Sandhya Thulasi Das

E-mail: s_thulasidas@yahoo.co.in

--------------------------------------------------------------------------------------------------------------------Senior Biomedical Research Scientist

Biomedical scientist with over 10 years of small animal based in vivo and cell based in vitro laboratory experience with publications in cancer genetics, drug discovery, pharmacology and toxicology. Additional publications related to chemokine biology, inflammation, asthma, epigenetics and innovative methods to study animal physiology and lung diseases. Proficient in designing and implementing experimental protocols involving rodent surgery, necropsy, tissue collection and preservation. Competent and well organized in compilation and analysis of experimental data and consolidation of these into manuscripts for publication in a timely manner. Capable of thinking outside the box and submitting fresh ideas for funding/ grant proposals. Interested in biology education and outreach.

--------------------------------------------------------------------------------------------------------------------Qualifications Summary
Cancer Cell Biology, Molecular Biology, Epigenetics, Genetics, Radiation Biology, In vivo rodent experiments, Rodent handling, Animal Physiology, Pulmonary Function Tests (PFTs) in rodents, Stereology, Protein Expression, Mammalian Cell Culture, Protein Expression and Purification, Lung Mechanics, High Performance Liquid Chromatography (HPLC), Toxicology, Immunohistochemistry, Critical Review of Scientific Literature, Data Analysis, Grant Writing, Teaching

--------------------------------------------------------------------------------------------------------------------EDUCATION:
DEGREE Postdoctoral Training INSTITUTION Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA Johns Hopkins University School of Medicine, Baltimore, MD, USA University of Texas Medical Branch, Galveston, TX, USA University of Mumbai, Mumbai, India DATE 09/2010-09/2012 FIELD Asthma, emphysema, lung mechanics, epigenetics Inflammation, lung fibrosis and cancer Inflammation, Chemokine Biology Life sciences-Radiation and Cancer Biology Zoology-specialization in Animal Physiology Zoology

Postdoctoral Training

02/2010-08/2010

Postdoctoral Training

08/2006-01/2010

Ph.D.

07/ 2006

MSc. BSc.

University of Mumbai, Mumbai, India University of Mumbai, Mumbai, India

07/ 1998 07/ 1996

PROFESSIONAL WORK HISTORY AND TEACHING EXPERIENCE:

2012- 2013 2010- 2012 2010-2011 2006- 2010 2002-2006 2000-2002 Junior Faculty (Research Associate) at Johns Hopkins University School of Medicine, Baltimore, MD, USA Postdoctoral Fellow at Johns Hopkins University, Baltimore, MD, USA Exhibit guide at the national aquarium at Baltimore, MD, USA-volunteer Postdoctoral Fellow at University of Texas Medical Branch, Galveston, TX, USA Research Scholar, Radiation Biology & Health Sciences Division, Bhabha Atomic Research Centre (BARC), India Research Scholar, Homi Bhabha Centre for Science Education, Tata Institute of Fundamental Research (TIFR), Mumbai, India

1999-2000 1998-1999 1997-1998

Junior Research Fellow, Bombay Natural History Society Mumbai, India High School Biology Teacher, Chate Coaching Classes, Thane, Mumbai, India Grade 3 full time substitute teacher at NBWS High School, Mumbai, India

HONORS:
2007-2009 2002-2007 2002 2000-2002 The McLaughlin Endowment Fund-Post-doctoral Fellowship, UTMB, TX, USA Department of Atomic Energy (DAE, India) Fellowship CSIR-UGC NET Fellowship Homi Bhabha Centre for Science Education research scholarship, Mumbai, India

ADDITIONAL INFORMATION: Journal Reviewer for

Journal of Anatomy (Ad-Hoc) PloS One (Ad-Hoc)

Grant Reviewer for

Boston Area Diabetes Endocrinology Research Center (BADERC) grants

PUBLISHED: A. ARTICLES IN PEER-REVIEWED JOURNALS:

1. Cheng RYS, Shang Y, Limjunyawong N, Dao T, Das S T, Rabold R, Sham JSK, Mitzner W and Tang WY. Alterations of Lung Methylome in Allergic Airway Hyperresponsiveness. Environ Mol Mutagen, 2013 (In Press). 2. Yan S, Das ST, Richard R, Sham JSK, Mitzner W and Tang WY. Epigenetic Alterations by DNA Methylation in House-dust- mite Induced Airway Hyperresponsiveness. Am. J. Respir. Cell Mol. Biol., 2013 (In Press). PMID: 23526225 3. Das ST, MacDonald KA, Chang HS and Mitzner W. A simple method of mouse lung intubation. J Vis Exp., 2013. (73):e50318. PMID: 23542122 4. Tran PT, Shroff EH, Burns TF, Thijagarajan S, Das ST, Zabuawala T, Chen J, Cho Y-J, Luong R, Tamayo P, Salih T, Aziz K, Adam SJ, Vicent S, Nielsen CH, Withofs N, Sweet-Cordero A, Gambhir SS, Rudin CM and Felsher DW. Twist1 suppresses senescence programs and thereby accelerates and maintains mutant Kras-induced lung tumorigenesis. PLoS Genetics, 2012-8(5):e1002650. PMID: 22654667. 5. Fallica J, Das ST, Horton M, and Mitzner W. Application of carbon monoxide diffusing capacity in the mouse lung. J Appl Physiol. 2011; 110(5):1455-9. PMID: 21310888. 6. Das ST, Rajagopalan L, Guerrero-Plata A, Sai J, Richmond A, Garofalo RP, and Rajarathnam K. Monomeric and dimeric CXCL8 are both essential for in vivo neutrophil recruitment. PLoS ONE, 2010- 5(7): e11754. 7. Joseph PR, Sarmiento JM, Mishra AK, Das ST, Garofalo RP, Navarro J and Rajarathnam K. Probing the role of CXC motif in chemokine CXCL8 for high affinity binding and activation of CXCR1 and CXCR2 receptors. J Biol Chem. 2010; 285(38): 29262-9. PMID: 20630874. 8. Sandhya T, Lathika KM, Pandey BN, Bhilwade HN, Chaubey RC, Priyadarsini KI, and Mishra KP. Protection against radiation oxidative damage in mice by triphala. Mutation Res. 2006; 609: 17. PMID: 16860592. 9. Sandhya T and Mishra KP. Cytotoxic response of breast cancer cell lines, MCF 7 and T 47 D to TPL and its modification by antioxidants. Cancer Lett. 2005; 238: 304. PMID: 16135398. 10. Sandhya T, Lathika KM, Pandey BN and Mishra KP. Potential of traditional ayurvedic formulation, TPL, as a novel anticancer drug. Cancer Lett. 2005; 231: 206. PMID: 15899544.

B. OTHER: Thesis/Dissertation
Investigations on the mechanisms of tumor radio-cytotoxicity in combination with drugs

Proceedings and Symposia

1.

Sandhya T and Nagarjuna G. A methodology for the analysis of biological knowledge base. In Proceedings of the International Conference on Science, Technology and Mathematics Education for Human Development. 2002; 1: 149. Tran PT, Shroff EH, Thijagarajan S, Das ST, Cho Y, Chen J, Luong R, Vicent S, Nielsen CH. Reactivation of Oncogene-induced Senescence In Kras Lung Tumors by Inhibition of Twist1. ASTRO conference abstracts in International Journal of Radiation Oncology Biology Physics. 2010; 78 (3): S128.

2.

Reviews
1. Sandhya T, Mishra KP. Radio-oxidative damage induced apoptosis: role of reactive oxygen species and lipid peroxidation with implications to cancer radiotherapy. Science Lett. 2002; 25: 327.

Book Chapters
1. Das ST and Mishra KP. Triphala. Book chapter in Phyllanthus Species: Scientific Evaluation and Medicinal Applications. 2011; CRC Press.

PUBLICATIONS UNDER PREPARATION

1. 2. 3. Kearson A, Limjuyawong N, Das ST and Mitzner W. Effect of point sampling density in quantifying mouse lung emphysema. Kumar, S, Thimmulappa, R, Das, ST, Kombairaju, P, Mitzner, W and Biswal S. Nrf2 critically regulates TSLP expression and Attenuates OVA-induced Experimental Asthma in Mice. Das ST and Mishra KP. Enhancement of radiation toxicity to tumor cells by Triphala, in vitro as well as in vivo.

PAPERS AND CONTINUING EDUCATION PROGRAMS:

Research Leadership -Johns Hopkins School of Medicine- Spring 2010

INVITED LECTURES AT SYMPOSIA AND CONFERENCES:

1. 2. UTMB Immunology Research in Progress, 12/3/08 JHMI Molecular and radiation sciences departmental talk 4/7/10

Selected Abstracts at Conferences

1. 2. 3. 4. American Thorasic Society International Conference, Philadelphia, May 17-22, 2013. Title: A nanoparticle based therapy to target bronchial angiogenesis. American Thorasic Society International Conference, Philadelphia, May 17-22, 2013. Title: Effect of sampling density in mouse lung emphysema. American Thorasic Society International Conference, San Francisco, California, May 18-23, 2012. Title: Inflammatory cell kinetics following an acute intratracheal elastase insult. American Thorasic Society International Conference, San Francisco, California, May 18-23, 2012. Changes in global DNA methylation in mice lungs following an acute intratracheal elastase insult: Role of IL-17a. American Thorasic Society International Conference, Denver, Colorado, May 13-18, 2011Abstract accepted for Poster Discussion Session. Title: Role of CD8+ T cells and IL-17 in elastaseinduced emphysema. American Society of Clinical Oncology ASCO Annual Meeting Chicago, Illinois, June 1-5, 2011- Title: Reactivation of oncogene-induced senescence in KRAS mutant non-small lung cancer by inhibition of TWIST1. Gordon Research Conference on Gradient Sensing and Directed Cell Migration, Galveston, Texas March 29-April 3, 2009. Title: In vivo neutrophil recruitment is regulated by chemokine CXCL8 monomer-dimer equilibrium. Annual McLaughlin Symposia on Infection and Immunity, UTMB, Galveston Texas, USA, March 2008. Title: Role of CXCL8 monomer dimer equilibrium in neutrophil recruitment: insights from a mouse lung model. International Symposium on Translational Research: Apoptosis & Cancer, Trivandrum, India, December 18-21, 2005. Title: Triphala, an anti cancer ayurvedic drug enhanced apoptosis in -irradiated MCF-7 cells.

5. 6.

7. 8.

INVITED LECTURES - OFF CAMPUS:

1. 2. 3. 4. Interview talk at University of Texas Southwestern medical School- 06/16/10 Interview talk at Washington University School of Medicine at St. Louis-07/06/10 Interview talk at University of Tennessee Health Science Centre- 07/21/10 Faculty interview talk at Homi Bhabha Centre for Science Education, TIFR, Mumbai- 10/18/13

OTHER ACTIVITIES:
Facilitator: Expanding Your Horizons to encourage young women to pur sue science, technology, engineering, and mathematics (STEM) careers. Volunteer at SOURCE, Johns Hopkins School of Public Health community outreach program to renovate a school in East Baltimore neighborhood. Volunteering as an exhibit guide to help visitors appreciate and understand the wildlife and natural environment we share with fellow beings through the exhibits at the National Aquarium at Baltimore.

SELECTED ABSTRACTS FROM PEER-REVIEWED PUBLICATIONS:

Epigenetic Alterations by DNA Methylation in House-dust- mite Induced Airway Hyperresponsiveness. Am. J. Respir. Cell Mol. Biol., 2013 (In Press). PMID: 23526225 Yan S, Das ST, Richard R, Sham JSK, Mitzner W and Tang WY. Asthma is one of the most prevalent chronic lung diseases affecting 235 millions of individuals around the world, with its related morbidity and mortality increased steadily over the last 20 years. Exposure to the environmental allergen, house-dust-mite (HDM), results in airway inflammation with a variable degree of airway obstruction. Although there has been much experimental work in the past using HDM-challenge models to understand mechanistic details in allergic inflammation and airway hyperresponsiveness (AHR), there has been no study on reprogramming of lung or airways mediated through epigenetic mechanisms in response to an acute HDM exposure. Male mice, 6-weeks of age, were administrated with HDM extracts or saline at Day 1, 14 and 21. Exposure of mice to HDM extracts caused significant airway inflammation and increased AHR. These HDM-challenged mice also exhibited a change in global DNA methylation as compared with saline-exposed (control) mice. Next, by employing Methylation Sensitive Restriction Fingerprinting (MSRF), we identified a set of genes, showing aberrant methylation status, associated with the HDM-induced AHR. These candidate genes are known to be involved in cAMP signaling (pde4d), Aktsignaling (akt1s1), ion transport (tm6sf1, pom121l2 and slc8a3) and fatty acid metabolism (acsl3). Slc8a3 and acsl3 were downregulated while pde4d, akt1s1, tm6sf1, and pom121l2 were upregulated in the mice exposed to HDM. Our results, hence, suggest that HDM exposure induces a series of aberrant methylated genes that are potentially important for the development of allergic AHR. Twist1 suppresses senescence programs and thereby accelerates and maintains mutant Kras-induced lung tumorigenesis. PLoS Genetics, 2012-8(5):e1002650. PMID: 22654667. Tran PT, Shroff EH, Burns TF, Thijagarajan S, Das ST, Zabuawala T, Chen J, Cho Y-J, Luong R, Tamayo P, Salih T, Aziz K, Adam SJ, Vicent S, Nielsen CH, Withofs N, Sweet-Cordero A, Gambhir SS, Rudin CM and Felsher DW. KRAS mutant lung cancers are generally refractory to chemotherapy as well targeted agents. To date, the identification of drugs to therapeutically inhibit K-RAS have been unsuccessful, suggesting that other approaches are required. We demonstrate in both a novel transgenic mutant Kras lung cancer mouse model and in human lung tumors that the inhibition of Twist1 restores a senescence program inducing the loss of a neoplastic phenotype. The Twist1 gene encodes for a transcription factor that is essential during embryogenesis. Twist1 has been suggested to play an important role during tumor progression. However, there is no in vivo evidence that Twist1 plays a role in autochthonous tumorigenesis. Through two novel transgenic mouse models, we show that Twist1 cooperates with Kras(G12D) to markedly accelerate lung tumorigenesis by abrogating cellular senescence programs and promoting the progression from benign adenomas to adenocarcinomas. Moreover, the suppression of Twist1 to physiological levels is sufficient to cause Kras mutant lung tumors to undergo senescence and lose their neoplastic features. Finally, we analyzed more than 500 human tumors to demonstrate that TWIST1 is frequently overexpressed in primary human lung tumors. The suppression of TWIST1 in human lung cancer cells also induced cellular senescence. Hence, TWIST1 is a critical regulator of cellular senescence programs, and the suppression of TWIST1 in human tumors may be an effective example of pro-senescence therapy. Application of carbon monoxide diffusing capacity in the mouse lung . J Appl Physiol. 2011; 110(5):1455-9. PMID: 21310888. Fallica J, Das ST, Horton M, and Mitzner W. In the past decade the mouse has become the primary animal model of a variety of lung diseases. To assess various mechanisms underlying such pathologies, it is essential to make functional measurements that can reflect the developing pathology. In this regard, the diffusing capacity for carbon monoxide is a variable that directly reflects structural changes in the lung. Although measurement of single-breath diffusing capacity of the lung for carbon monoxide (DL(CO)) has also been previously reported in mice by a number of investigators, a number of technical issues have precluded routine and widespread use of this metric in mouse models. In the present report, we describe a means to quickly and simply measure a dimensionless variable closely related to the DL(CO) in mice, termed a diffusion factor for carbon monoxide (DF(CO)). The DF(CO) procedure involves a 9-s lung inflation with tracer gases in an anesthetized mouse, followed by a 1-min gas analysis time. We have tested the approach with two common models of lung pathology, elastase-induced emphysema and bleomycin-induced fibrosis. Results show a significant

15% reduction in DF(CO) in emphysema, and a 41% reduction in the fibrosis model. Repeat measurements within a mouse were found to be highly reproducible. This pulmonary function test can thus be used to detect structural changes with these pathological models. The method can also be used to measure changes in pulmonary blood volume, since the uptake of CO is highly dependent on this variable in addition to the gas exchange surface area. Monomeric and dimeric CXCL8 are both essential for in vivo neutrophil recruitment . PLoS ONE, 2010- 5(7): e11754. Das ST, Rajagopalan L, Guerrero-Plata A, Sai J, Richmond A, Garofalo RP, and Rajarathnam K. Rapid mobilization of neutrophils from vasculature to the site of bacterial/viral infections and tissue injury is a critical step in successful resolution of inflammation. The chemokine CXCL8 plays a central role in recruiting neutrophils. A characteristic feature of CXCL8 is its ability to reversibly exist as both monomers and dimers, but whether both forms exist in vivo, and if so, the relevance of each form for in vivo function is not known. In this study, using a 'trapped' non-associating monomer and a nondissociating dimer, we show that (i) wild type (WT) CXCL8 exists as both monomers and dimers, (ii) the in vivo recruitment profiles of the monomer, dimer, and WT are distinctly different, and (iii) the dimer is essential for initial robust recruitment and the WT is most active for sustained recruitment. Using a microfluidic device, we also observe that recruitment is not only dependent on the total amount of CXCL8 but also on the steepness of the gradient, and the gradients created by different CXCL8 variants elicit different neutrophil migratory responses. CXCL8 mediates its function by binding to CXCR2 receptor on neutrophils and glycosaminoglycans (GAGs) on endothelial cells. On the basis of our data, we propose that dynamic equilibrium between CXCL8 monomers and dimers and their differential binding to CXCR2 and GAGs mediates and regulates in vivo neutrophil recruitment. Our finding that both CXCL8 monomer and dimer are functional in vivo is novel, and indicates that the CXCL8 monomer-dimer equilibrium and neutrophil recruitment are intimately linked in health and disease. Probing the role of CXC motif in chemokine CXCL8 for high affinity binding and activation of CXCR1 and CXCR2 receptors. J Biol Chem. 2010; 285(38): 29262-9. PMID: 20630874. Joseph PR, Sarmiento JM, Mishra AK, Das ST, Garofalo RP, Navarro J, Rajarathnam K. All chemokines share a common structural scaffold that mediate a remarkable variety of functions from immune surveillance to organogenesis. Chemokines are classified as CXC or CC on the basis of conserved cysteines, and the two subclasses bind distinct sets of GPCR class of receptors and also have markedly different quaternary structures, suggesting that the CXC/CC motif plays a prominent role in both structure and function. For both classes, receptor activation involves interactions between chemokine Nloop and receptor N-domain residues (Site-I), and between chemokine N-terminal and receptor extracellular/transmembrane residues (Site-II). We engineered a CC variant (labeled as CC-CXCL8) of the chemokine CXCL8 by deleting residue X (CXC CC), and found its structure is essentially similar to WT. In stark contrast, CC-CXCL8 bound poorly to its cognate receptors CXCR1 and CXCR2 (K(i) > 1 m). Further, CC-CXCL8 failed to mobilize Ca(2+) in CXCR2-expressing HL-60 cells or recruit neutrophils in a mouse lung model. However, most interestingly, CC-CXCL8 mobilizes Ca(2+) in neutrophils and in CXCR1expressing HL-60 cells. Compared with the WT, CC-CXCL8 binds CXCR1 N-domain with only 5-fold lower affinity indicating that the weak binding to intact CXCR1 must be due to its weak binding at Site-II. Nevertheless, this level of binding is sufficient for receptor activation indicating that affinity and activity are separable functions. We propose that the CXC motif functions as a conformational switch that couples Site-I and Site-II interactions for both receptors, and that this coupling is critical for high affinity binding but differentially regulates activation. Protection against radiation oxidative damage in mice by triphala. Mutation Res. 2006; 609: 17. PMID: 16860592. Sandhya T, Lathika KM, Pandey BN, Bhilwade HN, Chaubey RC, Priyadarsini KI, and Mishra KP. Protection against whole body gamma-irradiation (WBI) of Swiss mice orally fed with Triphala (TPL), an Ayurvedic formulation, in terms of mortality of irradiated animals as well as DNA damage at cellular level has been investigated. It was found that radiation induced mortality was reduced by 60% in mice fed with TPL (1g/kg body weight/day) orally for 7 days prior to WBI at 7.5 Gy followed by post-irradiation feeding for 7 days. An increase in xanthine oxidoreductase activity and decrease in superoxide dismutase activity was observed in the intestine of mice exposed to WBI, which, however, reverted back to those levels of sham-irradiated controls, when animals were fed with TPL for 7 days prior to irradiation. These data have suggested the prevention of oxidative damage caused by whole body radiation exposure after feeding of animals with TPL. To further understand the mechanisms involved, the magnitude of DNA damage was studied by single cell gel electrophoresis (SCGE) in blood leukocytes and splenocytes obtained from either control animals or those fed with TPL for 7 days followed by irradiation. Compared to irradiated animals without administering TPL, the mean tail length was reduced about three-fold in blood leukocytes of animals fed with TPL prior to irradiation. Although, similar protection was observed in splenocytes of TPL fed animals, the magnitude of prevention of DNA damage was significantly higher than that observed in leukocytes. It has been concluded that TPL protected whole body irradiated mice and TPL induced protection was mediated through inhibition of oxidative damage in cells and organs. TPL seems to have potential to develop into a novel herbal radio-protector for practical applications. Cytotoxic response of breast cancer cell lines, MCF 7 and T 47 D to TPL and its modification by antioxidants . Cancer Lett. 2005; 238: 304. PMID: 16135398.

Sandhya T and Mishra KP. The cytotoxic effects of Triphala (TPL), an Indian Ayurvedic formulation with known anti-cancer properties, has been investigated on two human breast cancer cell lines differing in their p53 status. In vitro studies showed that MCF 7 with wild type p53 was more sensitive to TPL than T 47 D, which is p53 negative. TPL induced loss of cell viability was determined by MTT assay. After 72h incubation, the IC 50 values for MCF 7 was found to be approximately 8microg/ml and that for T 47 D was approximately 26microg/ml. Moreover, TPL inhibited the clonogenic growth of MCF 7 cells, which was significantly recovered by pifithrin-alpha, the p53 inhibitor. However, pifithrin-alpha, did not modify TPL induced cytotoxicity in T 47 D cells. Exogenous addition of antioxidants, glutathione (GSH) and N-Acetyl-Cysteine (NAC) inhibited the anti-proliferative ability of TPL in both MCF 7 and T47 D. Annexin-V and propidium iodide double staining of cells treated with TPL for 2h revealed that TPL induced significant apoptosis in both the cell lines in a dose dependant manner but magnitude of apoptosis was significantly higher in MCF 7 than in T 47-D cells. TPL was also found to induce dose and time dependent increase in intracellular reactive oxygen species in both the cell lines. Present results have demonstrated that MCF 7 and T 47 D cells exhibited differential sensitivity to TPL, which seems to be dependant on their p53 status. Inhibition of anti-proliferative ability of TPL by antioxidants suggests a role for TPL induced ROS in the induction of apoptosis. It is concluded that p53 status of cancer cells formed an important factor in predicting the response of cancer cells to prooxidant drugs. Potential of traditional ayurvedic formulation, TPL, as a novel anticancer drug . Cancer Lett. 2005; 231: 206. PMID: 15899544. Sandhya T, Lathika KM, Pandey BN, Mishra KP. The cytotoxic effects of aqueous extract of Triphala, an ayurvedic formulation, were investigated on human breast cancer cell line (MCF-7) and a transplantable mouse thymic lymphoma (barcl-95). The viability of treated cells was found to decrease with the increasing concentrations of Triphala. On the other hand, treatment of normal breast epithelial cells, MCF-10 F, human peripheral blood mononuclear cells, mouse liver and spleen cells, with similar concentrations of Triphala did not affect their cytotoxicity significantly. The drug treatment was found to induce apoptosis in MCF-7 and barcl-95 cells in vitro as determined by annexin-V fluorescence and proportion of apoptotic cells was found dependent on Triphala concentration. MCF-7 cells treated with Triphala when subjected to single cell gel electrophoresis, revealed a pattern of DNA damage, characteristic of apoptosis. Studies on Triphala treated MCF-7 and barcl-95 cells showed significant increase in intracellular reactive oxygen species (ROS) in a concentration dependent manner. ROS increase was, however, found to be insignificant in MCF-10 F as well as in murine spleen and liver normal cells. In vivo, direct oral feeding of Triphala to mice (40 mg/kg body weight) transplanted with barcl-95 produced significant reduction in tumor growth as evaluated by tumor volume measurement. It was also found that apoptosis was significantly higher in the excised tumor tissue of Triphala fed mice as compared to the control, suggesting the involvement of apoptosis in tumor growth reduction. These results suggest that Triphala possessed ability to induce cytotoxicity in tumor cells but spared the normal cells. The differential effect of Triphala on normal and tumor cells seems to be related to its ability to evoke differential response in intracellular ROS generation. The differential response of normal and tumor cells to Triphala in vitro and the substantial regression of transplanted tumor in mice fed with Triphala points to its potential use as an anticancer drug for clinical treatment.