Graduate Fellowship Awardees

2025 Awardees

Kubra Calisir Unsal headshot

Kubra Calisir Unsal

LOWVELO HCC Graduate Fellow

Project: Targeting Triple Negative Breast Cancer with High Chromosomal Instability

Mentor: Ozgur Sahin, Ph.D.

My research focuses on triple-negative breast cancer (TNBC), which accounts for 10–15% of all breast cancer cases and is associated with a more aggressive phenotype, earlier recurrence, and poorer overall survival compared to non-TNBC subtypes.

Chemotherapy remains the primary treatment option; however, most TNBC patients ultimately develop resistance. TNBC is characterized by high chromosomal instability (CIN)—a hallmark of aggressive tumors that is poorly tolerated by normal cells but frequently exploited by cancer cells. CIN contributes to poor prognosis, metastasis, and therapeutic resistance. Thus, effective targeted therapies for CIN-high TNBC remain lacking. Through my work, we have identified TACC3, a member of the transforming acidic coiled-coil protein family, as a novel vulnerability in TNBC.

My current study aims to elucidate the molecular mechanism of TACC3 in TNBC, advancing our understanding of CIN-driven cancers and paving the way for new therapeutic strategies.

Pritika Sahani headshot

Pritika Shahani

LOWVELO HCC Graduate Fellow

Project: Identifying translational drug combinations for medulloblastoma treatment

Mentor: Jezabel Rodriguez Blanco, Ph.D.

Brain tumors are the leading cause of cancer-related deaths in children, with medulloblastoma (MB) being the most common. MB is classified into four molecular subgroups: WNT, Sonic Hedgehog (SHH), Group 3, and Group 4. This classification has improved our understanding of these malignancies and allowed for the development of targeted therapies.

Despite these advances, most children with MB are still treated with standard-of-care protocols, including surgery followed by radiation and chemotherapy targeting highly proliferative cells. While these treatments can be curative, they leave survivors with long-term side effects.

Targeted therapies offer a less toxic alternative, but many oncogenic drivers in MB, such as the Glioma-associated (GLI) oncogene, are difficult to target directly. Bromodomain and Extra-Terminal (BET) inhibitors (BETi) have shown promise by indirectly blocking the transcriptional activity of this oncogene, thereby reducing tumor growth in the SHH MB subgroup. However, dose-limiting toxicities observed in clinical studies threaten BETi translation. My research in SHH MB models suggests that combining drugs that synergize with BETi can reduce the required BETi dose, minimizing toxicities while preserving efficacy.

My research is aimed at finding drug combinations that by acting synergistically allow a reduction in BETi dosing, minimizing toxicities while preserving efficacy. The successful completion of this project will pave the way for clinical trials aimed at improving outcomes for children with SHH MB. Moreover, given the involvement of GLI in driving other malignancies, this therapeutic approach could be easily extended beyond MB patients.

2024 Awardees

Russell Cochrane headshot

Russell Cochrane

LOWVELO HCC Graduate Fellow

Project: Engineering CAR Tregs for solid tumor immunotherapy

Mentor: Leonardo Ferreira, Ph.D.

Solid tumors are the deadliest and most common form of cancer. Chimeric Antigen Receptor (CAR) T-cell therapy has shown immense success against blood cancers. Researchers hope to translate this type of therapy to solid tumors. However, CAR-T cells struggle to infiltrate and survive in the harsh dense environment of solid tumors.

One subtype of immune cell that accumulates and thrives in the solid tumor environment is the regulatory T cell (Treg). Unfortunately, Tregs help protect tumors from immune attack, as their primary function is to calm down the immune system. Recently, we discovered that high affinity CAR signaling shifts Tregs' function from suppressive to inflammatory while still maintaining the key characteristics of Treg identity.

My project aims to harness this discovery. By utilizing the CAR in Tregs, we can target Tregs directly to tumor cells and harness their ability to penetrate and survive in the tumor environment but change their role from calming the immune system to eliminating the cancer. We are turning Tregs into a ‘Trojan Horse’ that can infiltrate the tumor and fight it from within. By studying these modified CAR-Tregs in the lab and in animal models, we hope to develop new and more effective treatments for solid tumors.

headshot of Valentin Kliebe

Valentin Kliebe

LOWVELO HCC Graduate Fellow

Project: Uncover the signaling mechanism facilitating medulloblastoma self-renewal

Mentor: Jezabel Rodriguez Blanco, Ph.D.

Medulloblastoma (MB), the most common malignant pediatric brain cancer, is currently classified into four major subgroups. The Sonic Hedgehog (SHH) subgroup accounts for one-third of all cases and is characterized by aberrant SHH signaling activation.

While 75% of children with SHH medulloblastoma survive, the remaining suffer from tumor recurrence. The survival upon relapse diagnosis averages only 10 months and no effective therapeutics aimed at preventing it are currently available. Our lab recently identified a subpopulation of MB progenitor cells that is treatment-resistant and responsible for tumor recurrence. Such progenitor cells remain often unharmed by traditional chemotherapy and are capable of self-renewing, just like healthy stem cells, to initiate tumor recurrence. We found that their growth is driven by GLI, the ultimate SHH pathway effector, and targeting this subpopulation by inhibiting GLI activity showed efficacy in preventing MB relapse. Nevertheless, a number of tumors in GLI inhibitor treated animals still recurred. These relapses indicate the involvement of additional signaling mechanisms helping these cells to self-renew.

In my project, I aim to uncover additional signaling mechanisms enabling these treatment-resistant cells to evade chemotherapy and to self-renew. The successful identification of these mechanisms will allow me to design future therapeutic strategies to prevent MB relapse.

headshot of Wyatt Wofford

Wyatt Wofford

LOWVELO HCC Graduate Fellow

Project: Lipid metabolism alterations drive PD-L1 dependent oncogenic signaling in TNBC

Mentor: Besim Ogretmen, Ph.D.

My research focuses on triple-negative breast cancer (TNBC), an aggressive breast cancer subtype with few effective treatment options and a high propensity to metastasize. Although immunotherapy shows promise for metastatic TNBC, it only works for a small percentage of patients. My study investigates how changes in lipid metabolism influence cancer cell resistance to immunotherapy via PD-L1 signaling. By better understanding how PD-L1 helps cancer cells evade immunotherapy, I hope to develop new strategies that make these treatments more effective for TNBC patients.

Past Fellows