Preventing Cancer with Personalised Medicine and Treating it

Reginald Nicholson^*
*Correspondence: Reginald Nicholson, Department of Cancer Sciences, University of Glasgow, Scotland, UK, Email:

Keywords

Pancreatic cancer • Damage response • Replication stress • Personalized medicine

Introduction

A cancer's response to a particular treatment can be impacted by specific gene or protein alterations. Even though they have the same sort of cancer, some people's malignancies contain gene changes that are distinct from those in other people's cancers. For instance, melanoma skin cancers don't always respond to a treatment in the same manner since they don't all have the exact same gene alterations. To assist decide which treatments are most likely to be effective, doctors can analyse the cancer cells for specific gene and protein alterations prior to beginning treatment. Giving treatments that are most likely to be effective while avoiding those that might not is the aim [1].

Literature Review

In precision medicine, clinicians create a care plan that typically includes precise recommendations using data from specific lab tests. In some circumstances, it can assist in making a more precise diagnosis and enhancing care. In other situations, it can assist individuals in making choices regarding healthy behaviours, earlier screening exams, and other actions they might take that may help lower their risk for a specific cancer. It's possible that your medical professionals won't employ "precision medicine" or "personalised medicine" exactly. Instead, they might discuss DNA, molecular, genomic, or genetic testing with you. Or they might discuss obtaining a genetic profile or running biomarker tests. These are some examples of how medical professionals and other healthcare specialists might apply a precision medicine strategy [2].

In cases where a patient's chance of developing a particular cancer is higher, precision medicine may be applied. For instance, a patient may discover that cancer runs in their family or a doctor may spot a trend of cancer in the patient's family. In these circumstances, the individual may consult with a licenced genetic counsellor and think about undergoing genetic testing. The testing can reveal whether they have a hereditary gene alteration that makes them more susceptible to developing particular types of cancer. If so, the doctor may advise screening and other tests (typically at a younger age than usual) to aid in the early detection of cancer, or they may propose medications or healthy lifestyle changes to assist reduce the patient's risk of developing the disease [3].

In cancer, where there is a greater focus on prevention and where severe short- and long-term toxicities are linked to surgical and chemo radiotherapy management regimens, personalised medicine is particularly crucial. The right patient selection for treatment has long been an essential component of standard clinical practise, but until recently, practitioners had few resources available to them to identify which patients might benefit and which could experience preventable toxicities. Exciting advances in personalised cancer medicine, such as the identification of prognostic and predictive biomarkers that allow for therapeutic targeting to patients most likely to benefit, are enhancing survival rates and are quickly taking centre stage in clinical practise [4].

Discussion

The development of Colorectal Cancer (CRC) is triggered by the accumulation of genetic mutations. 9 Familial Adenomatous Polyposis coli (FAP), an autosomal dominant condition with complete penetrance that results in truncation of the protein product and deregulation of the downstream signalling pathway, is responsible of colon cancer cases. By the time people are 40 to 50 years old, CRC is frequently developing due to the formation of hundreds of polyps. Genetic testing finds carriers and makes prophylactic bowel resection possible. In patients with FAP, this use of tailored medication has reduced the incidence of improved overall survival; but, just as with surgical prophylaxis for breast cancer above, surgery does not provide total avoidance of cancer development [5].

This strategy has recently been used to treat individuals with polymerase inhibitors. Homologous recombination DNA repair processes do not work in cells with BRCA mutations. However, base-excision DNA repair mechanisms continue to work, "rescuing" a tumour cell from apoptosis after a cancer treatment that damages DNA. By blocking base-excision repair drugs selectively kill tumour cells in BRCA-deficient cells while sparing healthy cells with functional homologous recombination pathways. A PARP inhibitor being tested in phase trials has a promising selectivity and sensitivity mutation carriers with ovarian, breast, and prostate cancer, with relatively low side effects. The greater risk was verified by a phase trial in women with advanced, previously treated high-grade serous ovarian cancer [6].

Conclusion

It’s still unclear how various people respond to therapies and how they develop diseases, despite the top scientists and physicians in the world. The way we create novel medicines for cancer patients has been completely transformed by translational research. One of the most significant developments in modern oncology is the shift from an organ-centric philosophy guiding therapy choice to thorough molecular analysis driving a tailored strategy. The ability to identify prognostic and predictive molecular changes has been considerably enhanced by a number of technologies, including RNA sequencing and next generation sequencing. The history of many diseases, both locally and metastatic ally, has been changed as a result of the discovery of gene mutations, amplifications, and fusions. This shift in viewpoint, which places the emphasis on the precise molecular changes within the tumour, has made individualised treatment possible. The rise in basket trials that choose certain molecular targets is a reflection of this predicament.

Acknowledgement

None.

Conflict of Interest

There is no conflict of interest by author.

References

1. Xavier, Ramnik J. and Daniel K. Podolsky. "Unravelling the pathogenesis of inflammatory bowel disease." Nature 448 (2007): 427-434.

Google Scholar, Crossref, Indexed at

2. Canavan, C., K. R. Abrams and J. Mayberry. "Meta‐analysis: Colorectal and small bowel cancer risk in patients with crohn's disease." Aliment Pharmacol Ther 23 (2006): 1097-1104.

Google Scholar, Crossref, Indexed at

3. Bye, William A., Christopher Ma, Tran M. Nguyen and Claire E. Parker, et al. "Strategies for detecting colorectal cancer in patients with inflammatory bowel disease: A cochrane systematic review and meta‐analysis." Am J Gastroenterol 113 (2018): 1801.

Google Scholar, Crossref, Indexed at

4. Sottoriva, Andrea, Haeyoun Kang, Zhicheng Ma and Trevor A. Graham, et al. "A big bang model of human colorectal tumor growth." Nat Genet 47 (2015): 209-216.

Google Scholar, Crossref, Indexed at

5. Guinney, Justin, Rodrigo Dienstmann, Xin Wang and Aurélien De Reynies, et al. "The consensus molecular subtypes of colorectal cancer." Nat Med 21 (2015): 1350-1356.

Google Scholar, Crossref, Indexed at

6. Sudhakar, Padhmanand, Dahham Alsoud, Judith Wellens and Sare Verstockt, et al. "Tailoring multi-omics to inflammatory bowel diseases: All for one and one for all." J Crohns Colitis 16 (2022): 1306-1320.

Google Scholar, Crossref, Indexed at