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SFM (Scientific Foundations of Medicine) > Lecture 13: Cell Cycle, Cancer, and Cell Death > Flashcards

Lecture 13: Cell Cycle, Cancer, and Cell Death Flashcards

1
Q

5 stages of M Phase

A
  1. Prophase - mitotic spindle assembly
  2. Prometaphase - nuclear envelope gone, spindle attach to chromosome
  3. Metaphase - chromosomes attach to mitotic spindle
  4. Anaphase - cohesion proteins cleaved, chromosomes pulled apart
  5. Telophase - nuclear membrane reconstitutes around chromosome sets
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2
Q

G0 phase, G1 phase, S phase, G2 phase

A

G0 - quiescent, non-cycling, intact proliferation capacity

G1 - between cell division and DNA replication initiation (build cell mass)

S phase - DNA replication (synthesis)

G2 phase - between DNA replication and initiation of cell division

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3
Q

When are Cyclins B, D1, E, and A active during the Cell Cycle?

A

D1 - G1 phase

E - end of G1 to S phase

A - S phase

B - G2 phase to M phase

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4
Q

What is the purpose of CAK (CDK activating kinase)?

A

phosphorylates threonine residue on T-loop of Cyclin Dependent Kinase

  • allows catalytic function of CDK to become activated
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5
Q

Cdc25 A and B phosphatase: what are their substrates and what do they promote?

A

Cdc25A:

  • Cdk1 –> G1 to S transition
  • Cdk2 –> G2 to M transition

Cdc25B:
- Cdk1 –> G2 to M transition

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6
Q

Cdk4/6: What are their cyclin partners and what is their function?

A

partners: D cyclin
function: passage of restriction point and E cyclin synthesis

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7
Q

Cdk2: What is its cyclin partners and what is its function?

A

partners: E and A cyclin
function: G1 to S transition

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8
Q

Cdk1: What is its cyclin partners and what is its function?

A

partners: A and B cyclin

function: G2 to M transition
- A destroyed in prometaphase
- B destroyed when chromosome attach to spindle

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9
Q

What are the CKIs for Cyclin D?

A

p16 (INK4A), p15 (INK4B), p18 (INK4C), p19 (INK4D)

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10
Q

What are the CKIs for Cyclin E, A, and B?

A

p57, p27, p21

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11
Q

What is the function of p21?

A
  • induced by p53 tumor suppressor
  • cell cycle arrest after DNA damage (NO DNA synth)
  • promotes cell cycle arrest in sensecence and terminal differentiation
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12
Q

What is the function of p27?

A
  • cell cycle arrest in response to growth suppressors (TGF-beta) and in contact inhibition/differentiation
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13
Q

What is the function of p16?

A
  • works w/retinoblastoma susceptibility protein in growth regulation and cycle arrest in senescence
  • altered in a high percentage of human cancers
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14
Q

What happens during G1/S transition?

A
  • D/Cdk4 hyperphosphorylates pRb, allowing E2F to increase transcription of cyclin E and E2F1 genes
  • E2F increases formation of cyclin E and E2F
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15
Q

G1 checkpoint during DNA damage

A

Fast pathway: Chk2 inhibits Cdc25, preventing Cyclin E - Cdk from being activated

Slow pathway: p53 stabilization, p21 upregulation, inhibition of Cyclin-Cdk complexes

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16
Q

G2 checkpoint during DNA damage

A
  1. Chk1/2 –> causes export of Cdc25 = inactive B1/Cdk1 accumulation
  2. p53 stabilization, p21 inhibits B1/Cdk1
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17
Q

Initiation of Carcinogenesis

A
  • irreversible, no threshold
  • caused by genotoxic agents (chemicals, radiation, viruses, ROS)
  • activation of oncogenes/inactivation of tumor suppressors
  • sequence change in cellular DNA
18
Q

Promotion of Carcinogenesis

A
  • occurs over long period of time, reversible in early stages
  • cellular selection and CLONAL EXPANSION
  • inhibition of cell death in initiated cells
19
Q

Progression of Carcinogenesis

A
  • irreversible changes in gene expression
  • selection for optimal growth in response to cellular environment
  • benign tumors into malignant neoplasms capable of invading and metastasizing distant sites
20
Q

Oncogenes vs Tumor Suppressors

A

Oncogenes: genes that stimulate division/growth

  • loss of control = unregulated cell growth/division
  • “gain of function” mutation
  • germline inheritance rarely involved

Tumor Supressors: check/inhibit cell division

  • loss of control = cell growth/division
  • “loss of function” mutation
  • germline inheritance frequently involved
21
Q

Three types of oncogenes

A
  1. Cellular proto-oncogenes –> retrovirus captured
  2. Virus-specific oncogenes –> behave like mutated cellular proto-oncogenes
  3. Cellular proto oncogenes –> mutated
22
Q

Papillomavirus: tumor type and cofactors

A

Tumor Type: anogenital cancers, some upper airway cancers and skin cancer

Cofactors: smoking, oral contraceptives and genetic disorder, UV light, immunosuppression

23
Q

Mechanism and Oncogenic element of: Type 1 retroviruses

A
  • Transducing Viruses
  • mech: oncogenic transduction of cellular gene
  • element: cellular oncogene carried in retrovirus
24
Q

Mechanism and Oncogenic element of: Type 2 retrovirus

A
  • Non-transducing Viruses
  • mech: cis-acting provirus
  • element: cellular oncogene via proviral insertion/integration
25
Q

Mechanism and Oncogenic element of: Type 3 retrovirus

A
  • Non-transducing Long Latency Viruses
  • mech: trans-acting proteins encoded by retrovirus
  • element: retroviral transactivating protein disrupting normal regulation of cellular transcription
26
Q

Mechanism and Oncogenic element of: Type 4 retrovirus

A
  • Retroviruses that contain envelope that signals
  • mech: trans-acting protein (envelope) encoded by retrovirus
  • element: inappropriate cellular signaling resulting from viral envelope/cell receptor interactions
27
Q

Oncogenes and their associated cancers:

  1. K-ras
  2. N-ras
  3. H-ras
  4. c-myc
  5. L-myc
  6. N-myc-DDX1
A
  1. K-ras –> lung, ovarian, colorectal, bladder carcinomas
  2. N-ras –> head and neck cancers
  3. H-ras –> colorectal carcinomas
  4. c-myc –> various leukemias, carcinomas
  5. L-myc –> lung carcinomas
  6. N-myc-DDX1 –> neuroblastomas, lung carcinomas
28
Q

What happens if p53 is damaged and cannot be repaired?

A

programmed cell death occurs

29
Q

What is the 2nd most commonly inactivated gene?

A

INK4A (p16)

30
Q

Chemotherapy:

  1. Alkylating Agents
  2. Intercalating Agents
  3. Antimetabolites
  4. Mitostatic Agents
  5. Platinum Derivatives
A
  1. Alkylating - denature certain macromolecules (cross-link DNA chains)
  2. Intercalating - interact between 2 DNA bases, changing structure and function
  3. Antimetabolites - structural analogs of purine/pyrimidine (block synth of corresponding base)
  4. Mitostatic - inhibit tubulin synthesis (cell spindle poisons)
  5. Platinum Derivatives - DNA binding
31
Q

Two molecules involved with regulating Necrosis and the mechanism

A
  1. Receptor-interacting protein 1 (RIP1)
  2. Poly [ADP-ribose] polymerase 1 (PARP-1)

Mechanism:

  • Calcium overload, mito uncoupling, inc. oxygen consumption
  • ATP depletion and excessive ROS
32
Q

Morphology of Necrosis

A

Cell membrane: swell/rupture

Cytoplasm: organelle degen., mito swelling

Nucleus: clumping, random degen. of nuclear DNA

Cells: ALL TYPES

Inflammation: YES

  • extensive failure of normal physiological pathways essential for maintaining cellular homeostasis
  • CASPASE INDEPENDENT
33
Q

Morphology of Apoptosis

A

Cell membrane: blebbing, fragment into membrane bound apoptotic bodies

Cytoplasm: fragment, shrinking

Nucleus: chromatin condensation/degradation by specific DNA cleavage = nuclear fragmentation

Cells: hematopoietic cells and malignant counterparts

Inflammation: NO

  • cell membrane loses asymmetry, phosphatidylserine exposed on cell surface; CASPASE DEPENDENT
34
Q

4 apoptotic mechanisms

A
  1. DNA damage (ATP and p53)
  2. Death receptor signaling
  3. cell membranes (hydrolysis of sphingomyelin to ceramide)
  4. mitochondrial damage - ceramide mediated process
35
Q

Bcl-2, Bax, Bak, BH3 (Apoptotic Signals)

A
  • Bcl-2 inhibits Bax and Bak

- BH3 binds to Bcl-2, allowing Bax and Bak to oligomerize (pore formation)

36
Q

Morphology of Autophagy

A

Cell membrane: blebbing

Cytoplasm: accumulation of two-membrane autophagic vacuoles

Nucleus: partial chromatin condensation; no fragments

Cells: ALL TYPES

Inflammation: NO

  • CASPASE INDEPENDENT, increased lysosomal activity
37
Q

Morphology and mechanisms (3) of Mitotic Catastrophe

A

Cell membrane: no change

Cytoplasm: larger cytoplasm; formation of giant cell

Nucleus: micro/multinucleation. formation of nuclear envelopes around individual clusters of missegregated chromosomes

Mechanisms:

  1. defects in cell cycle checkpoints
  2. hyperamplification of centrosomes
  3. caspase-2 activation during metaphase (delayed apoptosis)
38
Q

Fate of Cells w/Abberant Mitosis (Mitotic Catastrophe)

A
  1. Mitotic Death (die in mitosis)
  2. Delayed Cell Death (division for many cycles)
  3. Senescence (exit mitosis, permanent G1 arrest)
39
Q

Morphology and two pathways of Senescence

A

Cell membrane: No change

Cytoplasm: flattening, inc. granularity

Nucleus: distinct heterochromatic structure

Cells: ALL TYPES

Inflammation: Yes, but induced by secretory factors from cell itself

Pathways (same as DNA damage checkpoints)

  1. p53 –> p21
  2. p16 –> Rb
40
Q

Rous Sarcolema: oncogene, type of oncoprotein, homologous oncogene in human tumors

A

oncogene: src
oncoprotein: non-receptor TK

homologous oncogene: colon carcinoma

SFM (Scientific Foundations of Medicine) (20 decks)

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