Bikul Das
Academic Appointments
- Postdoctoral Research fellow, Medicine
Contact Information
- Academic
Offices
Personal Information Email
Professional Snapshot
Honors and Awards
- Harold E.Johns Fellowship award, Canadian Cancer Society (2009)
- Grand Challenges Explorations Grant, Bill and Melinda Gates Foundation (2009)
- Schweisguth Prize, International Society of Pediatric Oncology (SIOP), Netherland (2008)
- Scholar-in-training award, American Association of Cancer Research (2007 and 2008)
- Hind-Rattan Award, Non-Resident Indian (NRI) Society, New Delhi (2006)
Professional Education
| Fellow in Stem Cell Program: | Sickkids, Toronto, (2009) |
| Doctor of Philosophy: | University of Toronto, (2007) |
| Fellow in Hematology & Oncology: | NAITP, Sickkids, Toronto, (2001) |
| WHO training course: | Ministry of Health, Bhutan, Tuberculosis control (1996) |
| Residency in Internal Medicine: | Guwahati Medical College, India, (1994) |
Faculty Advisor
Community & International Work
Web Site Links
Scientific Focus
Research Interests
Cancer is considered as a disease of cellular evolution to reach a state of self-sufficiency and immortality. The final stage of this evolution is the appearance of aggressive and metastatic cancer cells. These aggressive cancer cells exhibit some molecular and cellular features of embryonic stem cells. During my clinical practice in India, while treating cancer patients, an important and disturbing question came to my mind: why should a cancer cell, towards the end of its evolution to become an aggressive cell exhibit features of embryonic stem cells? After all, embryonic stem cell creates life, whereas aggressive cancer cell kills life. During my PhD and fellowship training in Toronto (Hospital for Sick Children), I found that exposure of cancer cells to oxidative stress could induce embryonic stem cell like state (the stemness state) to cancer cells. This oxidative stress-induced stem cell like cancer cell state (cancer stemness state) is aggressive, and highly fluctuating (unstable) unlike the normal stemness state, which is stable and less fluctuating. Thus, one possible explanation of why cancer cell switch to an embryonic stem cell like state is that there are two kind of stem cell states: stable state (life-supporting), and an unstable state of aggression (life-destroying). Cancer cell may evolves into the unstable stemness state. At Stanford's Felsher laboratory, I am focusing on developing an appropriate experimental system to study the stable vs unstable state of stemness state. Prof. Dean Felsher's vast experience in Oncogene research will help my project tremendously. Furthermore, Prof. Peter W Andrews of the University of Sheffield will be my co-supervisor for the project.
Ref:Other interest
Since my early days of medical practice in India, I have a strong interest to understand how acute infectious disease process enters into an asymptomatic /latent phase, and then re-appear again. My hypothesis is that adult stem cell niche may play a...
Publications
- The Idea and Evidence of Tumor Stemness Switch Book Series: Stem Cell Biology and Regenerative Medicine, Humana Press. 2009: 473-487
- Cisplatin treatment increases survival and expansion of a highly tumorigenic side-population fraction by upregulating VEGF/Flt1 autocrine signaling. Oncogene. 2008; (28): 3923-34
- Hypoxia enhances tumor stemness by increasing the invasive and tumorigenic side population fraction. Stem Cells. 2008; (7): 1818-30
- A hypoxia-driven vascular endothelial growth factor/Flt1 autocrine loop interacts with hypoxia-inducible factor-1alpha through mitogen-activated protein kinase/extracellular signal-regulated kinase 1/2 pathway in neuroblastoma. Cancer Res. 2005; (16): 7267-75
- Squalene selectively protects mouse bone marrow progenitors against cisplatin and carboplatin-induced cytotoxicity in vivo without protecting tumor growth. Neoplasia. 2008; (10): 1105-19
Help