Cancer Biology Track

Faculty and Their Research Interests in Cancer Biology

Click on the faculty member’s name for a more in-depth description of their research and publications.


Ivana de la Serna, Ph.D.Ivana de la Serna, Ph.D.

Associate Professor
University Of California, Davis, 1998

In eukaryotes, DNA is packaged into chromatin, the basic unit of which is the nucleosome.  Chromatin structure plays a critical role in the regulation of gene expression by imposing topological constraints and by creating a barrier for general transcription factors and other regulators.  Dr. de la Serna studies the functional role of mammalian SWI/SNF chromatin-remodeling enzymes in the regulation of gene expression during melanocyte differentiation and to determine how SWI/SNF function is de-regulated in melanoma. The effects of DNA damage and repair pathways on chromatin remodeling are also under investigation.

Kathryn Eisenmann, Ph.D.Kathryn Eisenmann, Ph.D.

Associate Professor
University of Minnesota, Twin Cities, 2000

Research focus #1

Understanding the role of Dia-interacting protein (DIP) in modification of the cellular actin cytoskeleton and amoeboid cell movement is providing novel insights of mechanisms controlling the transition towards cell migration/invasion and metastasis by cancer cells. Dr. Eisenman's lab is using recent findings to further probe amoeboid conversion in response to CXCL12 chemokine signaling with the goal of providing novel molecular targets for alternate therapeutic avenues.

Research focus #2

At the heart of the extreme lethality of glioblastoma (GBM) is an aggressive capacity to invade into surrounding healthy tissue. Rho GTPases coordinate actin dynamics to support GBM invasion, but little is known about their downstream effectors, the mDia formins, to GBM invasion. Using small molecules that directly inhibit mDia-midiated f-actin assembly, the Eisenmann lab is exploring the role of mDia formins in GBM invasion. They have recently uncovered a role in GBM cell motility and identified a possible anti-invasive therapeutic strategy for GBM.

Research focus #3

Epithelial ovarian cancer (EOC) is a deadly disease often detected after it has metastasized within the peritoneal cavity. Multi-cellular spheroids are enriched in the ascites of EOC patients and they represent an invasive and chemoresistant cellular population fundamental to metastatic dissemination. The molecular mechanism triggering single cell invasive egress from spheroids has remained enigmatic, but the Eisenmann lab has recently discovered that multiple GTPase effectors must be suppressed to fully block invasive egress from ovarian cancer spheroids. These results indicate a possible therapeutic anti-invasive avenue for targeting these multicellular structures.

Saori Furuta, Ph.D.Saori Furuta, Ph.D.

Assistant Professor
University of California, Irvine, CA, 2007

Over 200,000 new cases of breast cancer are diagnosed in the U.S. each year, affecting 1 in 8 women in their life-time. Despite the recent advances in diagnostic tools, breast cancer mortality rate has only declined slowly, justifying the urgent need for a better diagnostic marker for a treatment success. The Furuta lab has been working to understand the primary cue that drives pre-neoplastic progression of normal breast cells. They are currently focusing on the role of nitric oxide, a gaseous signaling molecule ubiquitously produced. They have previously shown that normal mammary epithelial cells (MECs) produce a significant amount of nitric oxide when they encounter certain types of the extracellular matrix proteins, whereas breast cancer cells do not. The Furuta group has been investigating novel hypotheses within this area of research by using high-resolution imaging techniques, including second harmonies generation on multiphoton microscope, time-lapse confocal microscopy and atomic force microscopy, as well as animal studies, 3D cultures (mono and co-cultures), histological studies of clinical samples and other molecular/cell biology/biochemistry techniques.

William A. Maltese, Ph.D.William A. Maltese, Ph.D. 

Professor and Chairman 
Syracuse University, Syracuse, NY, 1977 

Current research of the Maltese lab centers on the molecular and cellular characterization of novel forms of non-apoptotic cell death and the development of novel anti-cancer agents designed to induce these forms of cell death in brain tumors. Past studies established that ectopic expression of activated forms of the Ras or Rac GTPases in glioblastoma and other types of cancer cells can trigger a unique form of cell death, involving accumulation of large cytoplasmic vacuoles, which the Maltese lab has termed "methuosis". Ongoing studies are aimed at 1) identifying the specific molecular targets of the methuosis-inducing compounds and 2) modifying the structures of these molecules to optimize their potency, pharmacokinetic properties and transport across the blood-brain barrier. Efforts are underway to define the mechanism of action of these compounds and to determine if they may have therapeutic advantages over existing microtubule-targeted chemotherapeutic agents. 

Dayanidhi Raman, B.V.Sc., Ph.D.Dayanidhi Raman, B.V.Sc., Ph.D.

Assistant Professor
Kansas State University, Manhattan, KS, 1995

Dr. Raman’s research group is focused on cell signaling, migration, local invasion and metastasis mediated by chemokine receptors CXCR2 and CXCR4 in breast cancer. Chemokine receptors are used for many normal cellular functions, however they are subverted in the tumor microenvironment to facilitate tumor progression and metastasis. His lab is currently working on elucidating the role of CXCR4 in controlling regulatory aspects of breast cancer cells. These processes are mediated through an adaptor protein called LIM and SH3 Protein 1 (LASP-1) by ligand activated CXCR4. The Raman lab has identified several key proteins that bind to nuclear LASP-1 in response to activation of CXCR4 by CXCL12 in breast cancer cells. Importantly, they have discovered that nuclear localized LASP-1 correlates inversely with patient long-term survival.

Randall J. Ruch, Ph.D.Randall J. RucH, Ph.D.

Associate Professor
Medical University of Ohio, Toledo, OH 1988

Dr, Ruch’s current research interests are to understand how gap junctions become defective in cancer cells and carcinogen-treated cells. Cells communicate with each other in many ways using secreted molecules (e.g., hormones, cytokines, growth factors, and nitric oxide), microvesicles, and direct cell contact through cellular junctions such as synapses, desmosomes, hemidesmosomes, adherens junctions, and gap junctions. Gap junction defects cause some forms of peripheral neuropathy, hereditary deafness, cardiac arrhythmia, cataracts, infertility, and skin disease, and are also involved in atherosclerosis, birth defects, and cancer.  

Cynthia M. Smas, D.Sc.Cynthia M. Smas, D.Sc.

Associate Professor 
Harvard University, Boston, MA, 1994

Obesity is now at epidemic proportions and is closely linked to co-morbidities including heart disease and diabetes. Dr. Sma’s group is studying adipogenesis and preadipocyte/adipocyte function in order to better understand and treat obesity. A particular interest of her lab is novel secreted products of adipocytes, termed adipokine. These molecules likely impact systemic physiology and as such have the potential to act as therapeutic targets in the fight against obesity and its co-morbidities. In addition, the Sma lab is investigating preadipocyte and the early stages of adipocyte lineage commitment, much of which remains to be elucidated.  By better understanding this cell type they can potentially target obesity before its formation, at the preadipocyte stage. 

Robert J. Trumbly, Ph.D. Robert J. Trumbly, Ph.D. 

University of California, Davis, CA, 1980

Dr. Trumbly’s present research focus is the use of bioinformatics, genetic, and biochemical approaches to analyze the role of transcriptional regulation in cancer, primarily prostate and breast cancer. Dr. Trumbly and colleagues have analyzed the patterns of gene expression from microarray data in prostate and breast cancer cells. In the case of prostate cancer cells, they have discovered a novel mechanism for androgen-independent growth, which involves gene activation by the androgen receptor in the absence of ligand. In a parallel result, they have found that gene activation by the unliganded estrogen receptor permits cell cycling in breast cancer cells, providing a mechanism for development of resistance to anti-estrogens.

Kandace J. Williams, Ph.D.Kandace J. Williams, Ph.D.

Professor and Associate Dean for College of Medicine & Life Sciences Graduate Program
Director, Cancer Biology track
Dartmouth Medical School, Hanover, NH, 1987

Dr Williams is the Associate Dean for the College of Medicine & Life Sciences (COM&LS) Graduate Programs, as well as the Director of the Cancer Biology research training track in the Biomedical Sciences Program. She is involved with all of the COM&LS graduate programs, including the MD/PhD dual degree program, all of the PhD and MSBS Biomedical Science Program training tracks, MSBS-Medical Science for premedical students, MSBS-Medical Physics, MSBS-Oral Biology for Dentistry residents, MSBS-Orthopedic Sciences, MSBS-Human Donation Sciences, MSBS-Physician Assistant studies, and MSBS-Assistant in Pathology. The majority of her time is focused on the Biomedical Science Program research training tracks. 

Kam C. Yeung, Ph.D.Kam C. Yeung, Ph.D.

Associate Professor 
University of South Alabama, Mobile, AL, 1990

Raf kinase inhibitor protein (RKIP) is a novel metastasis suppressor gene in and its expression is diminished in breast cancer metastases. Restoring RKIP expression is sufficient to inhibit cancer metastasis in experimental mouse models suggesting RKIP can function alone to regulate metastasis. One current focus of the Yeung lab is to define the mechanisms through which loss of RKIP promotes metastasis and determine the clinical validity of findings using human breast cancer tissues. An additional project is under investigation because the Yeung lab has observed that the expression of RKIP correlates with oncogenic activation of the PI3K and Ras/Raf pathways. Importantly, germ-line deletion of RKIP increases incidence of prostate cancer and promotes metastasis in a transgenic mouse model driven by PI3K and Ras/Raf mutations. Another area of investigation focuses on elucidating the function of micro-non-coding RNAs (miRNAs) in the malignant transformation of melanocytes into melanoma. High-throughput-sequencing of cancer genomes has identified oncogenic mutations in BRaf genetic locus as one of the critical events in melanomagenesis. Recent in vitro results in the Yeung lab suggest that miR-10b is an important mediator of oncogenic BRafV600E activity in melanoma. To better define the role of miR-10b, they will continue to investigate add-in and knock-down effect of miR-10b on melanoma in mouse models, clinical nevus and melanoma samples.


James C. Willey, M.D.James C. Willey, M.D.

Professor of Medicine and Pathology
George Isaac Chair in Cancer Biology
Medical College of Ohio, 1978

Dr. Willey’s research group studies the expression of multiple genes simultaneously by quantitative, competitive RT-PCR in normal and tumor respiratory epithelial and alveolar macrophage cells. These studies have provided a molecular signature that allows for a prediction of how aggressive a tumor may become. His specific current research interests using this quantitative technique are::

  • Determining molecular genetic basis of cancer risk 
  • Development of molecular diagnostic tests for better diagnosis and more optimized, individualized treatment of cancer
  • Gene regulation in normal and malignant human lung cells
  • Development of standardized, quantitative gene expression measurement technologies, including standardized RT-PCR and standardized immunoPCR.


David C. Allison, M.D., Ph.D.David C. Allison, M.D., Ph.D.

University of Michigan College of Medicine, Ann Arbor, MI, M.D.
University of Chicago, Chicago, IL, Ph.D.

Dr. Allison’s laboratory is studying the mechanisms responsible for the selection of chromosomal abnormalities in aneuploid cancers.  They are specifically testing the possibility that chromosomal abnormalities are conserved to retain cell-survival genes required for tumor-cell growth coincident with the loss of chromosomal regions containing tumor suppressor genes retarding tumor growth, or losses of heterozygosity (LOHs).  Special attention is paid to the possibility that tumor LOHs might prove to be an important indicator for breast cancer patients.  Techniques employed in the laboratory include Gene Mapping and Expression Arrays, Spectral Karyotyping analysis of cancer chromosomes, and Laser Capture Microdissection of breast cancer cells in paraffin-embedded tissue blocks. 

Last Updated: 9/13/16