My S.O.P.

This is the statement of purpose (SOP) that I used when applying to PhD programs:

Cancer is a very elusive disease since it involves various genes, pathways, and mechanisms, most of which are still being investigated. But with what we already know about Cancer, we have saved many lives and alleviated the quality of life of many terminal cancer patients. Most prominently, we have identified cancer genes such as BRCA1 and BRCA2 for breast cancer, and have been screening patients for mutations in these genes, and doing our best to prevent the disease from ever occurring. However, even with BRCA1 and BRCA2, the risk of a patient to develop breast cancer is still variable, ranging from 20-80%, indicating a possible involvement of other genes and pathways. Thus, it is mandatory to determine better prognostic markers in order to increase the efficiency of preventive medicine programs. This is the cardinal reason why I am interested in pursuing a Ph.D. in Molecular Epidemiology, or a related field involved in studying cancer pathogenesis and improving the prevention of the disease.

I was first cognizant of cancer and its treatment and diagnosis while I was completing my undergraduate degree in De La Salle University in Manila, Philippines. I majored in pre-med physics, which had a curriculum that included fundamental pre-med courses, and a concentration on basic biomedical physics courses, which explored radiation therapy, medical imaging, and medical instrumentation. The gist of my undergraduate education was the diagnosis and treatment of cancer through the application of medical physics concepts, such as in doing Positron Emission Tomography (PET) scans and the use of the Linear Accelerator (LINAC) in radiation therapy. I culminated my undergraduate studies by writing a thesis that investigated the protective effect of Vitamin E (α-Tocopherol) against X-ray(LINAC)-induced chromosome lesions in peripheral blood lymphocytes. My thesis partner and I concluded that the protective effect is significant when compared to the absence of any antioxidants, but that the avoidance of exposure is still imperative. However, The study was not published due to a limited sample size.

Nonetheless, when doing the literature review for my undergraduate thesis, the fact that chromosomal lesions can induce cancer piqued my interest. I was curious about how DNA damage causes cells to either go through apoptosis or become cancerous. This led me to pursue a Masters of Science degree in Biology at California State University-Northridge (CSUN), focusing on molecular genetics, to explore further how genes are involved in the pathogenesis of cancer, as well as other diseases. I was fortunate enough to work in the lab of Dr. Aida Metzenberg, who is also the director of CSUN’s genetic counseling program. I found myself not only learning about molecular genetics theories and research methods but I was also exposed to a clinical medical genetics perspective, since I shared a number of classes with the genetic counseling students. One of such classes was the Clinical Cancer Genetics course that was taught by Kathleen Blazer, a genetic counselor and head of the cancer genetics education program, and Dr. Jeffrey Weitzel, director of Clinical Cancer Genetics, both from the City of Hope, a well-known Cancer Hospital. Through this class, I learned about the different hereditary cancers and the known cancer gene mutations, as well as the clinical impact of their discovery – that today, patients with a family history are screened for these mutations, and if they are found to be positive, everything is done to prevent the disease from manifesting. This fits well with my own philosophy in medicine – that by knowing the root cause of the disease, we may be able to stop it from ever occurring, rather than employing band-aid solutions.

With my insistence to pursue research in cancer genetics, Dr. Metzenberg referred me to Dr. Victoria Cortessis, my current adviser at the University of Southern California’s Norris Comprehensive Cancer Center. As her apprentice, I am presently in the process of doing a tumor microarray study on Testicular Germ Cell Tumors to identify protein expression of a handful of candidate genes. Testicular Germ Cell Tumors (TGCTs) are the most common cancer in men aged 15 to 35 years old, and is also the leading cause of cancer deaths in men of this age range, despite its overall curability. No specific genes have been identified to contribute to TGCT pathogenesis, although a relatively high familial risk, which is about 9 to 12 times the general population in brothers of affected individuals, suggests an unmistakable genetic component. My thesis will investigate the protein expression of genes selected from mouse models. If we are able to detect a gene with a significant contribution to TGCT development, we may be able to improve prognosis of TGCTs and help in the preventive process.

An emerging interest of mine, through the context of my current research, is the involvement of RNA interference (RNAi) and posttranscriptional regulation in cancer etiology. Specifically, one of my genes of interest is HIWI, a protein found in male germ cells and in hematopoietic stem cells that is involved in posttranscriptional regulation, and is required for the production of a subset of microRNAs, which are involved in RNAi, and PIWI-interacting RNAs, with which it interacts, possibly to enable its function. I am interested in learning about other cancers where RNAi and posttranscriptional regulation are involved in the development and maintenance of the tumor. I am also agog to the prospect of using RNAi to treat cancer, probably by repressing genes that are overexpressed.

All of these experiences have led me to pursue a Ph.D. in Cancer Biology in order to do research that can facilitate a better prognosis in cancer, by evaluating candidate genes. As Benjamin Franklin said, “An ounce of prevention is better than a pound of cure.” It is my hope that by elucidating the etiology of cancer, we can cut it at its roots and prevent it from manifesting, especially in patients with a mutation associated with hereditary cancer, and who are at high risk of developing the disease. Furthermore, current clinical cancer genetics, though facilitative, have the potential to be sharpened further in terms of precision. With the example of BRCA1 and BRCA2, there is the possibility of the involvement of other genes and pathways in the pathogenesis of breast cancer, and if we can determine these genes, we may be able to hone the prognosis. Lastly, I am interested in unraveling the role of RNAi and posttranscriptional regulation in cancer pathogenesis, and probably its prospective role in cancer treatment.