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CLS > Cancer > Flashcards

Cancer Flashcards

1
Q

What enzymes are needed in DNA repair and in what order

A

Helicase unwinding the helix
Endonucleases cut the strand
Gap is filled by DNA polymerase
Sealed by ligase

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2
Q

what does lack of ability to remove TT diners mean for repair

A

During replication DNA polymerase does not know how to proceed so leaves gaps in new DNA. Induces SOS

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3
Q

What is the problem with SOS

A

It makes many mistakes itself and may leave errors in TSG or Oncogenes= cancer initiation

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4
Q

What is xeroderma pigmentosuim

A 
Autosomal recessive disease
Unusual response to sunlight 
Pigmentation abnormalities
Skin cancer 
-lack endonuclease activity needed for DNA repair
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5
Q

What are PAHs

A

Polycyclic aromatic hydrocarbons. Eg benzo(a)pyrene benzanthracene formed by incomplete combustion of organic matter, burnt food, coal tar, cigarette smoke.

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6
Q

What is AHH

A

Aryl hydrocarbon hydroxylase. Enzyme that is activated by benzos, acts to remove them from our body by making more water soluble (add O2) but makes ultimate carcinogenic (benzapyrenediol epoxide) in the process
A) detoxified and excreted
B) attacked by electron rich atoms eg guanine in DNA causing mutations

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7
Q

How does bp diol epoxide cause mutations

A

A)causes incorrect bases pairing when DNA replicates, may cause a point mutation in an oncogene/TSG
B) can cause SOS repair, which has a high error rate- mutations in oncogene/TSG

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8
Q

What is the significance of AHH inducers

A

Genetically determined, high inducers are at higher risk of cancer

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9
Q

What gene mutation predisposes to breast cancer

A

BRCA1/2

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10
Q

What gene mutations predispose to colorectal cancer

A

APC

HNPCC

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11
Q

What is variable expression

A

Mutation in a single cancer gene can predispose to different rumours of the same individual

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12
Q

What is age related penetrance

A

Time needed for other outside hits to accumulate to cause a tumour

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13
Q

In what can inherited cancer predisposing genes occur

A

Protoncogenes
Tumour supressor genes
Mutator genes

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14
Q

Give two examples of mutations in protoncogenes

A 
RET- multiple endocrine neoplasia type 2 
Medullary thyroid cancer
Parathyroid tumours
Phaeochromocytoma 
MET-hereditary papillary renal carcinoma
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15
Q

Give four examples of mutations in tumour supressor genes

A

TP53 - li fraumeni syndrome
BRCA1/2
APC-familial adenomatous polposis coli
PTEN-breast cancer, particular skin tumours and thyroid cancer, together make Cowden syndrome

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16
Q

What is the difference between BRCA 1 and 2

A

1- cumulative risk of breast and ovarian cancer
Contra lateral tumour risk
Prostate cancer
2- cumulative risk of breast and ovarian cancer, also prostrate, pancreatic and male breast cancer

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17
Q

What is APC linked to p

A

Familial adenomatous polyposis coli -FAP
Greater than 100 colorectal adenomatous polyps or fewer than 100 polyps + fdr with FAP
7% of untreated develop CRC by 21
Extra colorectal cancers- thyroid, duodenum, pancreas, liver

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18
Q

What mutations are in mutator genes?

A

hMLH1 and hMLH2, problems with mismatch DNA repair
Causes colorectal, endometrial, ovarian, ureteric, or renal pelvis
And brain cancer

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19
Q

What is HNPCC

A

Hereditary non-polyposis colorectal cancer.
Ovarian
Endometrial
And bowel cancer

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20
Q

Name 6 key features when looking at familial cancer predisposition

A 
Early onset rumours
Multiple tumours in close relatives
Multiple tumours in an individual 
Clusters of different tumours in a pattern
Breast cancer in males
First degree relatives with cancer
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21
Q

Name and uncommon cancer predisposition syndrome

A 
Von Hippel-Lindau syndrome
Cluster of:
Harmangioblastomas
Renal cell carcinoma/multiple renal cysts/ phaeochromocytoma
Multiple pancreatic cysts/tumours
22
Q

What options are there for reducing risk in familial predisposition

A

Surveillance
Prophylactic surgery/chemo prevention
Diagnostic and predictive molecular genetic testing

23
Q

What mediators of growth control are there (5)

A 
Secreted growth factors
Environmental growth inhibitors
Secreted growth inhibitors
Intrinsic programme of differentiation/apoptosis 
Tumour immune response
24
Q

For a tumour to become malignant what three things does it need

A

Limitless replication
Angiogenesis
Invasion and metastasis

25
Q

Name 6 factors that lead to tumourigenesis

A 
Evading apoptosis
Tissue invasion and metastasis
Insensitivity to anti-growth signals
Sustained angiogenesis
Limitless replicating potential
Self sufficiency in growth signals
26
Q

How can mutations occur (4)

A 
Sequence change 
Gene amplification 
Gene deletion
Gene silencing (epigenetic)
27
Q

How can a tumour gain self-sufficiency of growth signals

A

Mutations that cause:
Increased secretion of GF’s
Up regulation of GF receptors
Activation of GF Receptors

28
Q

How might a mutation allow evasion of apoptosis

A

Up regulation of anti-apoptotic factors
Down regulation of pro-apoptotic factors
Loss of function of pro-apoptotic factors

29
Q

What are PAHs

A

Polycyclic aromatic hydrocarbons. Eg benzo(a)pyrene benzanthracene formed by incomplete combustion of organic matter, burnt food, coal tar, cigarette smoke.

30
Q

What is AHH

A

Aryl hydrocarbon hydroxylase. Enzyme that is activated by benzos, acts to remove them from our body by making more water soluble (add O2) but makes ultimate carcinogenic (benzapyrenediol epoxide) in the process
A) detoxified and excreted
B) attacked by electron rich atoms eg guanine in DNA causing mutations

31
Q

How does bp diol epoxide cause mutations

A

A)causes incorrect bases pairing when DNA replicates, may cause a point mutation in an oncogene/TSG
B) can cause SOS repair, which has a high error rate- mutations in oncogene/TSG

32
Q

What is the significance of AHH inducers

A

Genetically determined, high inducers are at higher risk of cancer

33
Q

What gene mutation predisposes to breast cancer

A

BRCA1/2

34
Q

What gene mutations predispose to colorectal cancer

A

APC

HNPCC

35
Q

What is variable expression

A

Mutation in a single cancer gene can predispose to different rumours of the same individual

36
Q

What is age related penetrance

A

Time needed for other outside hits to accumulate to cause a tumour

37
Q

In what can inherited cancer predisposing genes occur

A

Protoncogenes
Tumour supressor genes
Mutator genes

38
Q

Give two examples of mutations in protoncogenes

A 
RET- multiple endocrine neoplasia type 2 
Medullary thyroid cancer
Parathyroid tumours
Phaeochromocytoma 
MET-hereditary papillary renal carcinoma
39
Q

Give four examples of mutations in tumour supressor genes

A

TP53 - li fraumeni syndrome
BRCA1/2
APC-familial adenomatous polposis coli
PTEN-breast cancer, particular skin tumours and thyroid cancer, together make Cowden syndrome

40
Q

What is the difference between BRCA 1 and 2

A

1- cumulative risk of breast and ovarian cancer
Contra lateral tumour risk
Prostate cancer
2- cumulative risk of breast and ovarian cancer, also prostrate, pancreatic and male breast cancer

41
Q

What is APC linked to p

A

Familial adenomatous polyposis coli -FAP
Greater than 100 colorectal adenomatous polyps or fewer than 100 polyps + fdr with FAP
7% of untreated develop CRC by 21
Extra colorectal cancers- thyroid, duodenum, pancreas, liver

42
Q

What mutations are in mutator genes?

A

hMLH1 and hMLH2, problems with mismatch DNA repair
Causes colorectal, endometrial, ovarian, ureteric, or renal pelvis
And brain cancer

43
Q

What is HNPCC

A

Hereditary non-polyposis colorectal cancer.
Ovarian
Endometrial
And bowel cancer

44
Q

Name 6 key features when looking at familial cancer predisposition

A 
Early onset rumours
Multiple tumours in close relatives
Multiple tumours in an individual 
Clusters of different tumours in a pattern
Breast cancer in males
First degree relatives with cancer
45
Q

Name and uncommon cancer predisposition syndrome

A 
Von Hippel-Lindau syndrome
Cluster of:
Harmangioblastomas
Renal cell carcinoma/multiple renal cysts/ phaeochromocytoma
Multiple pancreatic cysts/tumours
46
Q

What options are there for reducing risk in familial predisposition

A

Surveillance
Prophylactic surgery/chemo prevention
Diagnostic and predictive molecular genetic testing

47
Q

What mediators of growth control are there (5)

A 
Secreted growth factors
Environmental growth inhibitors
Secreted growth inhibitors
Intrinsic programme of differentiation/apoptosis 
Tumour immune response
48
Q

For a tumour to become malignant what three things does it need

A

Limitless replication
Angiogenesis
Invasion and metastasis

49
Q

Name 6 factors that lead to tumourigenesis

A 
Evading apoptosis
Tissue invasion and metastasis
Insensitivity to anti-growth signals
Sustained angiogenesis
Limitless replicating potential
Self sufficiency in growth signals
50
Q

How can mutations occur

A 
Sequence change 
Gene amplification 
Gene deletion
Gene silencing (epigenetic)
51
Q

How can a tumour gain self-sufficiency of growth signals

A

Mutations that cause:
Increased secretion of GF’s
Up regulation of GF receptors
Activation of GF Receptors

52
Q

How might a mutation allow evasion of apoptosis

A

Up regulation of anti-apoptotic factors
Down regulation of pro-apoptotic factors
Loss of function of pro-apoptotic factors

CLS (12 decks)

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