Cancer Biomarkers & Targeted Therapies

Zhiyuan Shen^*
*Correspondence: Zhiyuan Shen, The Cancer Institute of New Jersey, Robert Wood Johnson Medical School, 195 Little Albany Street, New Brunswick, NJ 08903, USA, Email:

Cancer is a disorder that showcases extraordinary atomic diversity among numerous individuals. Patients with the similar clinically analyzed cancer regularly fluctuate in their response to a similar therapy in light of the fact that each instance of malignancy has a one of a kind atomic signature and obsessive advancement. In this way, individualized treatment is foremost for improving of malignancy treatment. The improvement of excused and individualized treatment is dependent on the distinguishing proof of the particular biomarkers, approval of the biomarkers to recognize the therapeutic targets, and drug development against the distinguished targets.

Cancer biomarkers are the quantifiable atomic changes to either carcinogenic or typical tissues of patients. Although the word “biomarker” most ordinarily refers to the modified articulation of certain quality items or strange DNA arrangements, changes to cell cycles like energy metabolism and DNA damage response can also be used as biomarkers from a more extensive perspective. Malignant growth biomarkers have different ramifications in disease intercession. A reliable biomarker can be utilized for disease determination, hazard and forecast evaluations, and for the surveillance of treatment adequacy.

All the more significantly, a few, but not all, biomarkers can be exploited as therapeutic targets. This is on the grounds that some biomarkers might be just “messengers” straightforwardly add to the tumor development and are hence not ideal therapeutic targets. Only the “driver” or “conspirator” biomarkers that straightforwardly add to tumor development might be focused on for treatment. Consequently, exertion in the advancement of targeted therapies should not just to distinguish biomarkers, yet in addition to comprehend the natural meaning of such markers to approve their convenience as potential therapeutic targets.

A widespread cancer biomarker is the Warburg impact, the shift of mitochondrial energy creation to a glycolysis subordinate metabolism that gives energy to cells as well as produces inter-mediate building materials for cancer cells to develop. Various controllers control this switch of energy metabolism. The article by Liang et al. rundowns the current comprehension on how the tumor suppressor gene p53 controls the cellular energy metabolism [1]. Altered DNA repair capabilities are considered a functional biomarker. Like normal cells, cancer cells encounter various forms of endogenous and exogenous DNA damage.

Legitimate elements of numerous DNA-repair pathways are fundamental for malignant cells to support their development and resist therapeutic DNA damage. Inadequate DNA repair not just adds to genomic in-stability and tumorigenesis [3], yet in addition offers an opportunity for targeted treatment. It is realized that some tumors with imperfections of an essential DNA-repair pathway might be dependent on another option or reinforcement DNA-repair pathway(s). This offers a likely-hood to focus on the elective DNA pathways, which would give engineered lethality to the cancer cells holding onto the original repair deformity. The articles by Santivasi and Xia [3] and by Zhang [4] talk about how to exploit the particular jobs of homologous recombination and non-homologous end participating in DNA double strand break fix and the capacity of homologous recombination in DNA single-strand break-fix for focused on treatments.

The paper by Yue et al. [5] examines the advantages and disadvantages of utilizing cytoskeleton protein filamin-An as a disease biomarker and possibly a remedial objective. Ultimately, the paper by Allaj et al. [6] sums up the parts of cyclooxygenase and prostanoid motioning in disease movement and as therapeutic target for the treatment. However, we hope that these articles offer readers a flavor of how alternations of specific genes, DNA damage response, and energy metabolism may be used as cancer biomarkers & for targeted therapies.

References

1. Liang Yingjian, Juan Liu and Zhaohui Feng. "The regulation of cellular metabolism by tumor suppressor p53." Cell Biosci 3 (2013):1-10.
2. Shen Zhiyuan. "Genomic instability and cancer: an introduction." J Mol Cell Biol 3(2011):1-3.
3. Santivasi Wil L and Fen Xia. "The role and clinical significance of DNA damage response and repair pathways in primary brain tumors." Cell Biosci 3(2013):1-6.
4. Zhang Junran. "The role of BRCA1 in homologous recombination repair in response to replication stress: significance in tumorigenesis and cancer therapy." Cell Biosci 3(2013):1-14.
5. Yue Jingyin, Steven Huhn and Zhiyuan Shen. "Complex roles of filamin-A mediated cytoskeleton network in cancer progression." Cell Biosci 3(2013):1-12.
6. Allaj Viola, Changxiong Guo and Daotai Nie. "Non-steroid anti-inflammatory drugs, prostaglandins, and cancer." Cell Biosci 3(2013):1-13