Flashcards in 7.0 Cancer Deck (35)
What can the genetic changes in cancer be due to?
- Anything that alters DNA sequence
- Methylation / histone modifications
- Tumour viruses bring extra genes into cell
What normally precedes a colorectal malignant tumour?
Common sites for metastasis:
3) Bone marrow
Where does breast cancer normally metastasise?
Local lymph nodes and bone
Where does colorectal cancer normally metastasise?
Benign fat cell tumour
Benign smooth muscle tumour
Benign tumour of glandular tissue
Malignant epithelial tumour
Malignant epithelial tumour of glandular origin
Malignant fat cell tumour
Malignant smooth muscle tumour
Malignant bone tumour
What are neuroblastomas / glioblastomas?
Both are malignant neural tumours
Difference between leukaemias and lymphomas:
Leukaemias = Liquid haematopoietic neoplasms
Lymphomas = Solid haematopoietic neoplasms (usually lymphocytic)
Define the following terms with examples:
General systemic wasting
Exact mechanism unknown - ?competition for metabolic resources?
Oncogenes vs tumour suppressor genes:
- Overactivity mutations
- Dominant in the cell
- Only one copy needs to be mutated
Tumour suppressor genes
- Loss of function mutations
- Recessive in the cell
- Both copies need to be mutated
What is the structure of p53?
This creates a unique form of mutation. It is a tumour supressor gene but only needs one copy of the gene to be mutated to have an effect. Losing both copies has a stronger effect
What are the two types of genetic instability in colon cancer?
1) Chromosomal instability (CIN)
- Rearranged chromosomes
- Due to loss of protective mechanisms against chromosome aberrations
2) Sequence instability
- Normal chromosomes
- microsatellite instability
- Mainly due to DNA mismatch repair inactivation
What are MLH1 + MSH2 needed for?
Defects seen in colon cancer
What is BRCA2 needed for?
Single + double strand repair
Defects seen in breast cancer
What are the hallmarks of cancer?
Proliferation and survival changes
1) Independence of growth signals
2) Resistance to growth inhibitory signals
3) Resistance to apoptosis
5) Differentiation block
6) Metabolic changes
What molecules are pro-apoptotic?
What molecules are anti-apoptotic?
What are the repeats in telomeres?
What can HPV do to Rb-1 and p53?
Bind to and inactivate
What is the major barrier to metastasizing cells?
Survival and growth in distant site (many cells can circulate body and exit circulation at different sites - most die because cannot survive and grow at this site)