New Bolton Center Kennett Square, PA
Emergencies & Appointments:
Ryan Hospital Philadelphia, PA

Cancer Biology & Oncology

Various types of cancers account for almost half of all disease related deaths in companion animals and are the second most common cause of death in people.  With the exception of “childhood cancers” which typically reflect defects in developmental pathways, the incidence of cancer increases exponentially in the last third of the average lifespan of most species including human and represents the number one natural cause of death in older pets; in this and other respects cancer is therefore considered a disease of aging. 


 Studies into the causes of cancer have focused on the inherited and somatic mutations that activate oncogenic pathways and inhibit tumor suppressor pathways intrinsic to the transformed cancer cells and this remains a fruitful area of research on the basic mechanisms underlying the development of cancer and progression to metastatic disease which is the major cause of cancer related deaths and continues to provide targets for the development of novel therapeutics.  However, it is now well-established that extrinsic signals provided by non-transformed cells and extracellular matrix are also critical to tumor initiation, progression and metastasis. Importantly, tumor stroma can confer resistance of many tumors against various therapeutic agents. 

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Our increasing understanding of these extrinsic mechanisms is revealing myriad of novel potential targets to inhibit tumor growth and to enhance delivery and efficacy of conventional tumor cell targeted therapies.  Better understanding of causes and mechanisms of cancer development and progression is required for improving the prevention, diagnostics and treatment of veterinary and human cancer patients suffering from oncologic diseases.  Members of the department are using cutting-edge technologies to conduct interdisciplinary studies in many areas of cancer biology including:

  • Intrinsic oncogene and tumor suppressor pathways
  • The tumor microenvironment
  • The relationship between inflammation/fibrosis and cancer
  • Mechanisms of age-tumorigenesis
  • Cancer stem cells and cancer stem cell niche
  • Drivers of metastasis and the metastatic niche
  • Developing novel tumor and stromal cell targeted therapies including immune-based therapeutic modalities and small molecule therapeutics


  • Dr. Serge Fuchs
    • Our lab focuses on the anti-tumorogenic effects of Type 1 fuch6121interferons – structures that play a major role in shaping immune defenses against tumors and inhibit the ability of the tumor to derive nutrition and oxygen. We study acute leukemia, malignant melanoma, breast, liver, and colorectal cancers, particularly in reference to tumor microenvironment associated stress stimuli.
  • Dr. Chris Lengner
    • Our lab is broadly interested in the mechanisms by which both Dr. Christopher Lengnersomatic and embryonic stem cells acquire and maintain developmental potency. We are also exploring how deregulation of these mechanisms can contribute to oncogenic transformation and tumorigenesis, and how we can learn to manipulate these mechanisms for application in disease modeling and regenerative medicine. In particular, we are focused on understanding how the Musashi (Msi) family of RNA binding proteins function to control normal stem cell activity in the intestinal epithelium and how their aberrant activation drives colorectal cancers.
  • Dr. Michael Atchison
    • Our lab studies genetic events underlying differentiation and maturation of B lymphocytes. We work towards determining the role of these mechanisms in development of B cell lymphomas. more content more content more content more content more content more content more content more content more content more content more content
  • Dr. Michael May
    • Our lab investigates the role of inflammatory cytokine signaling in tumorogenesis.  We study this process as it occurs in different tissue types, and our work has included the study of the development and progression of thyroid and pancreatic cancers.
  • Dr. Frank Luca
    • The mechanisms controlling cell growth and proliferation are fundamental for the proper development and function of cells, tissue and organs. Defects in growth control can give rise to a wide variety of developmental disorders and diseases, including cancer. Our laboratory applies a variety of molecular and genetic approaches in yeast and mammalian cells to elucidate the basic molecular mechanisms that govern eukaryotic cell growth and proliferation. The lab is particularly interested in revealing how NDR family protein kinases and their associated signaling networks spatially and temporally coordinate diverse molecular and cellular processes associated with cell growth and proliferation.
  • Dr. Anna Kashina
    • The goal of our research is to investigate the physiological role of a Dr. Anna Kashinapreviously uncharacterized posttranslational modification, protein arginylation, and its role in regulating the motility and invasion of cancer cells.
  • Dr. Ellen Puré
    • Our lab studies the role of stromal cells and extracellular matrix remodeling, chronic inflammation, and fibrosis in tumorigenesis. We are particularly interested in the contribution of those factors to age and high-fat diet/obesity related carcinogenesis, especially in breast, lung and pancreatic cancers and in regulating anti-tumor immunity. We are also developing the use of small molecule inhibitors of matrix modifying enzymes as well as immune-based stromal targeted therapies that we expect to be applicable across a wide variety of tumor types.
    • Learn more about Dr. Puré...
  • Dr. Narayan Avadhani
    • Our laboratory investigates the role of mitochondrial stressDr. Narayan Avadhani signaling in cancer progression and metastasis with emphasis on mammary, lung and eusphageal cancers. The mitochondrial retrograde signaling, also known as mitochondria stress signaling initiated by dysfunctional mitochondria involves Ca2+/Calcineurin activation and activation of NFkB, C\EBPd, CREB, NFATC transcription factors and hnRNPA2 as a co-activator. Recent results show that hnRNPA2 is HAT (histone acetyl transferase) activity, which regulates the expression >120 nuclear genes in addition to regulating telomere function.