Hunain Alam, PhD

Odyssey Fellow
Department of Molecular & Cellular Oncology
The University of Texas MD Anderson Cancer Center
1515 Holocombe Blvd. Rm Y7.6020
Houston, Texas-77030, USA

Biography

EDUCATION QUALIFICATION
• (1998-2001) BSc, Chemistry, Aligarh Muslim University, Aligarh, India
• (2002-2004) MSc, Toxicology, JamiaHamdard, New Delhi, India
• (2005-2011) PhD, Biochemistry, Cancer Research Institute (CRI), ACTREC, India

Research Interest

His current research is to investigate the Oncogenic functions of epigenetic modifiers in the development of Non-Small Cell Lung Cancer (NSCLC). Specifically, he plan to validate the tumor promoting functions of various histone demethylases and readers proteins using lung specific knockout mouse model and try to understand underlying tumor promoting mechanisms using Microarray and ChipSeq analysis.

Scientific Activities

AWARDS AND FELLOWSHIPS
• (2013) Odyssey Fellowship Award, MD Anderson Cancer Center
• (2005) Shortlisted for Shyama Prasad Mukherjee Fellowship Test
• (2004) Council of Scientific and Industrial Research National Eligibility Test- Junior Research Fellowship
• (2004) Council of Scientific and Industrial Research National Eligibility Test- Junior Research Fellowship
• (2004) Indian council of Medical Research Junior Research Fellowship
• (2004) Graduate Aptitude Test in Engineering

PROFESSIONAL SOCIETIES/MEMBERSHIP
• American Association for Cancer Research (AACR)
• American Society for Cell Biology (ASCB)
• All India Cell Biology Society (AICB)
• Indian Association for Cancer Research (IACR)

Publications

1. Klause W, Alam H, Giri U, et al. KDM2A promotes lung tumorigenesis by epigenetically enhancing ERK1/2 signaling. J Clin Invest. 2013. doi: 10.1172/JCI68642
2. Dhar SS, Alam H, Li N, et al. Transcriptional repression of histone deacetylase 3 by the histone demethylase kdm2a is coupled to tumorigenicity of lung cancer cells. J Biol Chem. 2014. doi: 10.1074/jbc.M113.521625
3. Alam H, Kundu S, Dalal S, Vaidya M. Loss of keratins 8 and 18 leads to alterations in α6β4-integrin-mediated signalling and decreased neoplastic progression in oral-tumor-derived cell line. J. Cell Science. 2011; 124(12): 2096-2106. doi: 10.1242/jcs.073585
4. Alam H, Sehgal L, Kundu S, Dalal S, Vaidya M. Novel function of keratin 5 and 14 in proliferation and differentiation of stratified epithelial cells. Molecular Biology of the Cell. 2011; 22(21): 4068-4078. doi: 10.1091/mbc.E10-08-0703
5. Alam H, Bhate A, Gangadaran P, et al. Loss of kertain 8 phosphorylation leads to increased tumor progression and correlates with clinico-pathological parameters of OSCC patients. PLoS One. 2011; 6(11): e27767. doi: 10.1371/journal.pone.0027767
6. Alam H, Bhate A, Gangadaran P, et al. Fascin overexpression promotes neoplastic progression in oral squamous cell carcinoma. BMC Cancer. 2012; 12: 32. doi: 10.1186/1471-2407-12-32
6. Dhar SS, Alam H, Li N, et al. Transcriptional repression of histone deacetylase 3 by the histone demethylase kdm2a is coupled to tumorigenicity of lung cancer cells. J Biol Chem. 2014. doi: 10.1074/jbc.M113.521625
7. Sehgal L, Mukhopadhyay A, Rajan A, et al. 14-3-3γ meditated transport of plakoglobin to the cell border is required for the initiation of desmosome assemblyin vitro and in vivo. J Cell Sci. 2014. doi: 10.1242/jcs.125807
8. Khapare N, Kundu S, Sehgal L, et al. Plakophilin3 loss leads to an increase in PRL3 levels promoting K8 dephosphorylation, which is required for transformation and metastasis. PLoS One. 2012; 7(6): e38561. doi: 10.1371/journal.pone.0038561
9. Iyer SV, Dange PP, Alam H, et al. Understanding the role of keratins 8 and 18 in neoplastic potential of breast cancer derived cell lines. PLoS One. 2013; 8(1): e53532. doi: 10.1371/journal.pone.0053532
10. Sawant S, Vaidya M, Chaukar D, et al. Clinical significance of aberrant vimentin expression in oral premalignant lesions and carcinomas. Oral Dis. 2014. doi: 10.1111/odi.12151