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Prevention is the ultimate approach to controlling cancer. The most promising approach is to focus on earliest manifestations of cancer. Pre-malignancies may display simpler genomic aberrations that can increase the likelihood of pinpointing targets for transformational therapies. Prevention efforts require a thorough understanding of the mechanism of carcinogenesis. Knowledge of the molecular basis of carcinogenesis is critical, elucidating signaling, metabolic pathways and defining genetic progression models. 

The use of this knowledge by transdisciplinary scientists to use natural, synthetic, or biologic agents and vaccines to inhibit or reverse pre-invasive or early stage carcinogenesis is called Cancer Chemoprevention

Cancer chemoprevention is the active way of combating cancer and carcinogenesis at earlier and earlier stages. The aims of the Cancer Chemoprevention initiative is to produce regression of prevalent precursors of cancer, suppress recurrent precursors and prevent incident precursors and/or cancer.

Since its establishment as a research interest group at Moffitt Cancer Center in 2010, this initiative has identified and tested several novel agents and combinations in laboratory and early human trials, publishing study results in leading scientific journals and receiving over 10 million in research funding from the National Institute of Health/National Cancer Institute.

The identification of chemopreventive agents holds tremendous promise in reducing the burden of cancer. Our experience from past trials of preventive agents offers important lessons that can inform the design and conduct of future trials. Trials of the past have clearly demonstrated the (a) need for more preclinical and early phase work before undertaking phase III trials; (b) imperative for broad, sensitive toxicological and human safety assessments; (c) safety can be improved in iterative generations of agents and trials; (d) synergy between agents can lead to lower doses, improved efficacy and fewer or less severe toxicities. Regarding cohorts, we have learned there are substantial benefits to employing germline, familial, or increased-risk cohorts, including, among others, more power over a shorter time frame. An assessment of endpoints in trials resulting in approval of a preventive agent reveals that nearly all have been approved on the basis of intraepithelial neoplasia, particularly in accessible organs. Lessons gleaned regarding the overall design of clinical trials underscore the importance of the randomized, placebo-controlled design and the need for long-term follow-up and monitoring to meet FDA requirements and promote acceptance in the marketplace.  


(a) Research:
In support of this mission and capitalizing on the transdisciplinary strengths of its members, the Cancer Chemoprevention initiative at the Moffitt Cancer Center will utilize a systematic, broad spectrum approach to:

  • Identify, characterize and develop agents that can modulate carcinogenesis for cancer chemoprevention and evaluate the safety, efficacy and mechanisms of action using in vitro and preclinical models.
  • Evaluate these agents for safety, efficacy in translational clinical trials targeting populations at risk due to exposure to carcinogenic agents, familial and genetic predisposition, or due to the presence of premalignant lesions, while validating intermediate end points of carcinogenesis and correlate these with clinical endpoints.

(b) Professional and Public Education
In addition to research, the Cancer Chemoprevention initiative disseminates current and authoritative information to patients, public, and health professionals towards integrating findings into evidence-based clinical practice. 



Our initiative is a member of two major National Cancer Institute Consortia:

Phase 0/I/II Cancer Prevention Clinical Trials Program (Consortia) The Division of Cancer Prevention conducts systematic early clinical development of promising preventive agents through its Phase 0/I/II Cancer Prevention Clinical Trials Program, also known as the Consortia for Early Phase Prevention Trials. Cancer prevention drug discovery is identifying many new agents, including an increasing number of agents that intervene in specific molecular pathways thought to be critical to cancer development.

The ECOG-ACRIN Cancer Research Group is a multidisciplinary, membership-based scientific organization that designs and conducts biomarker-driven cancer research involving adults who have or are at risk of developing cancer. The Group is dedicated to its stated purpose, which is to achieve research advances in all aspects of cancer care and thereby reduce the burden of cancer and improve the quality of life and survival in patients with cancer. ECOG-ACRIN is supported primarily through research grant funding from the National Cancer Institute. 


1R01 CA122060-Supplement   Kumar NB (PI)

National Institute of Health/National Cancer Institute

A Phase II Clinical trial of Polyphenon E in Prostate Cancer.

1R01CA129227-01A1   Malafa, M (PI)

National Institute of Health / National Cancer Institute.

Intervention of Pancreatic Oncogenic Pathways with Dietary Tocotrienol

1P20 MD003375-01   Kumar NB (Study Chair)

National Institute of Health /National Center on Minority Health and Health Disparities

Phase II Clinical Trial of Purified Isoflavones in Prostate Cancer: Comparing Safety, Effectiveness and mechanism of action between African American and Caucasian men.

Prostate Cancer Chemoprevention:

Based on the initial findings of the molecular targets of green tea catechins in prostate carcinogenesis by Dr. Aslam Kazi, Dr. Kumar and her multidisciplinary team have systematically characterized Green tea catechins for prostate cancer chemoprevention.Funded by the NCI (R01 CA12060), the team proposed a novel model in which GTCs, particularly epigallocatechin-3-gallate, targets prostate carcinogenesis via six major mechanisms that work simultaneously and dependently, largely driven through proteasome inhibition- induced regulation of the NFκB pathway (Connors, et al, Nutr Cancer 2011) (R01 CA122060-Supplement).Following these studies, the research team ledby Drs. Park and Kumar, in collaboration with Drs. Chornokur and Connors demonstrated the safety and effectiveness of green tea catechins in reducing the number and size of metastatic tumors in a preclinical (TRAMP) mouse model. (Kim, et al, Cancer Prev Res 2014). With the safety of green tea catechins established in preclinical and phase I trials, an intra-and inter-programmatic research team led by Dr. Kumar in collaboration with Drs. Chornokur, Egan and Pow-Sang, Dickinson SI, Sebti S  and Quinn G recently completed a phase II randomized clinical trial (R01 CA12060; NCT00596011) that evaluated (Kumar, et al, J Clin Trials 2012) and reported (Kumar, et al, Cancer Prev Res 2015) the safety (Kumar et al. Oncotarget, 2016)  and effectiveness of a standardized green tea catechin (IND 77626) containing 400mg of epigallocatechin-3-gallate in preventing progression to prostate cancer among men diagnosed with high-grade prostatic intraepithelial neoplasia or atypical small acinar proliferation of the prostate. Although  no significant differences in prostate cancer rates between the two study arms were observed at one year, results from this trial demonstrated that among men diagnosed with high-grade prostatic intraepithelial neoplasia at baseline, a significantly fewer number of men progressed to ASAP or prostate cancer in the treatment arm compared to placebo.  This trial also demonstrated that green tea catechins lowered levels of serum prostate serum antigen and that daily intake of the standardized, decaffeinated catechin mixture over a one-year period accumulated in plasma and was well tolerated. This is the first botanical agent that has shown promise in modulating early stages of  prostate carcinogenesis.

Based on these findings, we have now proposed a national trial of Green tea catechins in preventing clinical progression of prostate cancer in men on active surveillance to the National Cancer Institute-ECOG-ACRIN. The study has undergone review by the ECOG-ACRIN Prevention and Early Detection as well as the genitourinary cancer committee and early Modalities subcommittee and has received enthusiastic support.

Other agents currently under evaluation include isoflavones. Using a molecular mechanism targeted approach, Dr. Kumar and her team [Drs. Pow-Sang J, Spiess PE (CBMM), Connors S, Chornukur G (CE), Bai W (CBMM)](P20 MD003375-01: NCT01036321) have completed a phase II trial examining isoflavones ( IND 61949) for prostate cancer chemoprevention, comparing response to intervention in African American men compared to Caucasian men ( Kumar et al., J Cancer Sci Ther. 2012). However, findings need to be validated in future, well-powered clinical trials.

Pancreatic Cancer Chemoprevention:

Pancreatic cancer is one of the most lethal cancers in the United States, ranking fourth among the leading causes of cancer-related deaths. Despite treatment developments, the death rate for patients with pancreatic cancer has overall remained unchanged for decades. Investigations into novel therapies and chemopreventive agents are clearly warranted.

Dr. Malafa and his team have evaluated agents including Vitamins -Tocotrienols (1R01CA129227-01A1) that are found in cereal grains that have been found to have been shown to have antitumor activity.  Tocotrienols are a group of four (α-, β-, δ-, γ-) unsaturated, naturally occurring vitamin E compounds that not only inhibit the proliferation of a variety of human tumor cells, including breast, colon, lung, and hepatocellular, but also exhibit chemopreventive properties. Dr. Malafa and his team  previously demonstrated that δ-tocotrienol exhibits the most potent anti-tumor activity among the four tocotrienol isoforms in pancreatic cancer cells. They demonstrated that δ-tocotrienol exerted significant cell growth inhibition pancreatic ductal cancer (PDCA) cells without affecting normal human pancreatic ductal epithelial cell growth. They also showed that δ-tocotrienol-induced growth inhibition occurred concomitantly with G1 cell-cycle arrest and increased p27Kip1 nuclear accumulation. This finding is significant considering that loss of nuclear p27Kip1 expression is a well-established adverse prognostic factor in PDCA. Furthermore, δ-tocotrienol inactivated RAF-MEK-ERK signaling, a pathway known to suppress p27Kip1 expression. To determine whether p27Kip1 induction is required for δ-tocotrienol inhibition of PDCA cell proliferation, we stably silenced the CDKN1B gene, encoding p27Kip1, in MIAPaCa-2 PDCA cells and demonstrated that p27Kip1 silencing suppressed cell-cycle arrest induced by δ-tocotrienol. Furthermore, δ-tocotrienol induced p27Kip1 mRNA expression but not its protein degradation. p27Kip1 gene promoter activity was induced by δ-tocotrienol through the promoter's E2F-1 binding site, and this activity was attenuated by E2F-1 depletion using E2F-1 small interfering RNA. Finally, decreased proliferation, mediated by Ki67 and p27Kip1 expression by δ-tocotrienol, was confirmed in vivo in a nude mouse xenograft pancreatic cancer model. (Hodal PJ et al , PLoS One. 2013; Husain C et al. Carcinogenesis. 2013;  Husain C et al. Cancer Prev Res (Phila). 2013; Wang C et al.  J Nutr Biochem. 2015)

These findings reveal a new mechanism, dependent on p27Kip1 induction, by which δ-tocotrienol can inhibit proliferation in PDCA cells, providing a new rationale for p27Kip1 as a biomarker for δ-tocotrienol efficacy in pancreatic cancer prevention and therapy.

Based on these findings, Dr. Malafa and his team completed a phase I dose-escalation clinical trial in pancreatic cancer patients, preliminary findings revealed that δ-tocotrienol had no obvious toxicity at up to 3200 mg/day, which is 5 times the predicted biologically active clinical dose (Springett GM et al EBioMedicine. 2015). These findings underscore the promise of δ-tocotrienol for pancreatic cancer intervention.

These studies are some of the first studies to show promise of the safety, effectiveness and mechanism which δ-tocotrienol can modulate pancreatic carcinogenesis to be further translated to early phase clinical trials. 

Lung Cancer Chemoprevention:

Currently, approaches to reduce lung cancer morality in these high risk populations include, screening using low dose CT (LDCT) for early detections and aggressively pursuing tobacco control and smoking cessation programs to improve lung cancer mortality. There are no chemoprevention strategies that are implemented in this high risk population of former smokers and populations on active surveillance who report anxiety, aware of their high risk  and eager to further reduce their lung cancer risk. 

We first examined the role of evaluated enzastaurin (Gray JE et al, Cancer 2013), a selective PKC-β inhibitor with antiproliferative and proapoptotic properties in former smokers (U01-CA10122, P50-CA119997 Bepler G). In pretrial investigations, we established the rationale for PKC-β inhibition and pathway interrogation in premalignant lesions and early stage lung cancer. In the intent-to-treat analysis, of 40 subjects randomized, there was no significant difference in the pre/post-treatment change of the Ki-67 LI between the enzastaurin and placebo groups (p = 0.53). Six subjects discontinued enzastaurin (n=4, AEs: abdominal distension, DVT, hyponatremia, and rash; n=2, subject decision) and one placebo (noncompliance). Two subjects had ≥1 serious AEs (bradycardia, DVT, and hypotension).  This represents the first chemoprevention trial with a non-FDA-approved, oral, small-molecule targeted agent. Although the primary endpoint was not met, enzastaurin was found to be tolerable for 6 months by 75% of subjects with a suggestion of response in a subset analysis restricted to metaplastic or dysplastic lesions.

We and others have shown that curcumin (CUR), a fat soluble compound and ω-3 fatty acids (omega 3 fatty acids) as well as when combined with piperine are effective at suppressing Stat3P a and NF-κB signaling pathways relevant to lung carcinogenesis and  suppresses proliferation of human lung tumor lines (adenocarcinoma and squamous cell carcinoma) and inflammation responses.

In our previously published work in lung cancer derived adenocarcinoma cell lines (5) and our recently findings demonstrate that curcuminoid C3 complex and CURPERINE (CUR+piperine) significantly suppresses Stat3 phosphorylation and reduces proliferation of two lung SCC lines (H157 and H2170) in a dose-dependent manner. We also observed that CUR as well as CURPERINE suppresses inflammation pathways (interleukins and NF-κB) in lung SCC and adenocarcinoma lines and modulates inflammatory cytokines in human lung tumor cells. Both H157 squamous and H322 adenocarcinoma cell lines constitutively release high levels of IL6 and IL8, and CURPERINE causes a dose-dependent suppression. In recent preclinical studies, including in rodent models, we and others have shown that CUR reduces Stat3-P and proliferative markers such as CycD1 and Mcm2, in mice lung tissues. In addition, CUR suppresses cigarette smoking-induced NF-κB activation and downstream gene expression in human non-small cell lung carcinoma cells by inhibiting IkB-α kinase.

More recently, evidence from cell lines, animal studies and early studies in humans has provided strong evidence of the role and mechanism of  ω-3 FA as  specialized fat mediators, with anti-inflammatory, anti-proliferative and pro-resolving properties towards resolution of cigarette smoke-induced lung inflammation in former smokers. Recent evidence has demonstrated that the when CUR which is fat soluble is available in the lung tissue when combined with ω-3 FA.

Based on this evidence, we have proposed 2 clinical trials to evaluate the safety and effectiveness of (a) CUR C3 complex® with Bioperine® (a combination we have developed and tested in preclinical and in vitro studies, CURPERINE) targeting populations at high risk for lung cancer and CUR C3 complex® + ω-3fatty acids  in asymptomatic former smokers with lung nodules detected during LDCT screening (Lung RADS 3). Results of the proposed trial may benefit former and current smokers, including those who are on surveillance using LDCT and other high-risk populations towards lung cancer prevention. The proposed studies are clearly related to reducing tobacco-related lung cancer risk. 


Nagi B. Kumar, Ph.D.Nagi B. Kumar, Ph.D.Professor in the Division of Oncologic Sciences at the USF College of Medicine and Senior member, Population Sciences Division and Director of Cancer Chemoprevention at the Moffitt Cancer Center.  As founding member/Director of Cancer Chemoprevention at Moffitt,  Kumar has forged collaborations with investigators in basic, population and clinical sciences, laying the foundation to develop a program to accelerate  chemoprevention agent development and validation at the Moffitt Cancer Center for cancer prevention and treatment. Using a multi-disciplinary science-based approach and the rigor with which we test other therapeutic agents, Dr. Kumar and her team have initiated several epidemiological, laboratory, preclinical and phase I-II clinical trials evaluating safety, effectiveness and potential molecular targets of several nutritional components including isoflavones, lycopene, green tea polyphenols, tannic acid, n-3 fatty acids, metformin, anthocyanins, curcumin and combination agents for cancer chemoprevention, in addition to multimodal interventions to characterize and ameliorate symptoms of hypothyroidism, cancer cachexia and cognitive impairment. The multi-institutional clinical trials that Kumar has led include: (a) Phase II, Randomized, Double-blind, Multi-centered Study of Polyphenon E in Men with High-grade Prostatic Intraepithelial Neoplasia (NCI R01 CA12060-01A1); (b) Phase II Clinical Trial of Purified Isoflavones in Prostate Cancer: Comparing Safety, Effectiveness and mechanism of action between African American and Caucasian men (NIH 1 P20 MD003375-01).    She has completed: (a) A Randomized Pilot Clinical Trial of the Action of Isoflavones and Lycopene in Localized prostate cancer (CaP): Administration Prior to Radical Prostatectomy, and; (b) The Specific Role of Isoflavones in Reducing CaP Risk. (NCI – UI0 CA81920A) and phase II trials of evaluating isoflavone in modulating hormonal and proliferative markers in breast and prostate cancers (NCI R03 CA72588-01A1). Dr. Kumar is the site PI of the Phase 0/I/II Cancer Prevention Clinical Trials Program (Consortia) and serves on the Prevention Committee of the ECOG-ACRIN Cancer Research Group.

Mokenge Malafa, MDMokenge Malafa, MD, Senior Member, and Head of the section of Pancreatic Oncology GI Oncology:   Dr. Mokenge Malafa is head of the section of Pancreatic Oncology within the Gastrointestinal Oncology Program at Moffitt Cancer Center. He is an associate professor in the Department of Oncologic Sciences at the University of South Florida Morsani College of Medicine. Dr. Malafa’s research interest focuses on pancreatic cancer, in particular the discovery, identification and characterization of the role of novel agents, including metformin and  Vitamins, specifically, bioactive vitamin E compounds in regulating biological processes in cancer cells. Dr. Malafa has led  a series of laboratory and preclinical studies identify the targeted signal transduction pathways of vitamin E δ-tocotrienol in pancreatic carcinogenesis as well as preclinical studies in transgenic mouse model of pancreatic cancer. His team also completed a Phase I Safety, Pharmacokinetic, and Pharmacodynamic Presurgical Trial of Vitamin E δ-tocotrienol in Patients with Pancreatic Ductal Neoplasia.

Dr. Jhanelle GrayJhanelle Gray, MD, Associate Member, Thoracic Oncology. Dr. Gray’s research focuses on the analysis of targeted therapies in patients with non-small cell lung cancer (NSCLC) and those at risk for lung cancer with hopes of optimizing the therapeutic benefit while minimizing the toxicity with the use of biomarker analysis to enhance the understanding of cancer biology and treatment. She was the principal investigator of a phase IIB randomized, placebo-controlled, double-blind study of enzastaurin (a protein kinase C inhibitor), investigating its efficacy in lung cancer prevention in former smokers (Gray JE et al, Cancer 2013). Through her continued work on this project, she was awarded an NIH Specialized Program of Research Excellence (SPORE) supplement grant (Research Supplements to Promote Diversity in Health-Related Research). Dr. Gray has served as co-investigator in the series of laboratory and preclinical studies identify the targeted signal transduction pathways of curcumin and piperine in lung  carcinogenesis(Alexandrow MG et al., E J Cancer Prev). Additional  chemoprevention trials include curcumin + ω-3 fatty acids for lung cancer chemoprevention in former smokers  with lung nodules.

Mark Alexandrow, Ph.D.Mark Alexandrow, Ph.D., Associate Member, Cancer Biology: The research in Dr. Alexandrow's laboratory is focused on two central areas: (1) the mechanisms by which positive growth factor signals or inhibitory TGF-beta signals regulate the assembly and function of pre-(DNA) Replication Complexes (preRCs) in late G1 phase, and (2) how the DNA replication machinery and preRCs utilize chromatin remodeling complexes to gain access to the DNA substrate during late G1 and S-phase. The preRC is composed of multiple protein subunits that assemble in a stepwise and tightly regulated manner: Origin Recognition Complex (ORC), Cdc6, Cdt1, and the Mini-Chromosome Maintenance (MCM) helicase. After this forms, other proteins are recruited, including Cdc45, Mcm10, PCNA, and DNA polymerases. At G1/S, this complex is triggered and S-phase begins. However, very little is known in mammalian cells regarding how preRC assembly is regulated at the molecular level, how growth factors modulate preRC assembly, and how preRC activation is triggered at G1/S by cell cycle factors such as cyclin-dependent kinases. Furthermore, there is little knowledge of how the regulation of preRC assembly and activation is deregulated in cancer cells. Loss of control over MCM loading and activation is known to lead to re-replication within one cell cycle, producing genomic instability that contributes to tumorigenesis, and this concept provides a strong argument for understanding the molecular and biochemical events that govern preRC dynamics. The long term goal of this research is not only to understand the regulation of preRC function and assembly in late G1, but also to identify novel protein-protein interactions and key regulatory steps that might serve as useful targets for small molecule drug design/intervention for the treatment of cancer.  Dr. Alexandrow works closely with clinical chemoprevention faculty, first with Dr. Gerold Bepler and now with Dr. Nagi Kumar on lung cancer chemoprevention studies.  He completed and published the first phase 2 randomized study of enzastaurin (LY317615) for lung cancer prevention in former smokers (Gray JE et al, Cancer 2013).  Dr. Alexandrow has led the series of laboratory and preclinical studies identify the targeted signal transduction pathways of curcumin and piperine in lung  carcinogenesis (Alexandrow MG et al., E J Cancer Prev). Additional  chemoprevention trials include curcumin + ω-3 fatty acids for lung cancer chemoprevention in former smokers  with lung nodules and sulfoaphane for secondary prevention of bladder cancer. 

Relevant Publications:

  • Kazi A, Daniel KG, Smith DM, Kumar NB, Dou QP. Inhibition of the proteasome activity, a novel mechanism associated with the tumor cell apoptosis-inducing ability of genistein. Biochem Pharmacol. 2003 Sep 15;66(6):965-76.  PMID: 12963483.
  • Kazi A, Urbizu DA, Kuhn DJ, Acebo AL, Jackson ER, Greenfelder GP, Kumar NB, Dou QP. A natural musaceas plant extract inhibits proteasome activity and induces apoptosis selectively in human tumor and transformed, but not normal and non-transformed, cells. Int J Mol Med. 2003 Dec;12(6):879-87.  PMID: 14612961.
  • Kumar NB, Cantor A, Allen K, Riccardi D, Besterman-Dahan K, Seigne J, Helal M, Salup R, Pow-Sang J. The specific role of isoflavones in reducing prostate cancer risk. Prostate. 2004 May 1;59(2):141-7.  PMID: 15042614.
  • Moyers SB, Kumar NB. Green tea polyphenols and cancer chemoprevention: multiple mechanisms and endpoints for phase II trials. Nutr Rev. 2004 May;62(5):204-11. Review.  PMID: 15212320.
  • Kumar N, Allen K, Riccardi D, Kazi A, Heine J. Isoflavones in breast cancer chemoprevention: where do we go from here? Front Biosci. 2004 Sep 1;9:2927-34. Review. PMID: 15353326.
  • Kumar NB. Green Tea Polyphenols (GT): Promising Substances for Prostate Cancer Chemoprevention. JEBIM. 2005; 2:1.
  • Kumar N, Shibata D, Helm J, Coppola D, Malafa M. Green tea polyphenols in the prevention of colon cancer. Front Biosci. 2007 Jan 1;12:2309-15. Review.  PMID: 17127241.
  • Kumar NB, Krischer JP, Allen K, Riccardi D, Besterman-Dahan K, Salup R, Kang L, Xu P, Pow-Sang J. Safety of purified isoflavones in men with clinically localized prostate cancer. Nutr Cancer. 2007;59(2):169-75.  PMID: 18001211;   PMCID: PMC2442460.
  • Kumar NB, Krischer JP, Allen K, Riccardi D, Besterman-Dahan K, Salup R, Kang L, Xu P, Pow-Sang J. A Phase II randomized, placebo-controlled clinical trial of purified isoflavones in modulating steroid hormones in men diagnosed with localized prostate cancer. Nutr Cancer. 2007;59(2):163-8.  PMID: 18001210;   PMCID: PMC2435485.
  • Dahan K, Fennal M, Kumar NB. Lycopene in the prevention of prostate cancer. J Soc Integr Oncol. 2008 Winter;6(1):29-36. Review.  PMID: 18302908.
  • Kumar NB, Besterman-Dahan K, Kang L, Pow-Sang J, Xu P, Allen K, Riccardi D, Krischer JP. Results of a Randomized Clinical Trial of the Action of Several Doses of Lycopene in Localized Prostate Cancer: Administration Prior to Radical Prostatectomy. Clin Med Urol. 2008 Apr 16;1:1-14.  PMID: 20354574;   PMCID: PMC2846655.
  • Kumar N, Titus-Ernstoff L, Newcomb PA, Trentham-Dietz A, Anic G, Egan KM. Tea consumption and risk of breast cancer. Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):341-5. doi: 10.1158/1055-9965.EPI-08-0819. PMID: 19124518;   PMCID: PMC3156033.
  • Kumar NB, Kang L, Pow-Sang J, Xu P, Allen K, Riccardi D, Besterman-Dahan K, Krischer JP. Results of a randomized phase I dose-finding trial of several doses of isoflavones in men with localized prostate cancer: administration prior to radical prostatectomy. J Soc Integr Oncol. 2010 Winter;8(1):3-13.  PMID: 20205984;   PMCID: PMC3277948.
  • Kumar NB, Kazi A, Smith T, Crocker T, Yu D, Reich RR, Reddy K, Hastings S, Exterman M, Balducci L, Dalton K, Bepler G. Cancer cachexia: traditional therapies and novel molecular mechanism-based approaches to treatment. Curr Treat Options Oncol. 2010 Dec;11(3-4):107-17. doi: 10.1007/s11864-010-0127-z. Review. PMID: 21128029;   PMCID: PMC3016925.
  • Connors SK, Chornokur G, Kumar NB. New insights into the mechanisms of green tea catechins in the chemoprevention of prostate cancer. Nutr Cancer. 2012;64(1):4-22. doi: 10.1080/01635581.2012.630158. Epub 2011 Nov 18. Review.  PMID: 22098273;   PMCID: PMC3665011.
  • Kumar N, Crocker T, Smith T, Pow-Sang J, Spiess PE, Connors S, Chornukur G, Dickinson SI, Bai W, Williams CR, Salup R, Fu W. Prostate Cancer Chemoprevention Targeting High Risk Populations: Model for Trial Design and Outcome Measures. J Cancer Sci Ther. 2012;2011(S3). pii: 007. Epub 2012 Jan 10.  PMID: 22422102;   PMCID: PMC3300067.
  • Kumar N, Crocker T, Smith T, Connors S, Pow-Sang J, Spiess PE, Egan K, Quinn G, Schell M, Sebti S, Kazi A, Chuang T, Salup R, Helal M, Zagaja G, Trabulsi E, McLarty J, Fazili T, Williams CR, Schreiber F, Anderson K. Prostate Cancer Chemoprevention Targeting Men with High-Grade Prostatic Intraepithelial Neoplasia (HGPIN) and Atypical Small Acinar Proliferation (ASAP): Model for Trial Design and Outcome Measures. J Clin Trials. 2012 Jan 21;2(1). pii: 1000105.  PMID: 24533253;   PMCID: PMC3924733.
  • Kumar N, Crocker T, Smith T, Pow-Sang J, Spiess PE, Egan K, Quinn G, Schell M, Sebti S, Kazi A, Chuang T, Salup R, Helal M, Zagaja G, Trabulsi E, McLarty J, Fazili T, Williams CR, Schreiber F, Slaton J, Anderson JK. Challenges and potential solutions to meeting accrual goals in a Phase II chemoprevention trial for prostate cancer. Contemp Clin Trials. 2012 Mar;33(2):279-85. doi: 10.1016/j.cct.2011.11.004. Epub 2011 Nov 11. PMID: 22101219;   PMCID: PMC3268882.
  • Alexandrow MG, Song LJ, Altiok S, Gray J, Haura EB, Kumar NB. Curcumin: a novel Stat3 pathway inhibitor for chemoprevention of lung cancer. Eur J Cancer Prev. 2012 Sep;21(5):407-12. doi: 10.1097/CEJ.0b013e32834ef194.  PMID: 22156994;   PMCID: PMC3319490.
  • Kumar N, Chornokur G. Molecular Targeted Therapies Using Botanicals for Prostate Cancer Chemoprevention. Transl Med (Sunnyvale). 2012 Dec 31;Suppl 2:005.  PMID: 24527269;   PMCID: PMC3920581.
  • Kumar NB, Vadaparampil ST, Mahajan N, Lilienfeld HS, Lee J, Laronga C, Hakam A, Heine JJ, Egan, KM, Arun B, Pal T.  Metformin – promising agent for chemoprevention in BRCA1 carriers. Hereditary Genetics. 2012; 1(2).   PMID:  26097796.  PMCID:PMC4474476.
  • Kumar NB, Dhurandhar M, Aggarwal B, Anant S, Daniel K, Deng G, Djeu J, Dou J, Hawk E, Jayaram B, Jia L, Joshi R, Kararala M, Karunagaran D, Kucuk O, Kumar L, Malafa M, Samathanam GJ, Sarkar F, Siddiqi M, Singh RP, Srivastava A, White JD. Proceedings of the Indo-U.S. bilateral workshop on accelerating botanicals/biologics agent development research for cancer chemoprevention, treatment, and survival. Cancer Med. 2013 Feb;2(1):108-15. PMID: 24279005;   PMCID: PMC3797562.
  • Chornokur G, Kumar NB. Prostate cancer chemoprevention in men of African descent: current state of the art and opportunities for future research. Cancer Causes Control. 2013 Aug;24(8):1465-80. doi: 10.1007/s10552-013-0241-x. Epub 2013 Jun 5. Review.  PMID: 23737026;   PMCID: PMC4184029.
  • Kim SJ, Amankwah E, Connors S, Park HY, Rincon M, Cornnell H, Chornokur G, Hashim AI, Choi J, Tsai YY, Engelman RW, Kumar N, Park JY. Safety and chemopreventive effect of Polyphenon E in preventing early and metastatic progression of prostate cancer in TRAMP mice. Cancer Prev Res (Phila). 2014 Apr;7(4):435-44. doi: 10.1158/1940-6207.CAPR-13-0427-T. Epub 2014 Feb 5. PMID: 24501325;   PMCID: PMC4123218.
  • Kumar NB, Quinn GP, Alexandrow MG, Gray J, Schell MJ, Sutton S, Haura, EB. Chemoprevention Trial Feasibility Using Botanicals in Exceptionally High Risk Populations for Lung Cancer. J Clin Trials.  2014;4:180-6. doi:10.4172/2167-0870.1000180. PMCID:  26101725.  PMCID:PMC4474484.
  • Kumar NB, Pow-Sang J, Egan KM, Spiess PE, Dickinson S, Salup R, Helal M, McLarty J, Williams CR, Schreiber D, Sebti S, Kazi A, Lang L, Quinn G, Smith T, Diaz K, Chornokur G, Crocker T, Schell MJ.  Randomized, Placebo-Controlled Trial of Green Tea Catechins for Prostate Cancer Prevention.  Cancer Prev Res (Phila).  2015;8(10):879-87. [Epub ahead of print] PMID:  258733370.  PMCID: PMC4596745. 
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