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FMS Week 6 > 6 Hallmarks of Cancer > Flashcards

6 Hallmarks of Cancer Flashcards

1
Q

The 6 hallmarks of cancer

A

1) sustaining proliferative signaling
2) evading growth suppressors
3) resisting cell death
4) enabling replicative immortality
5) indicing angiogenesis
6) activating invasion and metastasis

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2
Q

6 hallmarks of cancer pic

A
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3
Q

Hallmark 1: sustaining proliferative signaling

A

malignant cells can proliferate without external stimuli

usually as a consequence of oncogene activation

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4
Q

Proto-oncogenes

A

Normal genes that turn into oncogenes through mutation

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5
Q

Role of oncogenes

A

oncogenes created by mutations in proto-oncogenes

oncogenes promite autonomous cell crowth in cancer cells

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6
Q

proto-oncogenes

A

unmutated counterparts of oncogenes

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7
Q

Onco-proteins

A

proteins encoded by oncogenes

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8
Q

Examples of oncogene

A

EGF receptor (ERBB1)

RAS

RAF

MYC

CCND1 (Cyclin D1)

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9
Q

Examples of oncogenes chart

A
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10
Q

Oncogenes in colon cancer

A

Activating KRAS mutation occurs in 40-50% of colon cancers

Activating BRAF mutations occur in a smaller subset of colon cancers

metastatic oclon cancers tested in clinical molecular lab for KRAS and BRAF mutations

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11
Q

Cetuximab (Erbitux)

A

EGFR inhibitor

Monoclonal antibody against EGFR (chimeric mouse/human antibody)

Treatment of KRAS wild type metastatic colon cancer

treatment of metastatic lung adenocarcinoma and head and neck cancers

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12
Q

Oncogenes in breast cancer

A

15-20% of breast CAs have amplification of ERBB2 (HER) gene

ERBB2 encodes Her2 receptor, a member of EGFR family

gene amplification results in over expression of Her 2 receptor

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13
Q

Trastuzumab (herceptin)

A

Monoclinan antibody that binds to Her 2 receptor

used to treat pts with Her2 amplified breast CAs

Trastuzumab binds to extracellular domain of Her2 -> cell cycle arrest

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14
Q

Hallmark 2: Evading growth suppressors

A

Tumor supressor genes in normal cells apply breaks to cell proliferation

Mutated tumor supressor genes in cancer cells fail to inhibit growth -> uncontrolled proliferation

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15
Q

Most tumor supressor genes encode

A

transcription factors, cell cycle inhibitors, signal transduction molecules, cell surface receptors, regulators of cellular responses to DNA damage

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16
Q

Normal p53 (guardian of the genome)

A

DNA damage -> p53 activation -> cell cycle arrest in G1

indiction of DNA repair

if successful DNA repair -> normal cells

if repair fails -> apoptosis

17
Q

Abnormal p53 (mutated or lost)

A

DNA damage -> no p53 activation -> no cell cycle arrest

DNA damage unrepaired -> genetically damaged cells grow

malignant tumor

18
Q

Most human cancers have

A

biallelic loss of function mutation of p53

19
Q

Rb

A

Governer of the cell

20
Q

Rb

A

RB is a key negative regulator of G1/S cell cycle transit

RB is directly inactivated in most human cancers

hypophosphorylated RB binds and inhibits E2F TF and blocks transcription -> antiproliferative effect

Hyperphosphorylated RB releases E2F transcription factor -> transcroptional activation -> proliferative effect

21
Q

Examples of tumor supressor genes

A
22
Q

Hallmark 3: resisting cell death

A

Apoptosis (programmed cell death)

is a pathway of cell death indices by tightly regulated cellular program

cells destined to ddie activate intrinsic enxymes that degrade DNA and proteins

Cells break up into fragments called apoptotic bodies that contain portions of cytoplams and nucleus

fragments are phagocytosed by macrophages

23
Q

Cancer cells can evade apoptosis

A

mutations in TP53

mutations in other genes that regulate apoptosis

overexpression of anto-apoptotic signaling molecules like Bcl-2

24
Q

Hallmark 4: Enabling Replicative Immortality

A

All cancers contain cancer stem cells

cancer stem cells have unlimited replicative potential- are immortal

most human cells can divide 60-70 times

then senescence or apoptosis

TELOMERES

25
Q

Telomerase

A

Cancer cells express a lot of telomerase allowing them to continue elongating telomeres and dividing more

26
Q

Telomeres

A

Specific DNA sequences at the end of chromosomes

Telomeres shorten with each division

When telomeric DNA is eroded -> DNA samage is sensed -> p53 upregulated ->apoptosis

27
Q

Hallmark 5: Inducing angiogenesis

A

tumors bigger than 1-2 mm outgrow blood supply

need for nutrients, oxygen, and evacuate metabolic waste and CO2

28
Q

angiogenesis

A

formation of new blood vessels

29
Q

Regulators of angiogenesis

A

VEGF

30
Q

VEGF inhibited by what drug

A

bevacizumab (avastin)

FMS Week 6 (12 decks)

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