The CBSO (Cancer Biology Student Organization) is a service organization designed to aid students in the USF Cancer Biology PhD Program. It is intended to foster scientific interaction, strengthen career development and encourage philanthropic activity focused on, but not limited to, cancer related issues. The CBSO will also serve as a source of information for first year students, as well as more experienced students.
President Vice President
Pat Innamarato Melissa Martinez
Chris Letson Daniel Lester
MEET THE REST!!!
Current Students Research Interests!
I study the role of carbonic anhydrase IX in acidification of the microenvironment and its role in the metabolic phenotype in breast and prostate cancer. I combine 2D, 3D and tumor and organ microtissue studies to gain an insight into overall metabolic phenotype and their differing responses to therapy.
The induction of lymphopenia by conditional chemotherapy in patients prior to the adoptive transfer of tumor infiltrating lymphocytes (TILs) improves anti-tumor responses. However, in the setting of lymphopenia, myeloid derived suppressor cells (MDSCs) have an enhanced proliferation and suppressive capacity relative to host T cell reconstitution. My research is focused on improving adoptive T cell therapies by studying the mechanisms by which MDSCs expand and suppress T cells after the induction of lymphopenia.
Drugs that target the protein Cereblon (CRBN) cause immune modulation of T cells but the normal function of CRBN is unknown. My work focuses on CRBN’s role in T cells to further our understanding of how targeting CRBN could enhance anti-tumor function of T cells in solid cancers.
Afua (Chu Chu) Akuffo
Characterize the role of cereblon depletion in the bone marrow. Specifically looking at cereblon’s role in the maintenance of long term hematopoietic stem cells.
The focus of my dissertation research is using quantitative proteomics to provide personalized patient care. To this effect, we are developing personalized mass spectrometry based assays using a proteogenomics approach to improve detection of minimal residual disease in Multiple Myeloma patients. In addition, we are using a multiplex liquid-chromatography multiple reaction monitoring (LC-MRM) platform to stratify non-small cell lung cancer patients by their kinase expression and phosphotyrosine signaling for novel treatment strategies.
The main focus of my research project centers around studying non-canonical targets of a number of clinically advanced targeted agents and the anticancer effects that result from their inhibition with a particular focus on identifying novel drug repurposing opportunities. To this effect I am applying a systems medicine approach that integrates phenotypic cancer drug screening with target and pathway identification through unbiased chemical and phosphoproteomics followed by in-depth functional validation. Through detailed elucidation of poly-pharmacologic mechanisms of action, we aim to design novel drug combination therapies and to identify mechanistic biomarkers that predict drug sensitivity.
Chen Hao Lo
Prostate cancer (PCa) frequently metastasizes to the bone. Patients with PCa bone metastasis suffer hypercalcemia, pathologic bone fractures and bone pain as their diseases manifest in the bone microenvironment. Therefore, it is critical to develop therapies, which may prevent cancer-induced dysregulation of the bone and improve the quality of life for patients. Osteal macrophages have important roles in mediating bone-remodeling processes, and their polarization into pro- and anti-inflammatory states (M1 and M2, respectively) may augment the growth of tumors. We currently aim to develop an in silico mathematical model that can recapitulate the biological interactions between various bone cell populations and with PCa, and accurately portray the physiological alterations to bone status as the disease progresses overtime. The ultimate goal of the project is to understand how the introduction of different conditions to the model may result in drastically different disease outcomes; to be able to predict the effects of various drugs, and potentiate new targets, which may have significant impacts on PCa progression.
In addition to their epigenetic role in regulating gene expression, histone deacetylases (HDACs) have been shown to exhibit immunoregulatory function. I am investigating the role of HDAC6 on the immunobiology of chronic lymphocytic and its potential as a therapeutic target. In addition, my research focuses on identifying novel combinatorial therapies for the treatment of B cell malignancies.
Bone metastatic prostate cancer is incurable and hallmarked by extensive bone formation. Mesenchymal stem cells (MSCs) give rise to multiple cell types including osteoblasts, bone forming cells. The bone is a natural reservoir for MSCs so my thesis project is to examine the cellular and molecular interactions of the prostate cancer cells and the MSCs to uncover novel therapies in combating prostate to bone metastases
Parathyroid hormone-related protein (PTHrP) is over-expressed by multiple cancers that metastasize to bone, including breast, prostate, and lung. In bone, it has been shown to mediate skeletal remodeling by influencing the activities of osteoblasts and osteoclasts, however proteolytic processing is first required to generate an active protein. We are studying how matrix metalloproteinases (MMPs), a family of enzymes that are also highly expressed in the tumor-bone microenvironment, cleave PTHrP to regulate its activity in the bone microenvironment.
Immune checkpoint therapy, which targets regulatory pathways in T cells to enhance antitumor immune responses, has elicited durable clinical responses but in a small fraction of patients. My dissertation project focuses on enhancing immune checkpoint therapy efficacy especially in KRAS mutant lung adenocarcinoma through combination therapy. My study includes determining the role and mechanism of KRAS downstream signals in cancer immune surveillance, and optimizing drug combination using preclinical models.
Genome wide association studies (GWAS) have identified several genomic loci associated with ovarian cancer risk, however, the vast majority of associated variants reside in non-coding regions, and the molecular mechanisms by which they predispose to ovarian cancer are unknown. My work is focused on performing functional analysis on the 8q24.21 ovarian cancer susceptibility locus to explore the regulatory landscape of this locus and provide a mechanistic basis to understand susceptibility to ovarian cancer.
Natural killer cells are the central mediators of the innate immune system and are the first line of defense against tumors. Recently, Pan-HDAC inhibitors have been found to severely dampen NK cell function against tumor cells, therefore it is vital to understand the role of HDACs in human NK function. Our hypothesis is that specific HDACs are pivotal in regulating NK functional activity against tumor cells, specifically Mantle Cell Lymphoma. Broadly, my research includes identifying selective HDAC inhibitors that enhance human NK functional responses against MCL.
My project involves using bioinformatics and biostatistics to discover novel prognostic and predictive signatures in lung cancer, specifically Squamous Cell Carcinoma. By taking into account DNA mutation profiles, gene expression patterns, and patient Meta data my project aims to increase our knowledge and understanding of the way we should be treating cancer on the basis of the individual rather than the disease.
The focus of my research is to determine the target profile of kinase inhibitors in lung cancer cells using chemical biology, an unbiased spectrometry-based drug affinity approach, combined to phosphoproteomics and functional validation. Understanding the important targets and mechanism of action in these cells can lead as to identify potent combination drugs.