Hi, I need help with essay on Individualising Cancer Patients Treatment Plan. Paper must be at least 2000 words. Please, no plagiarized work!Download file to see previous pages... Should excess myelos

Hi, I need help with essay on Individualising Cancer Patients Treatment Plan. Paper must be at least 2000 words. Please, no plagiarized work!

Should excess myelosuppression be observed in a cancer patient under multiple therapies, it is very hard to identify the specific drug causing the condition. To resolve such issues and allow for individualisation of cancer treatment, it is important that the patient be tested for his or her TPMT genotype. TPMT status testing has also been included into therapeutic procedures at St Jude Children's research Hospital from 1991.1

Some genotype therapy combinations are capable of affecting the late effects of cancer treatments for lymphoblastic leukaemia which is capable of causing second tumours. Defective TPMT activities and prior mercaptopurine treatment have been known to lead to irradiation-linked brain tumour and etoposide-related severe myeloid leukemias. This calls for a confluence of genetic features and treatment interaction to help in creating danger groups.

Evidence from reliable sources has shown that increased TGN leverage can boost carcinogenesis. Although is possible to make out patient subgroups capable of tolerating drugs that would otherwise be dangerous for others, it is vital to bear in mind both the long term and short term effects of this medicine.

In the UK, 5-FU is commonly prescribed for cases of solid tumours like colorectal and breast cancer. It has bee observed that over 80 per cent of 5-FU is deactivated by DPD, which varies from 8 to 21 times among patients. Patients showing signs of low DPD action may not effectively deactivate 5-FU, which could lead to gastrointestinal, neurological and haematopoietic toxicity, which could turn out to be fatal.

Even though it is not clear on the number of patients who have mutations reducing DPD function, acute toxicity happens after 5-FU treatment in patients who have low DPD activity. An estimated 3 per cent of the UK population is believed to be a carrier of a heterozygous mutation which inactivates DPD, while a negligible number are homozygous for deactivating any mutation.

Nature of cancer treatment

A number of cancer therapeutics destroy tumour cells, but a majority of them cannot differentiate these cells from the host cells, thereby destroying both the cancerous and non-cancerous cells. Drugs such as these have a very narrow therapeutic range because they have a relatively small ratio of the drug associated with anti-humour efficacy to that associated with toxicity. 2

For instance, even though anticyclones effectively treat breast cancer, its therapy is restricted to a particular cumulative dose due to the cardio-toxic effects of the drugs' high doses. If patients with genetic factors closely related to lesser likelihood of anthracycline-induced cardiac toxicity, then it will be easier to give higher, more efficient doses to these patients, therefore increasing the therapeutic range for this category of patient population.

A number of tumours undergo mutations, or acquire somatic mutations, making them resist drug therapy, with some tumours not expressing the target where the treatment should be directed. Other cancer therapies are simply not effective due to host genetic polymorphisms in the genes encoding enzymes, thus limiting the exposure of cancerous cells to drugs.

Response to tumour treatment is still commonly assessed by measuring of the tumour size through imaging.