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Health and Disease: Genes > Wright Cancer > Flashcards

Wright Cancer Flashcards

1
Q

What are the 2 types of cnacer growth?

A

Hyperplastic: too many cells
Dysplastic: mutant cells

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2
Q

What variation can observed in dysplastic growths?

A

Changes to nuclear size, shape, dye uptake, cytoplasmic ratio
Increased mitosis
Lack of cytoplasmic features

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3
Q

Which cells are most cancers derived from?

A

90% epithelial

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4
Q

How can primary tumours spread?

A

Via intravasation and dispersion of cells through blood and lymph systems

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5
Q

What are the 2 types of epithelial cancer?

A

Squamous cell carinomas

Adenocarcinoma

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6
Q

What are the main types of cancer?

A

Epithelial carcinomas
Connective tissue sarcomas
Haematopoetic leukaemias and lymphomas
CNS

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7
Q

How does cancer arise?

A

Somatic driver mutations aquired over a period of time

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8
Q

What are passenger mutations?

A

Mutations aquired during tumour development, contributing to genomic instability

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9
Q

What features do cancer cells have in culture?

A 
No contact inhibition
limitless replication
Less growth factor dependance
Refractile
Disarrayed actin
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10
Q

What are the 6 hallmarks of cancer?

A 
Evasion of apoptosis
Invasion and metastases
Sustained angiogenesis
Deregulated proliferation
Block of differentiation
Limitless replication
Evasion of immune system
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11
Q

What test measures mutagenicity?

A

Ames

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12
Q

How does the Ames test work?

A

Mutations disrupt histidine degrading gene so cells die in excess-histidine medium

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13
Q

What is the relationship between mutagenicity and carcinogenicity?

A

Linear correlation

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14
Q

What was the first oncogenic virus to be studied?

A

Rous Sarcome Virus

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15
Q

How did RSV aquire v-Src?

A

Reterovirus inserts as provirus adjacent to c-Src gene

Uptaken during replication

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16
Q

How does RSV cause cancer?

A

Acutely transforming with v-Src under control of consitutive strong 5’LTR

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17
Q

How can c-Src be detected?

A

Hybridisation of v-Src probe to uninfected tissues

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18
Q

How do slowly transforming reteroviruses cause cancer?

A

Insertational mutagenesis upregulates oncogene

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19
Q

How can oncogenes be upregulated?

A

Amplification
Point mutations
Chromosome translocations

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20
Q

What are Her2 related cancers caused by?

A

Gene amplification and overexpression of RTK

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21
Q

What cancers are caused by chromosome translocations?

A

BCR-Abl in chronic myleogenous lymphoma

c-myc BCL in Burkitt’s lymphoma

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22
Q

Where does ALV insert?

A

upstream of the c-myc oncogene

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23
Q

How can point mutations be detected?

A

Inserting gene into mouse cell results in fibroblast formation
Southern blot to detect gene
Detect critical region of fragment by recombinant techniques to reduce size
sequence

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24
Q

What is an example of an activating point mutation in an oncogene?

A

Ras oncogene mutated and activated in codon 12

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25
Q

What are the main oncogene functions?

A 
RTK
Cytoplasmic TK
Ser/Thr Kinase
Steroid growth factor receptors
nuclear TFs
GTP-binding proteins
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26
Q

What kind of mutation is found in src?

A

Absence of phosphorylation of RTK C-terminal regulator so no autoinhibiton

27
Q

What kind of mutation is v-ErbB?

A

Truncated ectodomain has ligand independant, constitutive activation

28
Q

What function does c-Src have?

A

Tyrosine kinase adapter protein with SH2/SH3 domains for PDGFr

29
Q

How is v-src constituitvely activate?

A

Phosphorylation of Y416 exposes kinase domain

No autoinhibition

30
Q

What are the main ways RTKs are mutated in cancer?

A

Overexpression
Autocrine signalling
Ligand independance
Lack of autoinhibition

31
Q

How is Ras signalling upregulated in cancer?

A

Overactivation of receptors
Loss of GTPase function
Loss of GAPs

32
Q

What cellular responses does Ras cause?

A

PI3K for PKB for proliferation
PI3K for Rho for cell shape and motility
MAPK for cell proliferation
RAL for motility

33
Q

What type of mutations are required to activate oncogenes?

A

Dominant

34
Q

What type of mutations are required to knock-out tumour suppressors?

A

Recessive (both alleles)

35
Q

How can tumour suppressor function be removed?

A

Deleting entire gene or critical region

Upregulation of inhibitor

36
Q

How can tumour suppressor genes be studied in culture?

A

Fusion of cancer cell with normal cell will halt tumour growth

37
Q

Which type of cancer gene can be inherited?

A

tumour suppressors

38
Q

What are the 2 types of Retinoblastoma?

A 
Sporadic mutations cause tumours in one eye 
Inherited form (40%) cause multiple tumours, both eyes and malignancy
39
Q

What function is the Rb gene shown to have by fusion with tumour cells?

A

Halts cell cycle in G1 phase

40
Q

What mutation causes retinoblastoma?

A

Chromosome 13 q14 deletion

41
Q

What functions do tumour supressors have?

A

Restrain cell proliferation

Promote apoptosis

42
Q

What are the targets of tumour suppressor genes?

A

Oncogene products

Signalling pathways

43
Q

What does NF1 encode?

A

Neurofibromin for 1000x increase in Ras GTPase

44
Q

What mutation does neurofibromatosis have?

A

Knock-out of tumour suppressor NF1 in schwann cells for consitutive activation of Ras

45
Q

How is p53 tumour suppressor function lost?

A

Mutations affect folding of DNA binding domain

Loss of ARF inhibitor of MDM2 causing degradation of p53

46
Q

What proportion of cancers shown p53 mutations?

A

50%

47
Q

What function does p53 have in normal cells?

A

DNA repair
Apoptosis
Cell cycle arrest
Block of angiogenesis

48
Q

What proportion of cancer is encoded epigentically?

A

50% of all germline cancers

49
Q

How do epigenetic changes cause cancer?

A

Methylation of CpG silences tumour suppressor genes

50
Q

When are epigenetic changes developed?

A

Early in tumour formation

51
Q

How is DNA methylation observed?

A

Stained dark

52
Q

What are examples of genes that can be methylated to cause cancer?

A

RASSF1A

P16INK4A

53
Q

How can cancer be detected without sequencing?

A

Measuring expression ratios of protein using mRNA/cDNA with microarray probes
Ratios can be compared to “normal”
Ratios/signatures determine prognosis

54
Q

How many genes can be compared in a gene expression assay?

A

20,000

55
Q

What are the 2 main classes of rational cancer treatment?

A

Antibodies

Low molecular weight compounds

56
Q

What type of mutations do rational protein treatments target?

A

Oncogenes

57
Q

How can antibodies be used in cancer treatment?

A

Neutralise overexpression of RTK by preventing ligand binding or dimerisation

58
Q

What is an example of antibody treatment of cancer?

A

Herceptin for Neu/Her2 Epidermal Growth factor receptor overexpression

59
Q

What are the advantages of Low Mw compounds to treat cancer?

A

Easier to produce

Penetrate tumour

60
Q

How do low Mw compounds block signalling mutations?

A

Target ligand independant RTKs to block ATP binding in kinase domain

61
Q

What is an example of the use of low Mw compounds to treat cancer?

A

Gleevec blocks Abl kinase domain in BCR-Abl translocations to prevent activation and TF activity

62
Q

What is the main problem with cancer therapy using low Mw compounds?

A

Resistance develops

63
Q

How are low Mw compounds developed?

A

Using structure based design

Health and Disease: Genes (6 decks)

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