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An NCI-designated Comprehensive Cancer Center, affiliated with the University of Pittsburgh School of Medicine
Research
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Dr. Bailey studies pediatric sarcoma biology. Specifically, Dr. Bailey's lab focuses on understanding the intersection of DNA damage and immunobiology in Ewing sarcoma. She is involved nationally in the Children's Oncology Group Bone Tumor Committee and is national Vice Chair of the COG clinical trial AOST2121.
Radiation therapy and many chemotherapies induce DNA damage. These therapies work because cancer cells divide more rapidly than normal cells and cancer cells acquire mutations that change their DNA damage responses and DNA repair mechanisms. Nevertheless, radiation and DNA damaging chemotherapies may not generate long-term responses as the dose of DNA damage required to kill all cancer cells may kill too many normal cells – dose limiting toxicity. The Bakkenist Lab studies how pharmacologic DNA damage response inhibitors can be used to increase the damage induced in cancer cells and potentiate anti-tumor immune responses. Our long-term goals are to develop new therapeutic approaches to manage human cancer.
Visit the Bakkenist Lab Website to learn more.
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Using a combination of multi-omics data integration, machine learning, and computer vision-assisted pathology image recognition, Dr. Bao’s work bridges methodological advances and biomedical applications with a direct impact on accelerating the knowledge discovery to new clinical trials that could benefit patients. Her lab focuses on the data-driven discovery of resistance mechanisms to cancer immunotherapy, with major contributions to the identification of WNT/ß-catenin activation as the first tumor-intrinsic mechanism that drives immune exclusion, commensal microbiome as the modulator of anti-PD1 efficacy, and systemic discovery of oncogenic pathways that contribute to the absence of immune infiltration across human solid tumors. Those findings are of particular importance because they provide the scientific rationale to new trials that combine therapeutic targets, such as IDH1 inhibitors, with anti-PD1. Dr. Bao is Co-Leader of Bioinformatics/Biostatistics in the Melanoma and Skin Cancer SPORE and Head and Neck Cancer SPORE programs. She also serves as the UPMC Hillman Cancer Center Informatics Committee, providing critical advice on data accessibility, analysis, integration, and infrastructure for translational research across the Cancer Center. Dr. Bao is a member of The American Association of Immunologists, Society for Immunotherapy of Cancer, and Medical Image Computing and Computer Assisted Intervention.
Dr. Barry is interested in breast and gynecologic cancer research specifically related to preoperative and salvage radiation therapies. Dr. Barry is a board-certified radiation oncologist and a Clinical Assistant Professor of Radiation Oncology at UPMC Hillman Cancer Center at UPMC Magee-Womens Hospital.
I am a behavioral scientist with a research focus on understanding and addressing cancer health disparities. My clinical training as a psychologist and extensive NIH-funded research history includes the design, evaluation and dissemination of behavioral and environmental interventions to address cancer and other chronic conditions. My approach relies heavily on community-based participatory research (CBPR) to identify sociocultural and environmental determinants of health among populations at greater risk of disease (e.g., African Americans, lower income populations, rural residents). For example, I served as PI for the Full Research Project on a community network partnership center grant (U54CA153719) that involved a cluster-randomized trial of a multi-level weight loss intervention for African American women at higher risk of cancer who live in the rural Deep South (Alabama and Mississippi) and a cluster-randomized trial testing the efficacy of a weight loss intervention for African American cancer survivors in the Black Belt of Alabama (R01CA160313). My collective work has cemented my expertise in outreach and engagement, the recruitment and retention of underrepresented groups into biobehavioral research, recruitment of family and non-family support, community-engaged research, mixed-method designs, and dissemination of research findings to multiple audiences (including participants and community partners). I believe membership in the HCC research program will afford me greater access to collaborations and resources to expand my work and adapt research originally conducted in the Deep South to populations in Pennsylvania.
Currently I work in cancer surveillance via survey methods to investigate factors related to disparities in cancer prevention, access to treatment, quality of life, and cancer-related protective and risk factors across the lifespan. As the Director of the HCC’s Population Survey Facility, I envision collaborations with HCC members that will ultimately result in interdisciplinary work through a population health lens focusing specifically on reducing cancer related health disparities in the HCC catchment area.
One of the major long-term research goals of my group is to explore the mechanisms by which environmental exposures increase the risk of liver disease and cancer in experimental and translational studies. Specifically, we explore the role of vinyl chloride (VC) exposure (at concentrations below the safety regulations) in the development of hepatocellular carcinoma (HCC). Although high occupational exposures to VC can directly cause liver injury and cancer, these studies have not considered interactions of low concentrations of VC with risk-modifying factors. We have demonstrated enhanced tumorigenesis in mice exposed to low-level VC. Our overall hypothesis is therefore that the concentrations of VC that a currently considered safe are sufficient to exacerbate hepatic pathology including HCC when combined with additional risk factors, such as overnutrition and that this may drive inter-individual risk. Importantly, such an interaction would imply that risk may be underestimated at this time. These studies are also entirely novel in the context of environmental health and are therefore expected to be highly impactful, especially in the light of the recent E. Palestine, OH train derailment that exposed hundreds of residents to toxic chemicals, such as VC.
Dr. Belcher’s research focuses on understanding and improving health outcomes among patients with cancer, particularly among patients with high cost and advanced cancers and among socioeconomically disadvantaged and historically excluded populations.
Her career development award is investigating how adherence to oral anticancer medication affects pain and quality of life and how financial hardship influences these relationships over time among patients with multiple myeloma. Her prior research identified predictors of poor health outcomes among adults with multiple primary cancers and relationships between financial hardship and quality of life among patients with advanced and high symptom burden cancers.
My lab is focused on development of human Organs-on-Chips (microphysiological systems) and bioinspired robotics in the context of lung and immune pathophysiology. I am interested in applying our Organ-on-a-Chip models to emulate cancer pathobiology preclinically and utilize these platforms for target discovery / therapeutic testing.
Dr. Berg’s research interests include contrast-enhanced mammography or MRI for improved screening, comparative effectiveness of new technologies in breast imaging, and artificial intelligence to improve breast ultrasound performance. Her clinical interests include supplemental screening for breast cancer based on risk and breast density, implementing new technologies, standardizing interpretive criteria, and educating referring providers on breast density and optimal screening.
Dr. Berg is the Chief Scientific Advisor for DenseBreast-info.org and holds the Bernard F. Fisher Chair for Breast Cancer Clinical Science.
My research focuses on understanding how non-coding RNA directs gene regulation. My current research goals are to understand how RNA conformational change within ribonucleoprotein complexes regulates gene transcription and genome replication. To do this, we will utilize complementary biochemical, structural and computational techniques.
Our research interests are focused on the mechanisms of cross-priming of antigens during immune responses to cancer, viruses and autoimmunity. The pursuit of this research area stems from the observations that in many situations, heat shock proteins (HSPs) are both necessary and sufficient for cross-presentation. HSPs are adept at this because of several unique properties, including their ability to:
HSPs thus elicit remarkable immune responses specific for the peptides they chaperone. The laboratory is using these observations to examine new facets of antigen presentation and also to develop novel immunotherapies for cancer, infectious disease and autoimmune disorders.
A related area of research examines how other ligands for the HSP receptor CD91 interact with the immune system. In the past few years, we have shown that a2-macroglobulin (a2M), a CD91 ligand, though not a bonafide HSP, shares the immunogenic properties of HSPs and can elicit immune responses specific to (peptide) substrates that it chaperones. We are currently exploring the identification of naturally formed a2M-substrate complexes and the potential use of these immunogenic complexes as therapeutic agents for cancer and infectious disease.
My research interest is focused on lncRNAs in breast cancer. I have strong collaborations with other members of the cancer center including Drs. Adrian Lee, Steffi Oesterreich, Partha Roy, and Uma Chandran. However, my primary role in the cancer center will be centered around training and diversity. I am the Director of the NCI (R25) and DDCF funded Hillman Academy that organizes ~70 internships to high school students annually with a special focus on training underrepresented minorities. I am also the vice chair of the education and training committee for the cancer center.
Interdisciplinary studies of: biobehavioral factors in cancer; the emotional, cognitive, behavioral, and biological consequences of breast cancer risk; the contribution of biobehavioral factors to side effects of medical treatments (surgery, chemotherapy, radiotherapy) and interventions that may ameliorate those effects; interactions between psychological and genetic factors in persistent smoking behavior; and, psychological influences on cancer screening decisions.
Research in the Brieno-Enriquez lab focuses on the regulation of gametogenesis in human and mouse and, more specifically, the fundamental mechanisms that are required to produce viable germ cells. Our studies include the analysis of all the different stages of germs cells including primordial germ cells (PGCs), spermatocytes, oocytes, as well as how age affects them. Our long-term goal is to test our overarching hypothesis that gene expression, epigenetic clock, and chromatin structure in the naked mole-rat can be hijacked for use in other species, allowing us to regulate the establishment and maintenance of the ovarian reserve, oocyte quality, and reproductive longevity.
Research in my laboratory is focused on cytochrome P450 enzymes (P450), their role in human health and disease, and their potential as drug targets. While most studies focus on steroidogenic P450 enzymes as drug targets for prostate and breast cancer treatment, my goal is to evaluate the potential of targeting fatty acid metabolizing P450 enzymes for cancer therapy. I am particularly interested in the CYP4F enzyme family of fatty acid -hydroxylases which, according to our findings, are upregulated in several cancer type. CYP4F enzymes are involved in the metabolism of arachidonic acid to the potent lipid mediator 20-hydroxyeicosatetraenois acid (20-HETE). While 20-HETE regulates the blood pressure in healthy individuals, it also promotes cell proliferation and migration and tumor angiogenesis in cancer. An unselective inhibition of 20-HETE producing CYP4 enzymes leads to a significant decrease of lung tumor size in mouse models. However, the clinical exploitation of these enzymes has not been realized yet due to high protein sequence similarities, the absence of isoform specific inhibitors, and a substantial lack of structural and functional information. Our long term goal is to establish CYP4F enzymes as novel potential drug targets for cancer therapeutics. Recent efforts in my lab were focused on the isoform CYP4F11 in lung cancer. My team has shown for the first time that a transient CYP4F11 knockdown in lung cancer cell lines leads to decreased cell proliferation and migration which is associated with decreased 20-HETE production. We also generated recombinant human CYP4F11 protein to conduct in-depth biochemical studies to probe enzyme function and to solve structures of CYP4F11 using X-ray protein crystallography. We aim to examine other CYP4F isoforms in various cancer types, unravel their cellular function in addition to 20-HETE production, and solve protein structures for the directed design of selective drugs.
Our work focuses on understanding: (1) how misfolded proteins are recognized and destroyed in normal and tumor cells, (2) how molecular chaperones mediate protein quality control “decisions”, (3) how protein quality control pathways can be targeted in disease models, and (4) how cellular stress responses (such as the Unfolded Protein Response, UPR) affect protein biogenesis and homeostasis, especially in cancer. The pursuit of these goals has employed biochemical, cell biological, and genetic tools using a range of models, including yeast, cell culture, and rodents. Our early work contributed to the discovery of the ER associated degradation (ERAD) pathway, which we named, and ongoing studies are deciphering the mechanisms underlying the ERAD pathway in yeast, mammalian cell culture, and rodent models, and its relationship to cellular stress responses. The importance of ERAD is underscored by the fact that >70 human diseases—including several cancers—are associated with this pathway. In parallel, new classes of small molecule modulators of chaperones and the ubiquitin-proteasome pathway have also been isolated, which we have used to probe the relationship between stress responses, protein homeostasis (“proteostasis”), and tumorigenesis. Ongoing work has capitalized on several of our tools and areas of expertise, including (1) an analysis of protein degradation pathways and the ubiquitin-proteasome system in breast and ovarian cancer, (2) the use of small molecules and drugs to target cancer vulnerabilities, and (3) measurements of cellular stress pathways in breast and ovarian cancer.
Dr. Brufsky's research interests include novel clinical therapeutics for breast cancer, bone-breast cancer interactions and therapeutics, molecular biology of metastatic breast cancer, and novel management strategies for metastatic breast cancer. Dr. Brufsky manages approximately 30 clinical trials investigating various aspects of breast cancer etiology and treatment. His main clinical interests are in breast cancer medical oncology with a particular interest in metastatic breast cancer.
Immunotherapy, specifically anti-PD1, has improved patient survival in a range of tumor types including head and neck squamous cell carcinoma (HNSCC) and non-small cell lung cancer (NSCLC). Despite the success of anti-PD1 therapy, only 20% of patients produce a durable response to this treatment. Further, there are some solid tumor types i.e. ovarian cancer, which yield very little therapeutic benefit from current standard of care immunotherapies. Thus, a need exists to develop additional therapeutic strategies to treat these patients, which includes evaluation of other tumor infiltrating immune cells that could further augment the CD8+ and CD4+ intratumoral T cell response. B cells represent a possible target for immunotherapy due to their predominance in the tumor microenvironment (TME) and crucial role in the immune response. However, B cell function in cancer and in the context of immunotherapy has been understudied. In fact, conclusions on an anti- or pro- tumor role for B cells in the TME remain incomplete. However, in multiple solid tumors, current evidence suggests an anti-tumor role for B cells. Specifically, detection of B cells within tertiary lymphoid structures (TLS) correlates with increased survival and immunotherapeutic response. While B cells have been identified in multiple tumor types, their complete phenotypic signature and interplay with other components within the TME have been understudied. Further, the complex composition of TLS in patient tumors is severely underappreciated, which is an overt focus of the Bruno laboratory. Specifically, we aim to understand B cell infiltration and TLS development within solid tumors to generate effective B-cell focused immunotherapies to augment the current successes of standard of care immunotherapies such as anti-PD1.
To this end, we take a multi-level approach to understanding B cells and TLS composition in human tumors. Specifically, we transcriptionally assess B cells via single cell RNAseq with paired BCR seq, we interrogate B cell subsets within patient tumors using multi-parameter flow cytometry (15-30 parameters), we locationally evaluate B cells within and outside TLS utilizing multispectral imaging (Vectra Polaris) and spatial transcriptomics (Nanostring GeoMax Digital Spatial Profiler), and we evaluate the function of B cells and their interplay with other important immune cells within the TME via micro-scale in vitro functional assays.
Ovarian cancer is a disease that has high rates of resistance to both chemotherapy and immunotherapy. This therapeutic resistance drives a poor prognosis for patients with ovarian cancer. A primary focus of my group is to understand therapeutic resistance and develop therapeutic approaches to overcome this resistance. We are working to understand both cancer cell inherent mechanisms of therapeutic resistance and how interactions with host cells in the tumor microenvironment increase therapeutic resistance.
We are currently focusing on understanding the biology of a population of slowly dividing/non-dividing or ‘quiescent’ cancer cells. These quiescent cells are inherently resistant to chemotherapy and radiation therapy – both of which kill fast growing cells. Upon exposure to chemotherapy, we find that these cells quiescent cells secrete novel factors to make neighboring cells resistant to both chemotherapy and immunotherapies. Following completion of chemotherapy treatment these quiescent cells can resume proliferation and drive disease recurrence.
Furthermore, following chemotherapy exposure, these cells secrete additional factors which create an immunosuppressive microenvironment. Given the critical role of these cells in therapeutic resistance, we are developing novel therapeutic approaches to kill these otherwise resistant cells. Based on our findings we are currently running two different clinical trials to determine if we can prevent chemotherapy or immunotherapy resistance.
Dr. Bukowinski is an assistant professor of pediatrics at the University of Pittsburgh School of Medicine. He cares for patients with a variety of oncologic diagnoses covering the spectrum of solid tumors, leukemia, and neuro-oncology. He serves as the UPMC Children's Hospital of Pittsburgh site Primary Investigator for the Pediatric Early Phase Clinical Trials Network (PEP-CTN) for clinical trials for the Children’s Oncology Group.
The mission of my research is to improve pain management and quality of life for patients with cancer. am currently funded by the Pitt CTSI KL2 to explore stigma around prescription opioids in adults with advanced cancer, who often have high rates of moderate-to-severe pain and prescription opioid exposure. The second aim of my work is to identify patients at risk for cancer-related pain and neuropathy as early as possible in order to improve access to effective pain management resources. In addition to my own research, I collaborate closely with my mentors Dr. Yael Schenker and Dr. Jessica Merlin, as well as other collaborators across the university, on other relevant projects. For example, I serve as co-I and site PI for a recently funded R01 (PI: Merlin) to understand risks, benefits, and stakeholder perspectives of opioid prescribing for patients with advanced cancer who are expected to live for years with their diagnosis.
Dr. Bunimovich is a faculty member of the Department of Dermatology at the University of Pittsburgh and the UPMC Hillman Cancer Institute, and a graduate faculty member in Molecular Pharmacology and Cellular & Molecular Pathology. He obtained PhD in Chemistry and Chemical Engineering from the California Institute of Technology, and MD from UCLA where he also completed postdoctoral fellowship in tumor immunology at the Crump Insitute for Molecular Imaging. Dr. Bunimovich's research program is focused on the neuroimmune regulatory mechanisms of cancer progression, with the emphasis on the roles of sensory neurons and neuroglia in the modulation of melanoma immunosurveillance. His laboratory is also investigating mechanisms of ferroptosis in cutaneous pathophysiology. His work is funded by the NIH/NCI, the American Cancer Society, the Skin Cancer Foundation, the American Skin Association. Dr. Bunimovich practices general medical and surgical dermatology, including treatment of cutaneous malignancies, atopic dermatitis, psoriasis, autoimmune, immunobullous and other skin conditions.
My research is focused on clinical and translational studies of soft tissue and bone sarcomas. Currently, I am investigating an immunotherapy utilizing an anti-PD1 inhibitor for patients with advanced sarcomas. In the future, I plan to further study novel immunotherapeutic approaches for advanced sarcomas, particularly with combinatorial strategies.
