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Block 3 : Cancer and Genetics > Cancer > Flashcards

Cancer Flashcards

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Biology 101 flashcards
1
Q

what is cancer and what is it caused by ?

A
  • complex group of more than 100 diseases affecting a wide range of tissues
  • caused by mutations in genes controlling cell growth after exposure to carcinogens
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2
Q

how is cancer characterised and how does it differ?

A
  • characterised by loss of growth control leading to an unregulated increase in cell number, metastasis and invasion of other tissues
  • cancers differ in tissue or origin, casual factors and molecular mechanisms
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3
Q

How do cancer tumours start?

A
  • when cells that have lost control of growth control proliferate to form a new growth (neoplasia), these cells don’t die via apoptosis which normally keeps number of cells constant
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4
Q

what are the two types of cancer?

A
  • benign

- malignant

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5
Q

Describe Benign tumours?

A
  • well differentiated and look like normal cells
  • may perform the normal function of tissue (eg secrete hormones)
  • cells grow slowly but this is not suppressed by apoptosis or contact inhibition
  • size may be limited to just a few mm due to a lack of blood supply
  • surrounded by a fibrous capsule and confined to original location
  • they don’t infiltrate, invade or metastasise
  • can damage nearby organs by compressing them
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6
Q

Describe Malignant tumours?

A
  • less differentiated and don’t look like normal cells
  • don’t perform normal tissue function
  • cells grow rapidly since they have lost ability to control proliferation and differentiation
  • no fibrous capsule
  • cells infiltrate and invade surrounding tissues and metastasise
  • can compress and/or destroy surrounding tissues
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7
Q

how are tumours classified?

A
  • classified according to tissue of origin
    Benign Tumours:
  • tissue name + “Oma”
    Malignant Tumours:
  • carcinomas = derived from epithelial cells
  • adenocarcinomas = derived from glandular epithelial cells
  • sarcoma= derived from mesenchymal cells
  • leukaemia = derived from haemopioetic cells
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8
Q

How does the body control cell number?

A

Most cells in the adult tissues are terminally differentiated and quiescent (non-dividing). within each tissue cell death by apoptosis or necrosis is balanced by cell division often of stem cells leaving the total number of cells constant .
Cell division is tightly regulated by growth factors which allow quiescent cells to enter the cell cycle and divide.

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9
Q

what are the six hallmarks of cancer?

A
  • self sufficiency in growth signals
  • in sensitivity to anti- growth signals
  • evading apoptosis
  • sustained angiogenesis
  • tissue invasion and metastasis
  • limitless replication potential
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10
Q

how does telomerase help to control cell lifespan?

A
  • telomerase is an enzyme which can elongate telomeres.
  • telomerase is essential for allowing cells to keep proliferating
  • as cells age, telomerase becomes inactive and hence telomeres shorten and cells lose ability to divide limiting lifespan
  • increase telomerase activity allows cells to proliferate indefinitely and leads to cancer
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11
Q

Cell proliferation is regulated by transit through the cell cycle, outline the four stages

A
  • G1 - gap between m and s phase
  • s phase- DNA synthesis/ replication
  • G2 - gap between S and M phase
  • M phase - mitosis, cytokinesis/ Division
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12
Q

cell cycle checkpoints control cell growth what controls these check points?

A
  • cyclin dependent kinases(CDK’s) and CDK inhibitors
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13
Q

what do CDK’s and CDK inhibitors ensure when controlling progression through the cell cycle?

A
  • correct sequence of phases (g1, s, g2,m)
  • cellular and environmental conditions are favourable
  • DNA is properly replicated and undamaged
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14
Q

what is being checked at the G1/S checkpoint and what is required for cells to progress

A
  • are growth factors present?
  • are nutrients available?
  • Is Dna changed?
  • Is cell big enough?

they need growth factors and intact DNA to progress

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15
Q

what is checked at the G2/M transition checkpoint?

A
  • Has DNA replicated

- Is DNA damaged

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16
Q

cancer is caused by gene mutations controlling cell number what are the two different types?

A
  • mutations that enhance cell proliferation and suppress cell death (apoptosis)
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17
Q

What does does mutation ind DNA repair genes cause and why is this an issue

A
  • it causes genome instability and makes further mutations more likely
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18
Q

What does “multi-hit hypothesis” mean

A
  • a single mutation is not enough , each cancer arises from an accumulation of several mutations over time (2-20 depending on cancer type)
19
Q

sequencing genes mutated in cancers can give a molecular finger print for each cancer (a list of genes that are mutated) how does this help us?

A
  • diagnosis and targeted treatments

- understanding mechanisms and new development therapies

20
Q

What are the two main types of mutated genes found in cancer?

A
  • pronto-oncogenes/oncogenes

- tumor supressor genes

21
Q

what are pronto-oncogenes?

A
  • are mutated forms of normal genes which positively regulate cell division
  • they encode components of growth factor signalling pathways allowing the progression of G1 to s Phase when growth factors are not present
22
Q

what are tumour supressor genes?

A
  • they negatively regulate cell division, preventing abnormal proliferation, suppressing tumorgenesis
  • they usually encode proteins at the cell cycle check points that block progression through if there is a problem
23
Q

what is the Ras-MAPK pathway and what happens when cancer causes a mutation in the ras protein?

A

the ras-mapk pathway activates cdk 4/6 and allows progression through the g1/s checkpoint and cell division. When cells have an activated ras protein the pathway is always active and cell division is then independent of growth factors

24
Q

P53 is known as the guardian of the genome what does it do?

A

it is a transcription factor activated by DNA damage and will cause cell cycle arrest inhibiting the transition from g1 to s phase.
50% of cancers have an inactivating mutation in P53 which consequently allows cells to divide even when dna is damaged
- P53 is a tumor supressor gene

25
Q

what are the three stages of cancer development

A
  • initiation
  • promotion
  • progression
26
Q

What takes place in the first stage of cancer development and what is it?

A

Initiation

  • exposure to chemical or physical carcinogen (activation or inactivation by metabolism or excretion)
  • damage to dna (may or may not be repaired; pronto-oncogene activation or tumor supressor gene inactivation)
27
Q

what happens in the second stage of cancer development and what is it?

A

Promotion

  • altered cells stimulated to divide by a tumour promoter
  • altered cells may remain dormant or be removed by immune system
28
Q

What happens in the third stage of cancer development and what is it?

A

Progression

  • may develop more mutations
  • uncontrolled cell replication and loss of specialisation
  • cell are more aggressive and invasive
29
Q

outline metastasis and invasion including intravastation, extravastation and angiogenesis

A

cells in a primary tumour develop the ability to wscape into the circulation (intravastation) through loss of adhesion or secretion of proteases to degrade basement membrane. they survive and travel in the blood or lymphatic system and then exit into surrounding tissues (extravastation) via proteases. Here they develop into secondary tumours or metastasis. Growth or new blood vessels (angiogenesis) enables rapid growth. Metastasis to multiple distant site and rapid growth is life threatening.

30
Q

what are four host risk factors of cancer development?

A
  • hereditary predisposition
  • Reproductive hormones (can act as tumour promoters)
  • obesity
  • immune surveillance of tumour antigens (some cancers express proteins to evade immune surveillance)
31
Q

What are 3 enviromental risk factors for the development of cancer?

A
  • chemical carcinogens
  • viruses and bacteria
  • radiation
32
Q

what are the local effects of the clinical manifestation of cancer (3)

A
  • physical effects due to the blockage or compression of structures close by
  • blood vessels - blockage or bleeding
  • effusions (build up of fluid) eg pleural effusion and ascites
33
Q

what are the systemic effects of the clinical manifestation of cancer (5)

A
  • various types of malnutrition (malabsorption, anaemia, anorexia and cachexia)
  • fluid and electrolyte imbalances
  • fatigue and sleep disturbaces
  • paraneoplastic syndromes
  • pain
34
Q

with cancer patients what is protein and energy malnutrition often due to?

A
  • increased energy demand of rapidly growing cancer cells

- decreased energy intake and malnutrition due to loss of appetite, altered taste and reduced absorption

35
Q

what are the seven cancer warning signs using the acronym CAUTION

A 
C= change in bowel/bladder habits
A= a sore that doesnt heal
U= unusual bleeding or discharge from any body orifice 
T= thickening or a lump in breast or elsewhere
I= indigestion/difficulty swallowing 
O= obvious change in wart or mole 
N= nagging cough or hoarseness
36
Q

what are the five ways of screening and diagnosing cancer and what are examples of each?

A
  • indirect, nonspecific testing ( liver function , blood in stools)
  • cytology ( pap smear, tissue biopsy)
  • diagnostic imaging ( x-ray, ct scan)
  • tumour markers( eg prostate -specific antigen )
  • Microrray technology ( gene chips to measure mRNAs checking the expression of specific cancer)
37
Q

what is tumour grading and how does take place?

A
  • measure of how different the tumour cells are from normal cells
  • microscopic/histologic examination of cells appearance and state of differentiation and number of mitotic cells
38
Q

there are four grades four tumour grading; outline these

A

grade 1 = cells are slightly different and well differentiated
grade 2 = cells are abnormal and moderately differentiated
grade 3 = cells very abnormal and poorly differentiated
grade 4 = cells are immature and undifferentiated

39
Q

what takes place during tumour staging?

A

clinical radiographic, surgical examination of the extent and spread of tumour to help with treatment and prognosis
specific for each type of tumour

40
Q

outline the TMN staging

A 
T1-4 = tumour size
N0-3= lymph node involvement 
M0-3= metastasis
41
Q

According to the American Joint committee on cancer what is the overall stage grouping (stage 0 - 4)

A 
stage 0 = cancer insitu 
1= tumour limited to tissue of origin
2= local spread (limited)
3= (extensive) local and regional spread
4= metastasis to distant sites
42
Q

what are 6 possible prevention methods that may reduce risk of developing cancer

A
  • avoidance of environmental exposure
  • diet, smoking, alcohol, obesity
  • use of protective product egs sunscreen and wearing a hat
  • vaccination (HPV)
  • routine screening
  • education through health promotion programmes
43
Q

what are six treatment methods for cancer and how do they help

A
  • surgery (excellent if no metastasis)
  • radiation therapy ( repeated low doses from a beam, implantation of radioactive source or systemic administration of radioisotopes. cells die through the apoptotic pathway)
  • chemotherapy (targets rapidly dividing cells often used in conjunction with radiation)
  • hormone and antihormone therapy (cancer responsive/dependent on hormones)
  • immunotherapy (stimulate immune system to kill cancers)
  • targeted therapies (mainly monoclonal antibodies that target specific proteins/processes)

Block 3 : Cancer and Genetics (1 decks)

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