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Principal Investigator: Milind M. Vaidya

Contact details

Office Phone: +91 22 27405055

Laboratory Phone: +91 22 27405338

Fax: +91 22 27405085

 

Research Area

One Key Research Area: Oral cancer, intermediate filament proteins

Special interests:Keratins, vimentin, If associated proteins, biomarkers

About us: A mission statement of the Laboratory in a line if any:

Focus of the laboratory is on understanding functions of IF proteins in cell transformation/differentiation and their use as biomarkers

Brief information on the activities of the Laboratory :

We have been working on developing keratins as specific markers for diagnosis and prognosis of human cancer and potentially malignant lesions. We are also exploring the possibility of using a battery of biomarkers which include Keratin associated proteins for prognostication of cancer. We are investigating the use of serum Keratin fragments as noninvasive prognostic markers for oral cancer. Studies related to possible role of Vimentin, K8/18 and their post translational modifications in governing processes like cell differentiation, transformation and apoptosis have been initiated. Our other interest includes development of chemical and transgenic models to study the process of oral carcinogenesis.

Projects

Projects: 

Project 1: Changes in keratin expression, localization and their interaction with membrane proteins in oral carcinogenesis using rat oral mucosa

Deepak Kanojia, Arvind Ingale, Anita Borges, Milind M. Vaidya

Oral cancer is the single largest group of malignancies in the Indian subcontinent. At present there is dearth of early diagnostic and prognostic markers for human oral cancer. Keratins (K) are being used as biomarkers in different epithelial disorders including cancer. K are associated with desmoplakin and α6β4 integrin which are components of desmosomes and hemidesmosomes respectively. in order to study the changes in keratin profile we uilised 4Nitroquinoline 1-Oxide (4NQO) , a carcinogen induced Sprague dwaley rat model for the development of various stages of oral carcinogenesis. Sprague dwaley rats treated with 4NQO resulted in dysplasia (80/120 days), papilloma in 160 days and SCC of tongue and buccal mucosa. we have analysed the alterations in CK and associated proteins during sequential stages of 4NQO induced oral carcinogenesis. Our results showed that the alterations primarily begin after the dysplastic changes in the lingual epithelium like the elevation of CK5/6a, ectopic expression of CK8, increase in suprabasal expression of α6 integrin and increase in desmoplakin levels. Most of these alterations persisted till the development of SCC except desmoplakin, the levels of which were downregulated in papillomatous lesions and SCC. Many of these alterations have also been documented in human oral carcinogensis.

Project2: Keratins 8 and 18 associated neoplastic progression through α6β4 integrin mediated signaling

Hunain Alam, Sorab Dalal, Milind M. Vaidya

Keratins 8 and 18 (K8 and K18) are predominantly expressed in simple epithelial tissues and perform both mechanical and regulatory functions. Aberrant expression of K8 and K18 is associated with neoplastic progression and invasion in squamous cell carcinomas (SCCs). To understand the molecular basis by which K8 promotes neoplastic progression in oral SCC (OSCC), K8 expression was inhibited in AW13516 cells. The K8-knockdown clones showed a significant reduction in tumorigenic potential, which was accompanied by a reduction in cell motility, cell invasion, decreased fascin levels, alterations in the organization of the actin cytoskeleton and changes in cell shape. Furthermore, K8 knockdown led to a decrease in α6β4 integrin levels and α6β4 -integrin-dependent signaling events, which have been reported to play an important role in neoplastic progression in epithelial tissues. Therefore, modulation of α6β4 integrin signalling might be one of the mechanisms by which K8 and K18 promote malignant transformation and/or progression in OSCCs.

Project 3: Role of Fascin in progression of oral squamous cell carcinoma:

Hunain Alam, Sorab Dalal, Milind M. Vaidya

Fascin is a globular actin cross-linking protein, which plays a major role in forming parallel actin bundles in cell protrusions and is found to be associated with tumor cell invasion and metastasis in various type of cancers including oral squamous cell carcinoma (OSCC). Previously, we have demonstrated that fascin regulates actin polymerization and thereby promotes cell motility in K8-depleted OSCC cells. In the present study we have investigated the role of fascin in tumor progression of OSCC. Fascin was overexpressed along with vector control in OSCC derived cells AW13516 and the phenotype was studied using tumorigenicity assays. Further, fascin expression was examined in human OSCC samples (N = 131) using immunohistochemistry and level of its expression was correlated with clinico-pathological parameters of the patients. Fascin overexpression in OSCC derived cells led to significant increase in cell migration, cell invasion and MMP-2 activity. In conclusion, our results indicate that fascin promotes tumor progression and activates AKT and MAPK pathways in OSCC-derived cells. Further, our correlative studies of fascin expression in OSCC with clinico-pathological parameters of the patients indicate that fascin may prove to be useful in prognostication and treatment of OSCC.

Project 4: Effect of loss of K8 phosphorylation in oral squamous cell carcinoma:

Hunain Alam, Sorab Dalal, Milind M. Vaidya

K8 and K18 undergo several posttranslational modifications including phosphorylation, which are known to regulate their functions in various cellular processes. Although, K8 and K18 phosphorylation is known to regulate cell cycle, cell growth and apoptosis, its significance in cell migration and/or neoplastic progression is largely unknown. In the present study we investigated the role of K8 phosphorylation in cell migration and/or neoplastic progression in OSCC. Our results provide first evidence of a potential role of K8 phosphorylation in cell migration and/or tumorigenicity in OSCC. Moreover, correlation studies of K8 dephosphorylation with clinico-pathological parameters of OSCC patients also suggest its possible use in prognostication of human OSCC.

Project 5: Role of K5/14 in proliferation and differentiation:

Hunain Alam, Sorab Dalal, Milind M. Vaidya

Keratin 14 (K14) is expressed in mitotically active basal layer cells, along with its partner keratin 5 (K5), and their expression is down-regulated as cells differentiate. Apart from the cytoprotective functions of K14, very little is known about K14 regulatory functions, since the K14 knockout mice show postnatal lethality. In this study, K14 expression was inhibited using RNA interference in cell lines derived from stratified epithelia to study the K14 functions in epithelial homeostasis. The K14 knockdown clones demonstrated substantial decreases in the levels of the K14 partner K5. These cells showed reduction in cell proliferation and delay in cell cycle progression, along with decreased phosphorylated Akt levels. K14 knockdown cells also exhibited enhanced levels of activated Notch1, involucrin, and K1. In addition, K14 knockdown AW13516 cells showed significant reduction in tumorigenicity. Our results suggest that K5 and K14 may have a role in maintenance of cell proliferation potential in the basal layer of stratified epithelia, modulating phosphatidylinositol 3-kinase/Akt-mediated cell proliferation and/or Notch1-dependent cell differentiation.

Project 6: Role of cytokeratin 8 and 18 in differentiation and transformation of epithelial cells

Sapna Iyer, Sharada S. Sawant, Sorab Dalal, Neelam Shirsat, Milind M. Vaidya.

The present study aimed at investigating the role of K8 and 18 in differentiation and transformation of mixed epithelia like breast. K8 was over-expressed in MDA MB 435 cells and down-regulated in MDA MB 468 (less invasive transformed cells) and MCF10 A (non-transformed) cell line .Significant differences were observed in the tumor volume, motility, in-vitro invasion assays and metastasis of K8 transfected cells as compared to vector control cells. K8 knockdown MDA MB 468 clones showed increase in cell growth, soft agar colony formation potential, motility and also invasion. Thus, our results indicate that K8 may play an important role in prevention of invasion and metastasis of mixed epithelia like breast. Differential gene expression of MDA MB 435 and MDA MB 468 clones was analyzed by microarray analysis and further validated using Real time PCR. K8 up-regulation in MDA MB 435 resulted in increase in mRNA levels of FGFRL1, THBS2, TUBB6 and decrease in mRNA levels of LEF-1.

Project 7: Global profiling of proteins in experimental rat buccal mucosal and lingual carcinogenesis : a sequential study

Biharilal Soni, Harsha Gauda, Akhilesh Pande, Arvind Ingale, Anita Borges, Milind M. Vaidya

We have explored the 4NQO induced rat model for tongue cancer because of its similar alterations in molecular pathways as seen in human. We obtained hyperplasia, papilloma, and carcinoma stages after 120, 160 and 200 days treatment of 4NQO respectively. In current study we used the 4 plex iTRAQ LC-MS proteomics approach to get the protein profile of each stage. In all we have identified 2223 proteins from the rat tongue tumor of which 415 proteins were found to be differentially expressed in tumor comparison to normal. We have also observed 333 proteins from papilloma and 109 proteins from hyperplasia, which followed differential expression pattern in tumerogenesis in compare to normal respectively. Several differential proteins previously reported in human OSCC like keratin 5(K5), K14, K17, K10, Vimentin, Transglutaminase 3 (TGM3), Periostin, MMP9, etc. have also been found to be differentially expressed in tumor of this model. We validated some of the known molecules like vimentin, fascin, periostin, transglutaminase 3 and cornulin in rat tissues. In addition we have also validated some of noble protein (protein whose expression is not reported in human cancer) like tenascin N in both rat and human samples. we found that up regualtion of vimentin, fascin and periostin and down regulation of transglutaminase3 and cornulin were also seen in human samples. Tenascin N was found to be upregulated in both rat and human tongue cancer.

Project 8: Prognostic value of tissue polypeptide antigen in oral squamous cell carcinoma

Sharada S. Sawant, Milind M. Vaidya, Devendra Chaukar, Shubhada Kane, Anil Dcruz

Human oral cancer has a high risk of locoregional relapse which is difficult to diagnose early due to lack of prognostic markers. We and others have shown aberrant expression of cytokeratin (CK) 8 and 18 in human oral cancer. Aberrant supra-basal expression of CK19 has been shown earlier. In this study, our aim was to develop a non-invasive test for prognostication of human oral cancer. Immunoradiometric assay (IRMA) was used to measure the circulating levels of TPA in the sera of 80 oral cancer patients before surgery and seven days after surgery. We have shown the presence of CK8, 18 and 19 fragments in the sera of oral cancer patients. We could correlate the higher TPA levels with tumour stage, recurrence and poor survival of the patients. We have also shown that the TPA levels remained high even after surgical removal of the tumour, which could be the result of presence of these proteins in the surrounding uninvolved areas.In conclusion, increased post surgery serum TPA levels could prove to be a useful marker of disease progression in human oral cancer and TPA could be used as a useful non-invasive prognostic assay.

Project 9: Use of cytokeratins as prognostic markers in human oral precancer and cancer

Sharada S. Sawant, Milind M. Vaidya, Devendra Chaukar, Shubhada Kane, Anil Dcruz

Our earlier studies have shown consistent changes in Keratin expression in both human oral pre-cancer and cancer. Two most common changes seen were non-expression of K5 and aberrant expression of K1, K8 and 18. In the present study we analyzed K1, K5, K8, and K18 in 122 precancerous lesions and 304 SCC with their respective cut margin tissues using immunohistochemistry. Results of IHC were correlated with the clinical parameters. Non expression of K5 and aberrant expression of K1, K8 and K18 significantly correlated with progressive grade of leukoplakia, while only K18 expression correlated with the progressive grade of fibrosis. Further, these two events that is loss of K5 and gain of K1, K8 and K18 independently as well as in different permutations and combinations also significantly correlated with local recurrence and overall survival of OSCC patients.

10: Role of aberrant vimentin expression in human oral pre-cancer and cancer

Crismita D’mello, Sharada S. Sawant, Devendra Chaukar, Shubhada Kane, Anil Dcruz, Sandeep Pagare, Milind M. Vaidya

Ability to clinically predict malignant transformation using histopathology is limited. Therefore, one of the keys to successful treatment and cure is early detection of tumour formation. Vimentin is an established EMT marker which is expressed in highly aggressive carcinomas while its role and mechanism in cancer initiation and progression remains unclear. Our published results have shown aberrant vimentin expression in human precancerous lesion, primary cultures derived from leukoplakia and in rat lingual carcinogenesis in 4NQO derived model. Hence this project revolves around understanding the vimentin associated molecular mechanisms governing the biological behaviour of initial and late stage of oral squamous cell carcinoma. We have initiated the development of invitro chemical carcinogenesis model to study the role of vimentin in the development of oral cancer. In the progression of oral cancer the role of vimentin is known however the molecular pathways involved are still unclear. Our recent studies indicate the different target molecules of vimentin through which it is able to confer a characteristic phenotypic to the cancer cell. The possible pathways operated by vimentin to contribute in oncogenesis are as demonstrated in the models. Currently our work focuses on decoding all the intermediate molecules in the pathways regulated by vimentin.

Project 11: Role of Keratin 8 phosphorylation in neoplastic progression of squamous cell carcinoma

Richa Tiwari, Sorab Dalal, Rahul Thorat, Milind M. Vaidya

Keratins were thought to be mere structural proteins whose known function was maintenance of structural integrity of cell. Recent progress in the field of keratin biology has indicated that, they do have key regulatory functions. We have previously shown role of Keratin 8 and 18 in malignant transformation in stratified epithelial cells. Our recent data suggests that K8 and K18 promote cell motility and tumor progression, possibly by deregulating β4 integrin signaling in OSCC. Our mutational studies suggest that loss of K8 phosphorylation leads to increased cell migration and tumorigenicity in OSCC cells. In addition, K8 dephosphorylation was also observed in human OSCC samples which correlated with tumor size, stage and lymph node metastasis. In present study we want to understand the role of K8 phosphorylation in neoplastic progression of SCC using a transgenic mouse model system so as to mimic the in vivo conditions. We also want to investigate role of K8 phosphorylation in cell lines derived from SCC of different origin like skin at phenotypic and molecular level so as to understand whether these effects are cell line specific and further to understand mechanism underlying the same. Results from these studies may help us to better understand the role of keratin 8 phosphorylation in tumor progression and in future it can be used as a promising prognostic marker and a new therapeutic target.

Project 12:The role of linker proteins in keratin mediated regulation of β4 integrin signaling in neoplastic progression of squamous cell carcinomas.

Pratik R. Chaudhari, Milind M. Vaidya

Previously, our laboratory has shown aberrant expression of keratin8/18 (K8/18) in human oral squamous cell carcinomas (OSCC). Subsequent work from our laboratory revealed that knockdown of K8 in Squamous cell carcinoma derived cell line (AW13516) resulted in alterations in levels α6β4 integrin proteins, α6β4 integrin mediated signaling, reduction in cell motility, downregulation of cell motility associated protein fascin and alteration in reorganization of the actin cytoskeleton. But how K8 and K18 modulate β4 integrin signalling and its downstream events is still unanswered. BPAG1e and Plectin are members of plakin family which anchor the keratin cytoskeleton network to the cell surface via β4 integrin. The importance of plakins in maintaining tissue integrity is well understood. However the role of these linker proteins in cell motility is not yet well studied. BPAG1e null animals display impaired wound healing in vivo. This observation indirectly implicates BPAG1e as a potential regulator of keratinocyte migration. Thus knockdown of BPAG1e in oral cancer derived cell line will enable us to understand the role of linker proteins in keratin mediated regulation of β4 integrin signaling in neoplastic progression of squamous cell carcinomas.

Project 13: Role of Keratins 8, 18 and Vimentin during epithelial mesenchymal transition (EMT) using oral organotypic co-culture model

Archana Singh, Vidhi Makani, Milind M. Vaidya, Sharada S. Sawant

Regional lymph node metastases and local recurrence are two major hurdles in the management of human oral cancer, the mechanism for which is largely unknown. Epithelialmesenchymal interactions are necessary for both, during development as well as maturation of the tissues. These interactions may also have an important role in neoplastic transformation and progression of the tumour. It is postulated that the highly invasive and metastatic activity of the tumour is the result of the interactions between cytoskeleton, cell surface receptors, and ECM components and not the gene expression alone. To study epithelial-mesenchymal interactions appropriate and functionally relevant experimental models are needed. The conventional monolayer cell culture models are not accurate representations of in vivo tissue because they grow two dimensionally. Connective tissue is known to have its influences on epithelial gene expression and therefore it will be important to establish a 3-D co-culture system in our lab so as to understand the interplay between epithelium & connective tissue. In this study we propose to 1) Develop in-vitro organotypic co-culture models from normal, dysplasia and SCC of human oral mucosa which grow in 3-D fashion and maintain its architecture which mimics in-vivo conditions. 2) Use this model to study the alterations in the interactions of cell–cell and cell ECM components during the various stages of oral carcinogenesis. In future, this model can be used to test anticancer drugs.

Project 14: Enrichment and characterization of cancer stem like cells: Applications in oral cancer

Archana Singh, Vidhi Makani, Milind M. Vaidya, Sharada S. Sawant

It is hypothesised that cancer stem cells (CSCs) are the cause for local recurrence. The development of new cancer stem cell (CSC) targeted strategies is currently hindered due to the lack of knowledge of the behaviour and fate determinant genes which increase resistance to the given anticancer therapies. In this study our aim is to understand the differential gene expression profile of primary tumour versus recurrent tumour using microarray analysis, further to study the molecular alterations associated with the development of resistance to chemo/radiation. In this direction, CSCs will be enriched from the cell line derived from human oral SCC using sphere formation strategy. The enriched and characterized CSCs will be injected into immunocompromized mice. The developed tumours will be surgically ressected and post-surgery animals will be treated with chemo/radiation. These animals will be allowed to live under normal conditions till the recurrent tumour developed or the death of the animal whichever is lesser period. These tumour cells will give us possibly chemo/radiation resistant population which will be further used for microarray analysis using whole human genome array. Microarray data will give us leads about the differential gene expression in primary tumour versus recurrent tumour. Short listed genes from microarray data will be validated using /RT- PCR. Depending on the results of this study efforts will be made to dissect the molecular signaling pathways associated with drug/radio resistance of cancer stem cells.

Project 15: Depicting the mechanism of K5 and K14 regulated cell proliferation/differentiation in stratified epithelial cells.

Saumya Shrivastav, Hunain Alam, Milind M. Vaidya

In stratified epithelial cells, Keratins exhibit well coordinated mechanism under tight regulation of differentiation program. The K5/K14 is the pair of keratins expressed in basal cells of stratified epithelia. Recent studies have demonstrated that K5/14 null mice died 2 days after birth and the loss of K14 cannot be compensated by the ectopic expression of any other keratin suggesting the role of keratin in normal development and functioning of basal cells and perform some unique regulatory role. The unique tissue specific role of K14 has been defined only recently. Recent study in our lab has provided evidence that K14 knockdown HAKAT cells demonstrated decrease in phosphorylation of Akt, decrease in cell proliferation and reduction in cell cycle progression markers (cyclin D1, PCNA, Ki67 and phosphorylated Histone H3. K14 deficient cells also exhibited increase in levels of activated Notch1 followed by increase in differentiation markers such as involucrin and K1. In addition, the tumorogenic potential of K14 knock down AW 13516 cells WAS found to be significantly reduced. However, the molecular basis of K5/K14 modulated cell proliferation and differentiation in basal keratinocytes is not completely understood. In the present study, we want to understand exact function of K5/K14 in cell proliferation and differentiation. We will explore molecule(s) that are involved in K5/K14 mediated cell proliferation downstream of Akt. We would also like to investigate the downstream signaling post Notch-1 activation. This information will provide us better understanding of K5/14 mediated cell proliferation and differentiation and an insight in the process of epithelial stratification and tumor progression.

Members

Laboratory Members:

Present members:

Milind Vaidya, Sharada Sawant, Rajesh Kadam, Shridhar Nadkar, Saumya Shrivastav, Biharilal Soni, Crismita Dmello, Richa Tiwari, Pratik Chaudhari, Archana Singh, Vidhi Makani.

Alumni

Deepak Kanojia, Hunain Alam, Sapna Iyer

Opportunities: If any for students Laboratory imparts six months short term trainee as a part of MSc/ BTec/ MTec dissertation and post MSc wet Lab experience.

Publications

Select Publications:

1. Sharada S. Sawant, Miline M. Vaidya, Devendra A. Chaukar, Hunain Alam, Crismita Dmello, Prakash Gangadaran, Sadhana Kannan, Shubhada Kane, Prerana P. Dange, Nigamananda Dey, Ranganathan K, Animal K. D’Cruz (2013). Clinical significance of aberrant vimentin expression in oral premalignant lesions and carcinomas. Oral Diseases. doi:10.1111/odi.12151.

2. Iyer SV, Dange PP, Alam H, Sawant SS, Ingle AD, et al. (2013) Understanding the Role of Keratins 8 and 18 in Neoplastic Potential of Breast Cancer Derived Cell Lines. PLOS One 8(1): e53532. Doi: 10.1371/journal.pone.0053532.

3. Deepak Kanojia, Sharada S. Sawant, Anita M. Borges, Arvind D.Ingle (2012), Milind M. Vaidya (2012). Alterations in keratins and associated proteins during 4- Nitroquinoline-1-oxide induced rat oral carcinogenesis. Journal of Carcinogenesis 11, 39-46.

4. Hunain Alam, Amruta V Bhate, Prakash Gangadaran, Sharda S Sawant, Shimul Salot, Lalit Sehgal, Prerana P Dange, Devendra A Chaukar, Anil K D’cruz, Sadhna Kannanl, Rajiv Gude, Shubhada Kane, Sorab N Dalal, Milind M Vaidya (2012). Fascin overexpression promotes neoplastic progression in oral squamous cell carcinoma. BMC Cancer, 12:32.

5. Alam H, Gangadaran P, Bhate AV, Chaukar DA, Sawant SS, Tiwari R, Bobade J, Kannan S, D'cruz AK, Kane S, Vaidya MM, (2011). Loss of Keratin 8 Phosphorylation Leads to Increased Tumor Progression and Correlates with Clinico-Pathological Parameters of OSCC Patients., PLoS One. 6(11):e27767. Epub 2011 Nov 17.

6. Hunain Alam, Samrat T. Kundu, Sorab N. Dalal and Milind M. Vaidya* (2011). Loss of keratin 8 and 18 leads to alterations in 6 4-integrin-mediated signalling and decreased neoplastic progression in an oral-tumour-derived cell line. Journal of Cell Science 124, 2096-2115.

7. Srikanth, B., Vaidya, M.M., Kalraiya, R.D (2010). O-GlcNAcylation determines the solubility, filament organization, and stability of keratins 8 and 18. Journal of Biological Chemistry, 285 (44), pp. 34062-34071.

8. Sawant SS, Zingde SM, Vaidya MM (2008). Cytokeratin fragments in the serum: Their utility for the management of oral cancer. Oral Oncol. 44(8), pp.722-732.

9. Vaidya MM, Kanojia D. (2007). Keratins: markers of cell differentiation or regulators of cell differentiation? J Biosci. 2007 Jun;32(4):629-34.

10. Raul UB, Sawant SS, Dange PP, Kalraiya RD and Vaidya MM. (2004) Implications of CK8 and 18 filament formation in stratified epithelial cells: induction of transformed phenotype. International Journal of Cancer, Vol.111, No.5, 662-668.

11. Upasani OB, Bhisey AN and Vaidya MM. (2004) The database of monoclonal antibodies to cytokeratins. Oral Oncology, Vol. 40, No.3, 236-256.

12. Sawant SS, Naresh KN, D’Cruz A, Ogale SB, and Vaidya MM (2003). Demonstration of cytokeratin-5 non-expression in tobacco related oral carcinogenesis-use of reverse transcriptase polymerase chain reaction as a sensitive assay. Oral Oncology 39:789-795.

13. Vaidya MM, Sawant SS, Borges AM, Naresh NK, Purandare MC and Bhisey AN. (2000) Cytokeratin expression in human fetal tongue and buccal mucosa. J. Biosci. 25: 235-242.

14. Vaidya MM, Sawant SS, Borges AM, Ogale SB and Bhisey AN (1998) Cytokeratin expression in precancerous lesions of the human oral cavity. Oral Oncol Eur J Cancer 34(4): 261-64.

15. Vaidya MM, Borges AM, Pradhan SA and Bhisey AN (1996). Cytokeratin expression in squamous cell carcinomas of the tongue and alveolar mucosa. Eur. J. Cancer Oral Oncol. 32: 333-336.

16. Vaidya MM, Borges AM, Pradhan SA, Rajpal RM and Bhisey AN (1989). Altered keratin expression in buccal mucosal squamous cell carcinoma. J. Oral Pathol. Med. 18: 282-286.

Links: Applications / online sources developed by the Department

Awards / Honors:

Invited speaker at Gorden conference on Intermediate filaments (2010, 2012), Executive committee member for Indian Society of Cell Biology 2013-15.

Sharada Sawant:

1. Received an excellent poster presentation international award for the Poster entitled “Use of cytokeratin as prognostic markers in squamous cell carcinoma of buccal mucosa” presented at Asian –Pacific Conference of Tumour Biology and Medicine, 2004 & 21st IATMO International Conference held at Xian- China during August 21-25, 2004.

2. Received Vocational Excellence Award from Rotary Club of New Bombay Hillside for excellent achievement in vocation on 1st November 2006.

3. Received best poster presentation award at “International Symposium on Intermediate Filament Proteins: Recent Trends in Keratin Biology which was held at ACTREC during September 28-29, 2007

4. Received best oral presentation award in the contest ‘National talent search in head and neck cancer research’ was held in the meeting ‘Indian Head and Neck Cancer Congress’ on 26th October 2009 at AIIMS-Kochi.

5. The Prof. Yasuzumi award for the second best oral presentation in Biological Sciences in the International Conference on ‘Advances in Electron Microscopy and related techniques and XXXI Annual Meeting of EMSI organized by Electron Microscope Society of India (EMSI) and Bhabha Atomic Research Centre (BARC) during March 8-10, 2010.

6. Received award for the poster presentation entitled,” Understanding the genetic determinants and their clinical significance in drug resistant recurrent tumours developed from CD44+ enriched cancer stem like cells” in the 4th international Conference on Stem Cells & Cancer during 19-22 October 2013 at Haffkine Institute, Mumbai, India.

Richa Tiwari:

Received award for poster presentation at The XXXVII All India Cell Biology Conference on Cell Dynamics and Cell Fate during 22-24 December, 2013 at Indian Institute of Science, Bangalore

Affiliations:

Member:Indian Association for Cancer Research, Indian Society of Cell Biology

Any other:

Webpage:http://www.actrec.gov.in/pi-webpages/MilindVaidya/milind-index.htm

Contact Us

Advanced Centre for Treatment, Research and Education in Cancer

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