CELLS AND MOLECULAR BIOLOGY OF CANCER Flashcards
what’s the prevalence of cancer in the UK?
1/2 people will be diagnosed with cancer during their lifetime
what is a tumour?
an abnormal growth of tissue that usually but not always forms a mass
simply, when does a tumour arise?
when the balance between cell division and cell differentiation/death is disrupted
which cells can’t become cancerous?
cells that can’t proliferate e.g. erythrocytes
what are the Hallmarks of cancer?
- evading growth suppressors
- avoiding immune destruction
- enabling replicative immortality
- tumour-promoting inflammation
- activating invasion and metastasis
- inducing angiogenesis
- genome instability and mutation
- resisting cell death
- deregulating cellular energetics
- sustaining proliferative signalling
what happens in G1 phase of the cell cycle?
There’s an increase in cell contents and DNA replication machinery
what happens in S phase of the cell cycle?
replication of DNA occurs, chromosomes becomes 2 sister chromatids
what happens in G2 phase of the cell cycle?
The cell prepares for division
which stages of the cell cycle make up interphase?
G1, S and G2
what happens in mitosis?
segregation of chromosomes and a division to produce 2 daughter cells
when are the checkpoints in the cell cycle?
at the end of G1, at the end of G2 and in mitosis (between metaphase and anaphase)
what is the cell cycle length?
it depends on the tissue type
which cell types never divide?
skin cells, erythrocytes, gut cell lining
what regulates the cell cycle?
an enzyme complex of a CDK and a cyclin
what is the cause of all cancers?
the mutation of genes involved in cell proliferation and survival
what are the 2 main classes of cancer critical genes?
oncogenes and tumour suppressor genes
what is the ‘two hit theory’?
he hypothesis that most tumor suppressor genes require both alleles to be inactivated to cause a phenotypic change.
What are oncogenes?
genes whose presence can trigger the development of cancer
how do oncogenes arise?
a result of mutations that increases the expression level or activity of a proto-oncogene (a gene which normally helps cells to grow)
what are tumour suppressor genes?
genes which normally provide negative control of cell division and activate apoptosis so when lost or inactivated can trigger the development of cancer
how do tumour suppressor genes lead to the development of cancer?
mutations of both alleles
what are the 3 classes of tumour suppressor genes?
gatekeeper genes
caretaker genes
landscaper genes
what are gatekeeper genes?
A class of genes which directly regulate tumour growth by inhibiting growth or by promoting cell death. its loss directly opens the gates to excessive cell proliferation
what are caretaker genes?
genes that control the maintenance of the genetic information integrity in each cell, not directly involved in cell proliferation
what are some examples of gatekeeper genes?
p53 and Rb
what are examples of caretaker genes?
BRCA1 and BRCA 2
what is retinoblastoma?
cancer of the retina
what is Rb?
a tumour suppressor gene first discovered in a case of retinoblastoma
outline how, under normal circumstances when a cell detects DNA damage, P53 works?
as cell detects DNA damage, P53 levels increase and acts as a transcription factor for P21 gene which inhibits CDK and cyclin… and the cell cycle is arrested. This gives the cell the opportunity to repair or, if not able, to undergo apoptosis
if this cant happen then we get mutations and cell proliferation
what are the links between obesity and cancer?
too much body fat can cause levels of growth hormones to rise = more cell division
more fat cells= more inflammation = cells divide faster
fat cells produce oestrogen after menopause so cells in the breast and womb divide more often
what type of cancers can obesity cause?
breast bowel pancreatic oesophageal gallbladder womb ovarian kidney liver upper stomach myeloma meningioma thyroid
how can HPV cause cervical cancer?
the viral genome encodes 2 oncogenic proteins, E6 and E7 (E6= P53 destruction, E7= Rb destruction)
