Topic 3: Genes and environment (Cancer) Flashcards
Define phenotype (2 points)
- the outward appearance of a characteristic or organism,
2. as a result of the genotype and sometimes the environment.
Define Tumour (2 points)
- a mass of unspecialised, abnormally growing cells,
2. which divide more quickly than normal cells.
Define metastasis (1 point)
- the spread of cancer cells to new areas of the body (often by way of the lymph system or bloodstream)
Define Malignant Tumour (1 point)
- a tumour that invades surrounding tissue and metastasises
Define benign tumour (1 point)
- a tumour that stays intact (does not spread/invade other tissues)
What are the 2 types of genes that produce proteins
that control the cell cycle?
- Proto-oncogenes
2. Tumour suppressor genes
Name 3 proteins that are important in the cell cycle and what they do
(1) Cyclins and (2) cyclin-dependent kinases (second) drive the cycle forward
3. Tumour suppressor proteins halt the cycle at checkpoints
What does the P53 protein do? (1 point)
- halts the cell cycle at the G1/S checkpoint
if p53 gene is expressed and protein is made it prevents DNA replication in ___ phase
S
some cancer cells have a mutated p53 gene, therefore p53 is not produced
these cancer cells therefore have _________ cell division (mitosis)
uncontrolled
Key Summary: Explain the effects of mutations in proto-oncogenes
(3 steps)
- When a proto-oncogene is mutated it becomes an oncogene
- Oncogenes lead to cell cycle being continually active –controls/stops/brakes on the cycle are not working
- Activated oncogenes can cause those cells designated for apoptosis to survive and proliferate instead.
Key Summary: Explain how mutations in tumour suppressor genes/p53 gene affect the cell cycle
(2 steps)
- Tumour suppressor genes produce proteins (eg.p53) that halt the cell cycle at certain stages
- Mutations in these genes may inactivate them, meaning controls/stops/brakes on the cycle are not working
Key Summary: How does cancer/a tumour arise?
5 steps
- environmental mutagen eg. UV light, radiation, carcinogen (read Q);
- mutagen leads to mutations in DNA of tumour suppressor genes/proto-oncogenes (resulting in oncogenes);
- cell cycle is disrupted/continually active leading to uncontrolled cell division –stops on cell cycle do not work, shorter interphase, faster cell cycle - so no Hayflick limit, cells do not become specialised, so growth cannot be controlled;
- Lack of apoptosis - rate of cell multiplication by mitosis is greater than the rate of cell death by apoptosis;
- an abnormal mass of unspecialised cells called a tumour forms, which may invade/invades surrounding tissue;
In which tissues is cancer more likely to develop? (1 point)
Why? (2 steps)
- in tissues with high rates of mitosis eg. lung, colon, bowel and bone marrow
- Greater number of cell divisions means more opportunities for errors in DNA replication which may lead to mutation in proto-oncogenes or tumour suppressor genes
- More mutations lead to greater risk of developing cancer
Key Summary: How do cancer cells spread to other tissues?
3 steps
- Some cancer cells break off a tumour
- Travel to other parts of the body in blood/lymph
- Causing secondary/metastatic tumours
Properties of normal body cells (4 properties)
Normal body cells can:
- reproduce when and where it’s needed
- stick together to form tissues in the right place in the body
- self destruct when they become damaged or too old
- become specialised (mature)