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FS YEAR 2 > Cancer traits 1 > Flashcards

Cancer traits 1 Flashcards

1
Q

Cancer is a disease of what?

A

genome

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2
Q

What do carcinogens do?

A

produce mutations

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3
Q

What do mutations in somatic cells cause?

A

transformation and carcinogenesis

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4
Q

What is initiation

A

initiation of cancer development is clonal
- mutation in one specific cell will give a rise to whole tumour

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5
Q

What is carcinogenesis?

A

normal cells transformed into cancerous cells

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6
Q

What is the process of tumour cells

A

continue accumulating mutations, can evolve -> sub-clonal selection offers growth advantage and explains cell heterogeneity in tumours
- cells get different mutations
mutations in germ cells can be inherited increasing cancer risk but rarely causing it immediately

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7
Q

What are the names if cells in processing to malignant tumour?

A

normal cell (initiation occurs)->initiated cell (promotion occurs)-> preneoplastic cell (progression occurs) -> neoplastic cell (metastasis occurs)-> malignant tumour

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8
Q

What is an abnormal cell cycle?

A

unreplicated, mutated or damaged DNA, blocks progression of cell cycle at checkpoints

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9
Q

What is the process of abnormal cell cycle?

A

initial mutation inactivates a negative cell cycle regulator -> next mutation over activates a positive cell cycle regulator -> third mutation inactivates a genome stability factor->additional mutations accumulate rapidly->cancer cell

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9
Q

What is the difference between a normal cell and a cancer cell during DNA damage?

A

normal cell will lead to apoptosis whereas cancer cell will continue dividing

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10
Q

What is missense mutation?

A

change of single DNA base resulting in change in amino acid sequence & change of protein function

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11
Q

What is frameshift mutation

A

addition or removal of DNA bases shift DNA & amino acid sequence; results in different protein

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12
Q

what is nonsense mutation

A

change of single DNA base creates stop codon that terminates translation; results in shorter protein with no or abnormal function

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13
Q

what are chromosome rearrangements?

A

piece of chromosome breaks & is lost entirely (deletion), moves to different location (translocation), flips direction (inversion), or is repeated (duplication)
Can alter several genes at once, generating fusion genes

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14
Q

What is proto-oncogenes

A

normal cellular genes which regulate cell growth &/or division & differentiation

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14
Q

What is an oncogene

A

a proto-oncogene that has been activated by mutation or over expression - results in deregulated cell division

15
Q

what are the sequences of stop codon in mRNA

A

UAA, UAG, UGA

16
Q

What are the features of sense DNA

A

DNA is responsible for storing & transferring genetic information
One strand of DNA is called the sense strand because when you read it in the right direction, it provides the code to make a protein
The sense strand is bonded to an opposite DNA strand that is called the antisense/noncoding strand
Antisense doesn’t carry the translatable code, but serves as a template during transcription

16
Q

What are the stop codon sequences in sense DNA

A

TAG, TGA, TAA

17
Q

What is HER2 + function

A

encodes human epidermal growth factor receptor 2, has tyrosine kinase activity

= breast cancer

17
Q

What is the cause of oncogene activation

A
  1. gene mutation: results in different oncoprotein than normal protein
    - point mutations: in proto-oncogene or in promoter/regulatory element
    - chromosomal translocation: fusion in proteins or disruption of regulatory elements
  2. oncoprotein are same as normal protein but overexpressed
    - gene amplification

one alteration in one copy of protocol-oncogene is enough to convert it into an oncogene
proto-oncogene mutation mainly affect somatic cells

17
Q

What are the examples of oncogenes?

A

HER2
KRAS
BCR-ABL1
MYC

18
Q

What is KRAS + function

A

GTPase (converts GTP->GDP)protein involved in signal transduction, controls cell growth and differentiation downstream of receptor tyrosine kinases, point mutation -> protein permanently active -> continuous proliferation

=lung cancer

19
Q

what is BCR-ABL1 + Function?

A

philadelphia chromosome: fusion protein due to reciprocal chromosomal translocation between chromosomes 9 & 22
- has consituitave (unregulated) tyrosine kinase activity

=chronic myeloid leukemia

20
Q

What is MYC and function?

A

family of photo-oncogenes that code for transcription factors
- pathogenic alterations in MYC involved activation, amplifications and translocations

= lymphoma (c-MYC)
= neuroblastoma (n-MYC)

21
Q

TSG function ?

A

-Encode proteins that maintain cell cycle checkpoints & control genome stability
-Inhibit replication & proliferation of damaged cells by:
-Repair of DNA damage (e.g. BRCA1/2)
-Apoptosis (TP53)

22
Q

What happens if TSG is inactivated?

A

Knudson’s 2-hit hypothesis: loss of function mutations in TSG are recessive in nature–> one normal allele is sufficient for cellular control
“Second hit” affecting normal allele–> disrupts gene function

Familial (heritable) cancers develop after additional loss of normal functional allele (loss of heterozygosity)

23
Q

What is heterozygous state?

A

indicates absence of a functional TSG copy - but people remain healthy as there is still one functional gene left on the other chromosome of the pair
- the other copy can be inactivated by point mutation or other mechanisms -> results in loss of heterozygosity event and leaving no TSG to protect the body
loss of heterozygosity doesn’t imply a homozygous state (which would require presence of 2 identical alleles in the cell)

24
Q

What is TP53 + function?

A

a TSG example
- codes for tumour protein p53
- detects cellular stress (DNA damage) -> cell cycle arrest -> damage repair or apoptosis
- over 50% of dancer contain TP53 gene mutations (missense)

25
Q

What is Li-fraumeni syndrome

A

people who inherit only one functional tp53 allele -> most likely will develop cancer

26
Q

What is RB1 + function?

A
  • example of TSG
  • codes for RB (retinoblastoma) protein
  • prevents cell growth by inhibiting cell cycle
  • when cells are ready to divide, RB is phosphorylated (inactivation) -> cell cycle progresses
  • RB mutation, gene deletion or loss of heterozygosity lead to retinoblastoma (eye cancer) -> affects young children
    40% germinal, 60% non
26
Q

What occurs if there are mutation in DNA repair gene?

A

accumulation of mutation -> genomic instability, activation of oncogenes and loss of tumour supressors

27
Q

What is BRCA and

A

an example of DNA repair gene
-BRCA1/2 inherited mutations increase risk of breast, prostate, ovarian cancers

28
Q

sustaining proliferative signalling in normal cells?

A

require growth factors to proliferate
- GF bind to cell-surface receptors, typically with intracellular tyrosine kinase domains
TKDs send intracellular signals regulating
- cell cycle progression
- cell growth
- cell survival
- energy metabolism

28
Q

What occurs in cancer cells in proliferative signalling

A

synthesise of GF’s/ligands -> autocrine proliferative signalling (positive feedback loop)
b. unregulated receptor expression -> increased sensitivity to ligand
c. stimulate normal cells to supply GF’s
d. constitutively activate signalling pathways downstream of receptors -> no need

29
Q

How do normal cells evade growth supressors

A

use antigrowth signals to maintain quiescence & homeostasis
- these signals block proliferation by forcing cells:
- to enter quiescent G0 state -> cell cycle arrest
- permanently lose their proliferative potential -> interim post-mitotic state, senescence, apoptosis

cells can re-emerge from G0 state on some future occasion when extracellular signals permit

30
Q

How do cancer cells evade growth supressors?

A

circumvent antigrowth programs (evade TGF-beta anti proliferative signalling)
- many antigrowth programs depend on tsg (tp53, PTEN &RB)
- complete loss of TSG
- accumulation of mutations that render genes inactive

31
Q

What can cancer cells become in growth signals?

A

self sufficient in growth signals
also become insensitive to antigrowth signals

32
Q

What are the different types of genetic mutations in cancer?

A

missense
frameshift
nonsense
chromosome rearrangements

FS YEAR 2 (10 decks)

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