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Ameen F. Cancer-Research to Treatment: an Accelerating Journey. Biosci Biotech Res Asia 2017;14(1).1).
Manuscript received on : 22 March 2017
Manuscript accepted on : 26 March 2017
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Cancer-Research to Treatment: an Accelerating Journey

Fuad Ameen

Department of botany and microbiology, Faculty of Science, king Saud University, Riyadh11451, Saudi Arabia.

Corresponding Author E-mail: alfouad2004@hotmail.com

DOI : http://dx.doi.org/10.13005/bbra/2444

ABSTRACT:

The discovery a single gene had a revolutionary impact on healthcare on the basis of work done by Dr. Mary-Claire King at the University of California in Berkeley because he discovered that a single gene was responsible for certain breast cancers and it changed the diagnosis. In the latter half of 1990, genetics was considered to be a vital aspect and hence the Human Genome Project was launched. The rate of Breast cancer had dramatically increased over the last decade with respect to the improvements in screening by mammograms but still thousands of women do not have access to screening or diagnostics because of a lack in funding. Hence, we were in need of a new testing method to inspire the genetic discovery of Dr. King but a link was not established between genetic and clinical practice in oncology and there raised an urge to investigate the concept of “personalized medicine”. In this review, we investigate the concept of personalized medicine.

KEYWORDS:

Dramatically; Mammogram; Screening; Diagnostics

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Introduction

Though the research work on breast cancer was not the area of expertise for Dr. King’s, she thought to apply genetics could to add some useful contribution to the research at that time and the focus was to identifying a gene that cause cancer. The National Cancer Institute in USA conducted a survey of 1,500 women with breast cancer as part of a study with oral contraceptives but Dr. King asked them to add a query about close relatives with breast cancer. During 1990, Dr. King named the gene as BRCA i.e. the gene involved in Breast Cancer. It also produces a protein called BRCA1 for suppressing the formation of tumors by repairing the damaged DNA. Mutations in the gene can lead to changes in the protein to stop it from functioning properly, so that the breast tumors are able to grow.

According to the National Cancer Institute, BRCA1 and BRCA2 1 with mutations can account for 25% 2 of hereditary breast cancers and the 5 to 10 % 3 of other breast cancers. If a parent has a mutation in one among the two genes, 4 their child will have a chance of inheriting the one among the two mutations.5 This effect will increase their risk of developing breast cancer i.e. about 12 % of women without a harmful BRCA1 mutation will develop breast cancer when compared to about 60%6 of women with a harmful mutation.

In Cancer, the genetic causes were not so clear. Although there is a link between certain harmful mutations in BRCA17 and the development of breast cancer, there are thousands of possible mutations and other genes that can affect a person’s risk of disease.

Recent Case Study

In March 2016, a phase 3 clinical trial was conducted with 257 womenwith a type of breast cancer – HER2 positive.9 It was observed that, treating them with a combination of drugs before surgery could lead to disappearing of their tumors.

Outcome

Tumors disappeared in 710-13 among the 66 women14,15 who received the combination therapy and only minute traces of the cancer remained in further 11.16-18 It is early, but this could mean that for certain types of HER2-positive breast cancer, women could have this combination treatment followed by surgery, without the need for chemotherapy.19,20

Future Prospective

In order to achieve success, the initiative will require huge amounts of genomic data, which will require institutions to collaborate and share information. In addition to develop a platform for data sharing, there is a need for analyzing the global cancer research to highlight the collaborations.

Further Challenges

Dealing with a huge influx of data associated with new research involves the results from clinical trial and medical knowledge. In 1950, it took 10 years for the world’s medical knowledge to double and it’s projected that the entire world’s medical knowledge will double every 73 days by 2020.

It’s not only healthcare professionals who will need to navigate the information and patients will be increasingly involved in their own treatment decisions.

Conclusion

Today’s research can be transformed into tomorrow’s treatment; patients should understand and embrace it. Cancer can be overwhelming and seems to be complicated for many patients and their families to understand. Genomics can also increase that complexity. So, there exists a challenge to overcome this last obstacle on the journey from bench to bedside.

The groundbreaking aspects of cancer research rely upon clinical trials and major initiatives like the Cancer Moonshot. As technology continues to develop, a better molecular imaging can be seen with a less invasive surgery and more targeted drugs. If patients are empowered to understand and apply the evidence-based information to their own treatment decisions, the path from basic research to clinical application will become shorter than ever.

References

  1. Perou C. M., Sørlie T., Eisen M. B., van de Rijn M., Jeffrey S. S., Rees C. A., et al. Molecular portraits of human breast tumours. Nature. 2000;406:747–52.
    CrossRef
  2. Slamon D. J., Clark G. M., Wong S. G., Levin W. J., Ullrich A., McGuire W. L. Human breast cancer: correlation of relapse and survival with amplification of the HER-2/neu oncogene. Science. 1987;235:177–82.
    CrossRef
  3. Anderson W. F., Chatterjee N., Ershler W. B., Brawley O. W. Estrogen receptor breast cancer phenotypes in the surveillance, epidemiology, and end results database. Breast Cancer Res Treat. 2002;76:27–36.
    CrossRef
  4. Cui X., Schiff R., Arpino G., Osborne C. K., Lee A. V. Biology of progesterone receptor loss in breast cancer and its implications for endocrine therapy. J Clin Oncol. 2005;23:7721–35.
    CrossRef
  5. Rakha E. A., El-Sayed M. E., Green A. R., Paish E. C., Powe D. G., Gee J., et al. Biologic and clinical characteristics of breast cancer with single hormone receptor positive phenotype. J Clin Oncol. 2007;25:4772–8.
    CrossRef
  6. Konecny G., Pauletti G., Pegram M., Untch M., Dandekar S., Aguilar Z., et al. Quantitative association between HER-2/neu and steroid hormone receptors in hormone receptor-positive primary breast cancer. J Natl Cancer Inst. 2003;95:142–53.
    CrossRef
  7. Lal P., Tan L. K., Chen B. Correlation of HER-2 status with estrogen and progesterone receptors and histologic features in 3,655 invasive breast carcinomas. Am J Clin Pathol. 2005;123:541–6.
    CrossRef
  8. Dowsett M., Allred C., Knox J., Quinn E., Salter J., Wale C., et al. Relationship between quantitative estrogen and progesterone receptor expression and human epidermal growth factor receptor 2 (HER-2) status with recurrence in the arimidex, tamoxifen alone or in combination trial. J Clin Oncol. 2008;26:1059–65.
    CrossRef
  9. Untch M., Gelber R. D., Jackisch C., Procter M., Baselga J., Bell R., et al. Estimating the magnitude of trastuzumab effects within patient subgroups in the HERA trial. Ann Oncol. 2008;19:1090–6.
    CrossRef
  10. Slamon D. J., Leyland-Jones B., Shak S., Fuchs H., Paton V., Bajamonde A., et al. Use of chemotherapy plus a monoclonal antibody against HER2 for metastatic breast cancer that overexpresses HER2. N Engl J Med. 2001;344:783–92.
    CrossRef
  11. Brufsky A., Lembersky B., Schiffman K., Lieberman G., Paton V. E. Hormone receptor status does not affect the clinical benefit of trastuzumab therapy for patients with metastatic breast cancer. Clin Breast Cancer. 2005;6:247–52.
    CrossRef
  12. Arpino G., Weiss H., Lee A. V., Schiff R.,Placido S. D., Osborne C. K., et al. Estrogen receptor-positive progesterone receptor-negative breast cancer: association with growth factor receptor expression and tamoxifen resistance. J Natl Cancer Inst. 2005;97:1254–61.
    CrossRef
  13. De Laurentiis M., Arpino G., Massarelli E., Ruggiero A., Carlomagno C., Ciardiello F., et al. A meta-analysis on the interaction between HER-2 expression and response to endocrine treatment in advanced breast cancer. Clin Cancer Res. 2005;11:4741–8.
    CrossRef
  14. Lipton A., Ali S. M., Leitzel K., Demers L., Chinchilli V., Engle L., et al. Elevated serum Her-2/neu level predicts decreased response to hormone therapy in metastatic breast cancer. J Clin Oncol. 2002;20:1467–72.
    CrossRef
  15. Osborne C. K., Schiff R. Mechanisms of endocrine resistance in breast cancer. Annu Rev Med. 2011;62:233–47.
    CrossRef
  16. Shou J., Massarweh S., Osborne C. K., Wakeling A. E., Ali S., Weiss H., et al. Mechanisms of tamoxifen resistance: increased estrogen receptor-HER2/neu cross-talk in ER/HER2-positive breast cancer. J Natl Cancer Inst. 2004;96:926–35.
    CrossRef
  17. Witters L. M., Kumar R., Chinchilli V. M., Lipton A. Enhanced anti-proliferative activity of the combination of tamoxifen plus HER-2-neu antibody. Breast Cancer Res Treat. 1997;42:1–5.
    CrossRef
  18. Witters L., Engle L., Lipton A. Restoration of estrogen responsiveness by blocking the HER-2/neu pathway. Oncol Rep. 2002;9:1163–6.
    CrossRef
  19. Marchiò C., Natrajan R., Shiu K. K., Lambros M. B., Rodriguez-Pinilla S. M., Tan D. S., et al. The genomic profile of HER2-amplified breast cancers: the influence of ER status. J Pathol. 2008;216:399–407.
    CrossRef
  20. Knowlden J. M., Hutcheson I. R., Jones H. E., Madden T., Gee J. M., Harper M. E., et al. Elevated levels of epidermal growth factor receptor/c-erbB2 heterodimers mediate an autocrine growth regulatory pathway in tamoxifen-resistant MCF- 7 cells. Endocrinology. 2003;144:1032–44.
    CrossRef
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