenes

A

EGF, Ras, Myc, cyclins, ATM

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8
Q

Four examples of tumor suppressor genes

A

P53, Rb, p14ARF, p16INK4A

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9
Q

Activity and level of CDKs and cyclins throughout cell cycle

A

CDKs: levels constant, activity changes
cyclins: levels change, activity changes

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10
Q

Major DNA damage trigger of cell death

A

DSBs

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11
Q

Why is cell death considered a cell cycle event?

A

Activation of cell cycle checkpoints

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12
Q

3 initiation and 3 executioner caspases

A

Initiators: 8, 9, 10
Executioners: 3, 6, 7

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13
Q

Examples of BH3 family proteins

A

Bid, Bim, Bad, Noxa, Puma

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14
Q

Function of autophagy

A

Degradation of long-lived proteins and organelles

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15
Q

What causes mitotic catastrophe?

A

Cell cycle checkpoint deficiencies

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16
Q

Three fates of the cell that undergoes mitotic catastrophe

A
  1. Mitotic death right away
  2. Delayed cell death -> divide for many cycles before dying
  3. Senescence: exit mitosis and undergo permanent G1 arrest
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17
Q

Replicative senescence

A

Due to telomere shortening

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18
Q

Tumor

A

Space-occupying lesion - may/may not be neoplasm

19
Q

Neoplasm

A

Relatively autonomous abnormal growth with abnormal gene regulation (benign or malignant)

20
Q

Cancer in two words

A

Malignant neoplasm

21
Q

Hallmarks of cancer

A
  1. Self sufficient
  2. Limitless replicative potential
  3. Insensitive to inhibitors
  4. Evade cell death and destruction
  5. Sustain angiogenesis
  6. Capability to invade and metastasize
  7. Create genome stability
  8. Promote inflammation
22
Q

Three stages of carcinogenesis

A

Initiation, promotion, progression

23
Q

Initiation of carcinogenesis

A

Genotoxic event causing mutation in 1+ gene that controls cell regulation (activation of oncogene or inactivation of tumor suppressor gene)

24
Q

Promotion stage of carcinogenesis

A

Epigenetic event involving change in gene regulation

25
Q

Is promotion in carcinogenesis irreversible? Is there a threshold?

A

It is reversible in early stages + threshold exists in time and dose (occurs over a long period of time)

26
Q

Progression in carcinogenesis

A

Clastogenic events that further change karyotype / make it unstable

27
Q

What does progression in carcinogenesis result in?

A

Conversion of benign tumor into malignant neoplasm

28
Q

What is notable about inactivation vs methylation of Rb gene?

A

Different alterations to the gene cause different clinical results (retinoblastoma vs brain tumor vs osteosarcoma, etc.)

29
Q

Three major cellular components of the tumor microenvironment

A
  1. Immune cells
  2. Fibroblasts and other stromal cells
  3. Blood vessel cells
30
Q

Three major components of the tumor microenvironment

A
  1. Cellular components
  2. Secretory factors
  3. ECM
31
Q

Secretory factors in the tumor microenvironment

A

Signaling molecules, GFs, inflammatory factors, enzymes

32
Q

Four reasons the tumor microenvironment is important

A
  1. Barrier for therapy
  2. Paracrine signaling occurs here
  3. Desmoplastic reaction
  4. Can promote tumor progression
33
Q

Fibroblast aging and cancer

A

Older fibroblasts may contribute to pancreatic cancer progression using ALOX12 and 12-HETE (inflammatory mediators) in the tumor microenvironment (Dr. Sarsour’s research)

34
Q

Most frequent malignancy in women

A

Breast cancer

35
Q

Three molecular features of breast cancer

A
  1. BRCA mutations
  2. HER2 activation
  3. Hormone receptor activation (estrogen and progesterone)
36
Q

Most common exocrine pancreatic neoplasm

A

PDAC: pancreatic ducal adenocarcinoma

37
Q

A typical early genetic event in pancreatic cancer

A

K-ras mutation

38
Q

Four types of cancer therapy

A
  1. Surgery
  2. Radiation
  3. Chemotherapy
  4. Immune therapy
39
Q

What cells are most affected by radiation

A

Cells with reproductive activity, long dividing future, and have the least fixed morphology and function

40
Q

Two mechanisms of radiation therapy

A
  1. Direct energy deposition to break DNA bonds

2. Hydrolysis of water to produce free radicals

41
Q

Five types of chemotherapy agents

A

Alkylating agents, intercalating agents, antimetabolites, mitostatic agents, platinum derivatives

42
Q

Two types of immune therapy for cancer

A
  1. Adaptive T cell therapy

2. Personalized recombinant cancer vaccines

43
Q

Adaptive T cell therapy

A

Isolated T cells from pt genetically modified to express CARs (ags) that can bypass MHC restriction -> cytotoxicity to target on surface of malignant cell

SFM Exam 2 (19 decks)

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