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Cancer Biology

Cancer biology is an academic discipline with a tangible end point: improving the prevention, diagnosis and treatment of human cancers. The Program in Cancer Biology provides students interested in pursuing a career in cancer biology with rigorous training in biochemistry, genetics, molecular and cell biology, as well as an understanding of the clinical aspects of cancer. The program is based in the Department of Molecular, Cell and Cancer Biology, but it also includes faculty from most basic science departments and several clinical departments. The strength and diversity of the faculty enable students to explore different approaches to the study of cancer in their laboratory rotations and to develop inter-departmental and interdisciplinary collaborations during their thesis research. This program is also an integral component of the UMass Cancer Center and it affords students the opportunity to participate in disease-based programs of the Cancer Center that are designed to translate achievements from the basic sciences to the clinical management of human cancers.


All Basic Biomedical Science students must complete the core curriculum as well as electives required by their program. Students in the Cancer Biology program must take 3 elective courses, two of which must be Histology and Tumor Pathology and Cancer Biology and Medicine

View PhD Program Schedule  |   View Courses



Dohoon Kim, PhD
Assistant Professor
email Dr. Kim
Visit the Kim lab site
  Arthur Mercurio, PhD
email Dr. Mercurio
Visit the Mercurio lab site

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Our faculty come from most basic science departments and several clinical departments. The strength and diversity of the faculty enable students to explore different approaches to the study of cancer in their laboratory rotations and to develop inter-departmental and interdisciplinary collaborations during their thesis research.

Research areas of our faculty inlcude:

  • Cancer Cell Biology and Immunology
  • Cancer Genetics

View the affiliated faculty listing for the Cancer Biology Program.


Many Cancer Biology students have been awarded NIH pre-doctoral fellowships and received other prestigious awards.  For example,  Nomeda Girnius  and Shawna Guillemente won the Dean's Award for Outstanding Thesis Research .  Our students have published in top journals including Cell, Science, Nature and Cancer Cell.  In addition to these accomplishments, our students organize an annual Cancer Biology Retreat and host a distinguished scientist as the keynote speaker for this retreat.   These speakers have included Robert Weinberg, Ron DiPinho, David Sabatini, Craig Thompson and Kornelia Polyak.  A monthly Cancer Biology Journal Club is also organized by our students.


Getting Results…
  • PhD candidate studies red blood cells; strives to increase diversity in STEM
    Education News, Media

    PhD candidate studies red blood cells; strives to increase diversity in STEM

    As president of UMass Chan Medical School’s chapter of the Society for Advancement of Chicanos/Hispanics and Native Americans in Science, PhD candidate Daniel Hidalgo provides cultural training and advocates for diversity in STEM fields.

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  • For GSBS class speaker Sumeet Nayak science brings hope
    Education News, Media

    For GSBS class speaker Sumeet Nayak science brings hope

    Sumeet Nayak’s research in the lab of Sharon B. Cantor, PhD, has led to a renewed understanding of how cancer develops and has opened up avenues to effectively advance anti-cancer therapies.

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  • Nick Peterson and Samantha Tse named Ruth L. Kirschstein National Research Service Award recipients
    Research News

    Nick Peterson and Samantha Tse named Ruth L. Kirschstein National Research Service Award recipients

    Two MD/PhD students in the lab of Read Pukkila-Worley, MD, have each received Ruth L. Kirschstein National Research Service Awards from the National Institute of Health.

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  • Anne Carlisle researches cancer cell metabolism at GSBS
    Education News, Media

    Anne Carlisle researches cancer cell metabolism at GSBS

    Anne Carlisle, PhD candidate in the Graduate School of Biomedical Sciences, came to Massachusetts from Nebraska in 2015. She is studying in the Dohoon Kim lab, investigating the role of selenium in cancer cells.

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    Discovery of a novel role of VPS13D in Autophagy

    Defects in autophagy, the self-degradation of cellular components, are linked to multiple disorders such as cancer, diabetes and neurodegenerative diseases. Autophagosomes, containing cargo marked for degradation, fuse with lysosomes to recycle cell resources, such as protein aggregates and damaged organelles. However, we know little about the mechanisms that regulate the association between autophagic cargoes and autophagosome formation. Here, I investigate the role of vps13d, an essential gene with relatively unknown function, in context-specific autophagy and cell death in the developing Drosophila intestine. Proteins that regulate autophagy and cell death are of particular interest given the roles they play in tumorigenesis. Previous studies of VPS13D identified a role in the clearance of mitochondria by autophagy, also known as mitophagy. Intriguingly, VPS13D also appears to be involved in dissolution of membrane contacts that are associated with autophagosome formation. Furthermore, little is known about the role of VPS13D in associating autophagy-bound cargo with the site of autophagosome formation, despite having links to the core autophagy machinery. I hypothesize that VPS13D facilitates context-dependent autophagy by associating ubiquitinated cargo with the autophagic machinery and disassembling membrane contact sites at the phagosome assembly site (PAS). Here I propose to determine if VPS13D functions as an autophagy receptor for ubiquitinated cargo and determine the relationship between VPS13D and membrane contact modulator Vacuole Membrane Protein 1 (VMP1). The association of VPS13D and mutations in other factors that regulate autophagic cargo recruitment with human disorders illustrates the importance of studying VPS13D function.

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  • Kevin O'Connor, Kelliher Lab, Funding Provided by National Institutes of Health

    Targeting dormant leukemia-initiating cells in T-cell acute lymphoblastic leukemia

    Therapy resistance is a major barrier to long term remission in pediatric T-cell acute lymphoblastic leukemia (T-ALL). The prognosis for children with relapsed or refractory disease is dismal. Leukemia-initiating cells (L-ICs) regenerate disease upon transplantation into mice. They also recapitulate the immunophenotypic complexity of the parent leukemia supporting that, as in normal hematopoiesis, there is a cellular hierarchy among leukemic cells. Our laboratory has previously demonstrated that the L-IC is a committed thymocyte progenitor and resides in the leukemic DN3 population, however, only a fraction of DN3 cells can give rise to disease. L-ICs rely on NOTCH1-induced MYC signaling for survival. Recent studies identified dormant, therapy resistant L-ICs in both murine models and T-ALL patient samples. The role of cell cycle restriction in L-IC latency is incompletely understood. In an effort to uncover pathways that govern L-IC function, we performed single cell RNA sequencing on thymocytes at varying stages of T-cell leukemogenesis using our transgenic Tal1/Lmo2 model. This approach identified a dormant DN3 cluster, marked by low Ki67 expression, which is observed in other murine T-ALL samples. Dormant DN3 cells exhibit high Notch1, but low Myc expression. The transcriptional signature of these cells shows enrichment of genes previously implicated in leukemia initiation or leukemia stem cell function. Dormant DN3 cells show enrichment of the non-canonical Wnt receptor Ryk, which is reported to maintain hematopoietic stem cell self-renewal by limiting proliferation and promoting quiescence. RYK is overexpressed in primary pediatric T-ALL and in Tal1/Lmo2-induced murine T-ALL compared to healthy thymus. This indicates that RYK may not be restricted to this rare subpopulation and moreover, there may be a therapeutic window for RYK inhibition in relapsed T-ALL. The central hypothesis of this proposal is that dormant DN3 cells are quiescent L-ICs that retain proliferative and differentiative capacity, which permits their therapy tolerance and subsequent expansion during relapse. This proposal will identify a gene signature of dormant DN3 cells and uncover the potential role of these cells in T-ALL relapse by evaluating their L-IC function and chemoresistance (Aim 1). Aim 2 will define the non-canonical WNT/RYK signaling network in T-ALL and uncover the role of these pathways in dormant DN3 cells and L-IC function by testing whether inhibition of RYK reduces the L-IC frequency of murine and patient T-ALL cells. Collectively, these studies will provide critical insight to TALL heterogeneity and will lay the foundation for development of L-IC targeted therapy for relapsed disease.

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    Integrin Regulation of Mammary Gland Development

    The mammary epithelium is composed of diverse cell populations that are responsible for regulating key processes in mammary gland development, especially lactation. Alveolar progenitor (AP) cells are partially differentiated stem cells that produce alveolar/milk-producing cells and these cells have recently been implicated as cells of origin in breast cancer. Through analysis of published single cell RNA-seq data, integrin β4, a protein known to function primarily in basal mammary epithelial cells to maintain structural integrity of the gland, was found to be expressed in the AP population. This unexpected result suggests that β4 plays a novel role in the AP population and may regulate dynamic processes within the developing mammary gland. This goal of this proposal is to understand the functional role of β4 in the AP cells of the nulliparous and lactating mammary gland and elucidate the mechanism by which β4 regulates this population. Preliminary studies have revealed that β4 expression is necessary to promote progenitor potential of the AP cells and identified LacdiNAc, a novel glycosylation modification, on β4 that we hypothesize is essential for its localization in lipid rafts that promotes its function in the AP population. Using an AP cell culture model as well as a Cre-lox mouse model to conditionally knock out β4 from the AP population, the function of β4 in the AP population will be assessed in vitro and in the virgin and lactating mammary gland. Also, glycomics analyses and biochemical approaches will identify novel glycans on β4 and help in understanding how LacdiNAc affects function of β4 in the AP population. This approach will further our understanding of the novel role of β4 in the AP population and a new mechanism involving LacdiNAc-β4 localization to lipid rafts to regulate alveolar differentiation. These studies have to potential to define novel mechanisms that regulate the AP population during normal mammary gland development as well as breast cancer progression.

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  • Jordan L. Smith, Xue Lab, Funding provided by National Cancer Institute

    Investigating YAP1 control of differentiation and metabolism in Hepatoblastoma

    Hepatoblastoma (HB), the most common pediatric primary liver tumor, affects children from infancy to five years of age. Surgical resection with adjuvant chemotherapy has saved many young lives. However, the five-year survival rate remains at 70%, and is worse for children with unresectable tumors. Meeting the clinical need for HB-targeted therapies requires a better understanding of how HB tumors are formed and maintained. The transcriptional co-regulator YAP1 is hyper-activated in 79% of HB cases, and recent studies suggest that YAP1 and the Wnt/β-catenin pathway act together to initiate HB tumors. But is YAP1 required to maintain HB tumorigenesis? Preliminary studies using a conditional mouse model of HB—driven by doxycycline-inducible hyperactive YAP1S127A and constitutively active β-catenin—suggest that YAP1 is essential for tumor maintenance. In the presence of doxycycline, YAP1 is expressed, and mice develop HB tumors; withdrawing doxycycline turns off YAP1, resulting in >90% tumor regression within 10 weeks. Transcriptional analyses revealed that hepatocyte differentiation factors and liver metabolic genes were induced in regressing tumors.

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    Integrin Function in Breast Cancer Initiation

    Breast cancer is the most common cancer diagnosis in women and is also one of the leading causes of cancer-related mortality in women who suffer from this condition. Tumors that originate in the breast consist of heterogeneous populations of cells. Breast cancer stem cells (BSCSs) are a subtype of tumor cells that have properties similar to normal, tissue stem cells such as the ability to divide slowly and give rise to differentiated cellular lineages. Furthermore, BCSCs have been implicated in tumor initiation, therapy resistance and metastasis to distant organs. Given this information, a greater understanding of the biological processes that sustain BCSCs will lead to the development of novel agents directed against this chemo- and radio-resistant population of tumor cells. The proposed work will explore the role of the α6 integrin splicing variants, α6Aβ1 and α6Bβ1, in the genesis of BCSCs, specifically addressing the mechanism of activation of the TAZ transcriptional coactivator. Integrins are a family of cell surface receptors that function in signal transduction and adhesion to the extracellular matrix. The α6Aβ1 integrin variant is expressed in differentiated, epithelial breast cancer cells and inhibits the acquisition of stem cell properties Conversely, the α6Bβ1 integrin variant is expressed in BCSCs and promotes tumor initiation by activating the Hippo signaling pathway transducer TAZ. TAZ has previously been shown to be important in the functioning of BCSCs, but the mechanism is unknown. Therefore, elucidating the relationship between the α6 integrin splicing variants and TAZ activation will provide insight into mechanisms of breast cancer progression. This proposal will use a cellular and molecular biology approach to establish the mechanism by which TAZ is suppressed in the α6Aβ1 expressing non-stem breast cancer cell population (Aim 1). Biochemical studies will also be undertaken with the purpose of connecting mechanisms of TAZ inactivation with classical Hippo pathway signaling in the non-stem breast cancer cell population (Aim 2). In summary, the studies included in this proposal will increase the understanding of integrin regulation of BCSCs. Our results can provide rationale in designing future targeted therapies for treatment resistant subtypes of breast cancer.

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  • Alec K. Gramann, Ceol Lab, Funding provided by National Institutes of Health

    Targeting BMP signaling to treat advanced melanoma and suppress therapeutic resistance

    Melanoma is the leading cause of skin cancer death in the United States, with the 5-year survival rate of 20% for patients with advanced disease. Despite improvements in therapy, many patients receive minimal survival benefit and often develop resistance to standard-of-care therapies. Furthermore, a population of patients exist who do not have the appropriate mutations or tumor characteristics to be eligible for new targeted and immunotherapies. In order to provide adequate treatment options for patients who develop resistance or are ineligible for current cutting-edge therapies, new therapeutic targets must be identified. Our lab has discovered a novel melanoma oncogene, growth differentiation factor 6 (GDF6), a secreted bone morphogenetic protein (BMP) ligand that promotes melanoma by regulating expression of specific neural crest factors, which has the dual effect of preventing differentiation and suppressing apoptosis9. In addition to these specific factors, we found GDF6 more broadly promotes a gene expression signature that mimics that of the embryonic neural crest. Neural crest identity has previously been identified as a key feature involved in melanoma initiation, progression, and therapeutic resistance. Our studies show knockdown of GDF6 suppresses expression of many of these neural crest genes. Taken together, these data indicate GDF6 is an optimal target for melanoma therapy. As a secreted extracellular protein, GDF6 is amenable to targeting by antibodies. We produced a panel of monoclonal antibodies to target the C-terminal binding region of GDF6 and developed multiple in vitro and in vivo assays to assess candidate antibodies with the most potent action against GDF6 and evaluate their effectiveness as potential melanoma therapeutics. I hypothesize that a subset of antibodies will effectively block GDF6 activity leading to increase differentiation and cell death of melanoma cells in vitro and in vivo. I further hypothesize that blocking GDF6 will suppress neural crest identity in melanoma cells, leading to less aggressive tumor cell characteristics and sensitizing previously resistant cells to standard-of-care therapy. I will evaluate a pre- screened panel of 42 monoclonal antibodies for in vitro and in vivo activity against GDF6 in melanoma cells to identify top candidates with the most potent activity, in parallel with characterizing pharmacokinetic and dynamic properties of the antibodies in vivo. I will further characterize the effects of GDF6 inhibition by these antibodies on neural crest expression profiles and key features of advanced melanoma such as therapeutic resistance, invasiveness, and anchorage independent growth. Additionally, I will analyze potential combinatorial therapies in vitro and in vivo to assess changes in pathway activity for known therapeutic resistance mechanisms. Results of this study will identify lead candidate anti-GDF6 antibodies for first-in-human (FIH) studies and provide appropriate pre-clinical safety data for submission of an FIH application. Furthermore, these data will provide broad insight into the tumorigenic features that are connected to neural crest identity and the result of reversing neural crest characteristics in established melanomas.

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  • Alec K. Gramann, Ceol Lab, Funding provided by Melanoma Research Foundation

    Examining BMP signaling as a regulator of neural crest identity during melanoma initiation and progression

    In many types of cancer, less differentiated tumors are more strongly associated with a poor patient prognosis. These tumors tend to be more aggressive: they have higher proliferation rates, a greater propensity for invasion and metastasis, and increased resistance to therapy compared to more differentiated tumors. Less differentiated tumors, by their nature, share characteristics with their embryonic cells of origin. In melanoma, these less differentiated tumors are associated with a neural crest identity that is acquired during early stages of tumor initiation and is present through tumor progression. Previous studies have shown that acquisition of a neural crest identity is a necessary step during initiation of early melanoma lesions and supports fundamental properties of aggressive tumors such as invasion and metastasis. However, the mechanisms of generating a neural crest identity are unknown. Recently, our lab has identified growth differentiation factor 6 (GDF6) as a novel melanoma oncogene. GDF6, a bone morphogenetic protein (BMP) ligand, is recurrently amplified in both human and zebrafish melanomas, and expressed in tumors but not normal melanocytes. We have shown GDF6 acts to prevent differentiation and suppress apoptosis in established melanomas, both in vitro and in vivo. Additionally, we have found that GDF6 regulates expression of multiple neural crest and melanocyte factors previously implicated in melanoma. Upon knockdown of GDF6, we observed downregulation of select neural crest factors coupled with upregulation of melanocyte differentiation factors, leading to melanoma cell differentiation and ultimately cell death. These results suggest that GDF6 plays a role in regulating oncogenic neural crest identity. Here, we look to identify the role of GDF6 and BMP signaling in establishing a neural crest identity during melanoma initiation and explore oncogenic characteristics imparted by GDF6 during melanoma progression. I hypothesize that GDF6-depenent BMP signaling acts to initiate a neural crest identity in melanomas to promote tumor initiation and aggressive tumor characteristics. I further hypothesize that loss of BMP activity leads to differentiation (and in tumors death of differentiating cells), making GDF6 an attractive target for differentiation therapy in melanoma.

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Graduates of the Cancer Biology Program have obtained post-doctoral fellowships at leading institutions including Harvard Medical School, MIT, NIH and Yale, and have obtained industry positions in reknowned companies such as Sanofi and Novartis.