CtDNA originates from dying tumour cells and can be present in a wide range of cancers but at varying levels and mutant allele fractions.
42.
This cycle of infection, replication and cell death is believed to be repeated until all tumour cells carrying an activated Ras pathway are destroyed.
43.
This result implicates that androgens in the physiological context may upregulate survivin, which contributes to the resistance of apoptosis observed in the tumour cells.
44.
Based on the reasoning that if tumour cells could be made to produce the herpes enzyme, ganciclovir could prevent them from copying their DNA.
45.
By uncovering this knowledge, the clinical evaluation of each individual patient can be improved and specific drugs which target the tumour cells can be identified.
46.
The tumour microenvironment may also contribute to tumour expansion, as it is capable of altering the selective pressures that the tumour cells are exposed to.
47.
Mutated forms of the p53 genes have been detected in tumour cells of patients with cancers of the colon, breasts, brain, lung, skin and bone.
48.
Survivin is known to be highly expressed in most tumour cell types and absent in normal cells, making it a good target for cancer therapy.
49.
Local cancer in many parts of the body can cause lymph nodes to enlarge, usually because of tumours cells that have metastasised into the node.
50.
The SFV virus was genetically modified with microRNA target sequences so that it only replicated in brain tumour cells and not in normal brain cells.
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