topic 17 Flashcards
what is benign cancer? malignant cancer?
benign cancer: doesn’t spread.
malignant: can spread to surrounding tissue.
what are the causes of cancer?
causes of cancer include the DNA damaging agents, genetic predisposition, and viruses.
what are some causes for DNA damage?
UV rays, X-rays, chemical mutagens, and replication errors
how is cigarette smoke a carcinogen?
cigarette smoke contains 69 chemicals known to cause cancer, including arsenic (rat poison), benzene, formaldehyde, and radioactive polonium 210.
what are the properties of a cancer cell? (4)
they have lost cell cycle control. they divide in the absence of growth factors
they are immortal. they don’t respond to signals that normally trigger cell death
they are genetically unstable
they multiple in abnormal places (metastasize)
briefly describe the stages of the cell cycle. also list the checkpoints in the cycle.
in G1, cellular contents excluding chromosomes are duplicated. in S, each of the 46 chromosomes are duplicated. in G2, cell double checks that all chromosomes have been duplicated and will make needed repairs. in mitosis, the cell divides.
during the cell cycle, there are several checkpoints where the cell checks for proper replication. prior to DNA replication. at G1, the DNA is checked for damage. at the G2 checkpoint, the cell checks whether DNA replication has occurred properly. healthy cells will stop cell division if DNA damage is detected. cancer cells do not stop at the checkpoints.
describe how mutations on the chromosomal level are a cause of cancer
cancer cells are genetically unstable. they have more point mutations, more copy number variations, and major chromosomal abnormalities. while only one gene may have a mutation, having a duplicate of this means there’s double the amount of gene expressed which can also be a cause of cancer.
what are the types of cancer causing genes? (2)
oncogenes and tumour suppressor genes
describe oncogenes. what do they and how? how are they created?
oncogene is the mutant form of a normal gene whose presence causes cancer (e.g. myc, ras, fos, jun, abl). oncogenes can cause cancer when they have mutations that cause them to be overactive (“gain of function”).
in a normal cell. there are 2 active copies of the proto-oncogenes (normal gene). a single mutation event creates the oncogene.
what are the different mutations that causes a proto-oncogene to become an oncogene? (3) describe them
mutation in protein encoding regions of the gene: normal gene sequence of proto-oncogene is mutated in the DNA. the mutation is carried on in the RNA and leads to a protein that’s hyperactive. the hyperactive protein is made in normal amounts, but the gain of activity increases overall activity in the cell.
gene amplification: there’s no mutation in the proto-oncogene. protein is exactly the same but in larger amounts. this leads to an increase in the amount of RNA and protein, increasing the functionality throughout the cell
chromosomal rearrangement: the protein encoding sequence isn’t changed and no change in the copy number. instead, there’s one proto-oncogene in a different location. instead of being produced in normal amounts, it may be produced in high amounts when nearby regulatory DNA sequence causes the normal protein to be overproduced or in another case, it re-fuses to actively transcribe genes nearby that produce a hyperactive fusion.
describe tumour suppressor genes. what do they do and how? how are they created?
tumour suppressor genes cause cancer with its absence and are characterized by underactivity mutations (“loss of function”). e.g. p53 and Rb. tumour suppressors are involved in DNA repair or the control of cell growth/differentiation or cell death.
in a normal cell, there are 2 copies of a certain gene. the mutation event inactivates one of those tumour suppressor genes. the 1st mutation usually has no effect but the 2nd mutation event inactivates the 2nd gene.
differentiate between oncogenes and tumour suppressor genes
tumour suppressor genes inhibit cancer. oncogenes stimulate cancer
what are the functions of cancer causing genes? (6) describe them
- growth factors and cellular receptors for growth: oncogenes are often growth factors that are stuck in the “on-position”. e.g. the epidermal growth factor receptor (EGFR) depends on an external growth factor to activate upon binding of the growth factor to initiate cell division. in the absence of a growth factor, the receptor is inactive. when the growth factor has been mutated, it is stuck on the on-position and becomes an oncogene, even in the absence of a growth factor, it will promote cell division.
- molecules involved in cell-cell interactions: oncogenes are found in regulatory pathways of cell-cell interactions. e.g. protein that promotes cell adhesion to the basal lamina may be mutated to now stabilize interactions with other cells, making cell growth independent of the cell’s position near the basal lamina.
- regulators of normal/programmed cell death: e.g. p53 aka “guardian of the genome”. p53 through other proteins, sense DNA damage or oncogene expression. p53 can then promote cell cycle arrest, apoptosis, or DNA repair among other processes. if p53 is mutated, it can’t fulfil its function. cancer cells don’t respond to normal signals that trigger cell death.
- transcription factors: proteins that initiate transcription of several other genes. a mutation in 1 transcription factor can affect the expression of many other proteins. cancer can be caused by too much or too little expression of the genes that regulate cell growth, differentiation, or cell death. mutation in transcription factors can have large effects on the cell’s protein.
- DNA repair proteins: if they’re mutated, cells will quickly accumulate a large number of mutations, eventually affecting key genes. e.g. xeroderma pigmentosum: melanomas develop from exposure of the skin to the sun’s UV rays, which cause pyrimidine dimers.
- molecules that directly control cell division and serve as normal “check point controls”.
why is the protein expression of cancer cells considered atypical?
they are expressed either at an unusual time or in unusual amounts.
what are the types of classic cancer treatment? (3) describe them
surgery: excises the tumour. capable of taking large amounts of cells out at a time. disadvantage is that cancer cells may be left behind.
radiation: so damaging to the cell’s DNA that the cells stop replicating. also damages adjacent cells and can cause secondary cancer.
chemotherapy: targets fast dividing cells (cancer cells). stops cells from replicating by damaging DNA or interfering with the mitotic machinery or reducing replication substrates.
