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Genetics > Lecture 10: Cancer 1 > Flashcards

Lecture 10: Cancer 1 Flashcards

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1
Q

cancer is a group of diseases in which cells develop malignant properties and become

A
  1. aggressive
  2. invasive
  3. metastatic
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2
Q

tumor

A

mad of abnormal growth of tissue, can be benign or malignant

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3
Q

neoplasia

A

formation of presence of new, abnormal growth

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4
Q

neoformation

A

new growth in reference to a tumor

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5
Q

malignancy

A

cells that are

  1. aggressive
  2. invasive
  3. metastatic
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6
Q

bening tumors

A

self-limitind in their growth and do not invade or metastasize
(not aggressive, invasive, or metastatic)

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7
Q

carcinoma

A

tissue of origin: epithelial tissue

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8
Q

sarcoma

A

tissue of origin: bone, cartilage, muscle, fat, connective tissue

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9
Q

leukemia

A

tissue of origin: bone marrow

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10
Q

lymphoma

A

tissue of origin: immune system

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11
Q

cns cancer

A

tissue of origin: brain and spinal cord

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12
Q

melanoma

A

tissue of origin: melanocytes

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13
Q

probability of being diagnosed with cancer

A

40%

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14
Q

probability of dying of cancer

A

20%

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15
Q

most common cancer types

A
  • prostate
  • lung
  • breast
  • colon, rectum

-pancreas (not that many cases but out of those cases majority die)

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16
Q

probability of being diagnosed and dying of a cancer in the oral cavity and pharynx

A

diagnosed –> 1%

dying–> 0.3%

17
Q

carcinogenesis

A
  • the accumulation of growth promoting mutation that results in cell transformation
  • occurs in already existing (somatic cells) –> not passed down
18
Q

mechanisms of carcinogenesis

A
  1. spontaneous gene or chromosome mutations
  2. mutagens or radiation
  3. tumor viruses (RNA and DNA)
  4. inherited predisposition; “cancer families”
19
Q

RNA tumor viruses

A

RNA tumor viruses (oncogenic retroviruses) contain viral oncogenes derived from cellular proto-oncogenes capable of transforming cells

20
Q

DNA tumor viruses

A
  • human papilloma virus (HPV) causes cervical cancer, oral caner
  • epstein-barr virus (herpes 4) causes burkitt’s lymphoma or nasopharyngeal cancer
  • human herpes virus 8 causes kaposi’s sarcoma
21
Q

DNA tumor viruses

A
  • human papilloma virus (HPV) causes cervical cancer, oral caner
  • epstein-barr virus (herpes 4) causes burkitt’s lymphoma or nasopharyngeal cancer
  • human herpes virus 8 causes kaposi’s sarcoma
22
Q

genes that are mutated in cancer

A
  1. proto-oncogenes
  2. tumor suppressor genes
  3. mutator genes
23
Q

proto-oncogenes

A
  • gain of function mutations: covert proto-oncogenes to oncogenes (“activates them”)
  • heterozygous
  • ex: point mutations, deletions, gene amplification, chromosomal translocation
  • genetic signature: limited number of mutations–> they are “drugable” (good targets for drug therapy)
24
Q

tumor suppressor genes

A
  • loss of function mutations: tumor suppressor genes result in cell transformation
  • homozygous
  • genetic signature: large number of mutation–> potential target for gene therapy
25
Q

mutator genes

A
  • loss of function mutations in enzymes involved in DNA replications and repair
  • enhance that rate of mutation accumulation
  • homozygous
26
Q

receptor tyrosine kinase signaling leads to

A

the activation of a transcription factors affecting growth and proliferation

27
Q

steps in receptor tyrosine kinase signaling

A

step 1: activation of receptor tyrosine kinase

step2: activation of KRAS
step3: activation of BRAF

28
Q

general structure of the receptor tyrosine kinase

A
  • extracellular domain (variable–> to recognize different ligands)
  • little transmembrane domain
  • intracellular domain which is a tyrosine kinase (phosphorylates other proteins on tyrosine residues)
29
Q

step 1: what happens when the ligand binds to the extracellular portion?

A

you get a dimerization, then they cross phosphorylate each other

30
Q

mutational events that activate EGFR

A

activating point mutations or deletions cause ligand independent dimerization (activate receptor) –> lead to epidermal growth factor receptors over expression

31
Q

epidermal growth factor receptor tyrosine kinase inhibitors

A
  • iressa: orally active EGFR tyrosine kinase inhibitor
  • traceva: used in lung and pancreatic cancer
  • caprelsa: used in medullary thyroid cancer
32
Q

step 2: activation of KRAS

A
  • once you activate the receptor the next step is KRAS
  • KRAS is not an enzyme (not easily inhibited)
  • small GTP binding protein (active when bound to GTP)
  • bound to the membrane
33
Q

KRAS mutations

A

if you have these mutations you can get stuck in the active form of KRAS (pathways keeps going)

  • almost always caused by the same type of mutation on codon 12 or 13
  • 20% of all tumors have a RAS mutation
34
Q

farnesyl trasnferase (FTase)

A

enzyme that helps in the anchoring of KRAS to the cell membrane
inhibiting this enzyme would inhibit KRAS

35
Q

step 3: activation of BRAF

A

RAS bind to and activates BRAF

  • BRAF is an enzyme which means there are powerful inhibitors for this step
  • mutations in the kinase domain, V600E is a common kinase activator
36
Q

BRAF mutations in which cancers

A

-melanoma
-colorectal carcinoma
papillary thyroid carcinoma
-some rare brain tumors

37
Q

philadelphia chromosome

A
  • a piece of chromosome 9 switches with a piece of chromosome 22
  • the new and shorter chromosome 22 contains abnormal BRC-Ab1 gene fusion
  • found in chronic myelogenous leukemia (CML) (95% carry this translocation)
  • gleevec is an effective treatment because it inhibits abnormal tyrosine kinase
38
Q

these lead to photo-oncogenes being converted to oncogenes

A

Activation of receptor tyrosine kinases (EGFR)
KRAS activation
BRAF activation
Philadelphia chromosome - BCR-Abl tyrosine kinase

Genetics (2 decks)

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