Gene expression and cancer

?
  • Created by: Hindleyc
  • Created on: 13-04-19 12:33
What is cancer
group of diseases caused by damage to the genes that regulate mitosis and the cell cycle
1 of 57
What does this lead to
unrestrained growth of cells
2 of 57
As a consequence what develops
tumour, a group of abnormal cells and constantly expand in size
3 of 57
What is it
common and destructive disease and to some extent avoidable and if diagnosed early enough successfully treatable
4 of 57
What aren't all tumour
cancerous
5 of 57
those that are cancerous are called
malignant
6 of 57
those that are not cancerous are called
benign
7 of 57
Features of B tumours
Can grow to a large size, grow v slow, cell nucleus relatively normal appearance, cells often well differentiated(specialised), cells produce adhesion molecules that make them stick together and so remain with the tissue from which they arise
8 of 57
what are these called
primary tumours
9 of 57
What are tumours surrounded by
capsule of dense tissue&so remain as compact structure, much less likely2be life-threatening but can disrupt functioning of vital organtend 2have localised effects on body&can usually removed by surgery alone and rarely reoccur after treatment
10 of 57
What are the features of malignant tumours
Can also grow to a large size, rapidly, cell nucleus larger and appears darker due to an abundance of DNA,cells can become de-differentiated (unspecialised)
11 of 57
what don't cells produce
adhesion molecules so they tend to spread to other regions of the body, a process called metastasis forming secondary tumours
12 of 57
what aren't tumours surrounded by
capsule and can grow finger like projections into the surrounding tissue, more likely to be life-threatening as abnormal tumour tissue replaces normal tissue and often have systemic whole body effects such as weight loss and fatigue
13 of 57
What does removal usually invovle
radiotherapy and or chemotherapy as well as surgery and can more frequently reoccur after treatment
14 of 57
How does a secondary tumour develop from a primary tumour
enlarging tumour develops blood and lymphatic vessels, tumour cells squeeze into blood and lymphatic vessels then circulating tumour cells can adhere to blood vessel walls and squeeze through to form distant metastases or metastasis in lymph node
15 of 57
What has DNA analysis of tumours shown
that in general cancer cells are derived from a single mutant cell
16 of 57
what does the initial mutation cause
uncontrolled mitosis in this cell
17 of 57
later what does a further mutation in one of the descendant cells lead to
other changes that cause subsequent cells to be different from normal in growth and appearance
18 of 57
What are the 2 main types of genes that play a role is cancer are
tumour surpressor genes and oncogenes- role of 2 genes, could be used in prevention, treatment and cure of cancer
19 of 57
What are most oncogenes
mutations of proton-oncogenes
20 of 57
What do promo-oncogenes do
stimulate a cell to divide when growth factors attach to a protein receptor on its cell surface membrane
21 of 57
What does it then activate
genes that cause DNA to replicate and the cell to divide
22 of 57
What if a proto oncogene mutates into an oncogene
it can become permanently activated (switched on) for 2 reasons
23 of 57
what are the first reason
the receptor protein on the cell surface membrane can be permanently activated so that cell division is switched on even in the absence of growth factors
24 of 57
2nd reason
the oncogene may code for a growth factor, that is, then produced in excessive amounts again stimulating excessive cell division
25 of 57
result
the cell divide too rapidly and out of control and a tumour of cancer develops
26 of 57
What are a few cancers inherited by
inherited mutations of proton-oncogenes that cause the oncogene to be activated but most cancer causing mutations involving oncogenes are acquired not inherited
27 of 57
What is an important difference between oncogenes and tumour suppressor genes
while oncogenes causes cancer as a result of the activation of proton-oncogenes tumour suppressor genes cause cancer wen they are inactivated
28 of 57
What do tumour suppressor genes do
slow down cell division, repair mistakes in DNA and tell cells when to die
29 of 57
what is that process called
apoptosis - programmed cell death
30 of 57
What do they therefore have opposite role from
proto-oncogenes
31 of 57
What does a normal TS gene maintain
normal rates of cell division and so prevents the formation of tumours
32 of 57
If a TSG becomes muted what happens
it is inactivated- switched off
33 of 57
as a result what happens
it stops inhibiting cell division and cells can grow out of control
34 of 57
What are the mutated cells that are formed
usually structurally and functionally different from normal cells
35 of 57
While most of these die what can those that survive make
clones of themselves and form tumours
36 of 57
What are there a number of
forms of tumour suppressor genes including TP53 ETC
37 of 57
What are some cancers caused by
inherited mutations of tumour suppressor genes but most are acquired not inherited eg more than half of human cancers display abnormalities of the TP53 gene which codes for the p53 protein
38 of 57
what do acquired mutations of the TP53 gene occur in
many cancers including lung and breast cancers- p53 protein is involved in process apoptosis (programmed cell death)
39 of 57
When is this process activated
when. cell is unable to repair DNA
40 of 57
But if gene for p53 not functioning correctly
cells with damaged DNA continues to divide leading to cancer
41 of 57
What is abnormal methylation of DNA
common In the development of a variety of tumours
42 of 57
What is the most common abnormality
hypermethyation (increased methylation)
43 of 57
How does it leads to cancer
hypermethylation occurs in a specific region (promotor region) of TSG leading to it being inactivated and as a result transcription of the promotor region of the TSG is inhibited so it is silenced (switched off)
44 of 57
result
as it normally slows rate of cell its inactivation leads to increased cell division and the formation of a tumour
45 of 57
What is abnormal methylation of this type thought to occur
in TSG known as BRCA1 and leads to development of breast cancer
46 of 57
What is another form of abnormal methylation
hypomethylation (reduced methylation) that has been found to occur in oncogenes where it leads to their activation and hence the formation of tumours
47 of 57
What does oestrogen play a central role in
regulating mensural cycle in women
48 of 57
What is it known that
after menopause womans risk of developing breast cancer increases and is thought to be due to increase in oestrogen conc
49 of 57
Why did it first seem paradoxical
because production of O from ovaries diminishes after the menopause
50 of 57
however what happens
fat cells of the breasts tend to produce more O after the menopause and these locally produced O appear to tigger Breast cancer in post menopausal women
51 of 57
Once tumour develops what happens
further increases O conc which therefore leads to increased development of the tumour
52 of 57
What also appears
that wbc's that are drawn to the tumour increase O production
53 of 57
What does this lead to
even greater development of the tumour
54 of 57
How does O cause T to develop
O activates a gene by binding to a receptor which promotes Transcription and if the gene that O acts on is one that controls cell division and growth then it will be acitvated and its continued division could produce a tumour
55 of 57
what is known that O causes
proto-o-genes of cells in breast tissue to develop into oncogenes therefore leads to development of a tumour (breast cancer)
56 of 57
so overall how are tumours developed
TSG and oncogenes, abnormal methylation of TSG and oncogenes and INC O conc in development of some breast cancers
57 of 57

Other cards in this set

Card 2

Front

What does this lead to

Back

unrestrained growth of cells

Card 3

Front

As a consequence what develops

Back

Preview of the front of card 3

Card 4

Front

What is it

Back

Preview of the front of card 4

Card 5

Front

What aren't all tumour

Back

Preview of the front of card 5
View more cards

Comments

No comments have yet been made

Similar Biology resources:

See all Biology resources »See all Biological molecules, organic chemistry and biochemistry resources »