The Alan and Sandra Gerry Postdoctoral Research Fellowship Recipients
The Gerry fellowship is awarded to an individual who has demonstrated excellence among their peers and whose work has a focus in metastasis research. This fellowship is set up through a generous gift from the Gerry family specifically for this purpose.
GMTEC’s 2025-2027 Gerry Fellow is Zainab Hussain.
Mentor: Mara Sherman
Project Title: Decoding the role of peripheral nerves and perineural invasion in pancreatic cancer metastases
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer often diagnosed after it has already spread, with a unique tendency to grow around and invade peripheral nerves—a process known as perineural invasion (PNI) and associated with poor prognosis. This study investigates the features of a distinct perineural niche within the pancreatic tumor microenvironment, characterizing nerve-educated cancer and stromal cells that promote tumor progression and spread to distant organs using nerves as a conduit. Through advanced cellular and spatial profiling of human pancreatic tumors, mouse models, and coculture systems with peripheral nerve ganglia, this research aims to uncover mechanisms by which nerve–tumor interactions promote metastasis and identify novel therapeutic targets by modulating nerve activity.
GMTEC’s 2024-2026 Gerry fellow is Ines Godet.
Mentor: Joan Massagué
Project Title: Uncovering the impact of current therapies on LUAD dormant metastasis
Despite recent therapeutic advances, LUAD remains a leading cause of mortality worldwide, with most deaths attributed to metastasis. Metastasis is mediated by disseminated metastasis initiating cells (MICs) that resist multiple physical, metabolic, immune, and therapeutic barriers, and can persist in a latent state in distant sites for months to years. Eventually, MICs drive metastatic relapse, which is clinically uncurable. Adjuvant therapy seeks to prevent cancer relapse by eliminating residual MICs during the latency period. However, efforts to improve adjuvant treatments are hindered by an insufficient understanding of the molecular mechanisms supporting the long-term viability of dormant MICs. Therefore, overt metastasis could potentially be prevented by leveraging an improved understanding of residual MICs to clear them prior to metastatic outbreak. Based on our findings, I hypothesize that MICs are early-stage progenitors with the ability to enter a quiescent state that confers protection against immune surveillance and against therapies targeting growth pathways. My preliminary results confirm that the metastatic dormant ability is associated with the SOX2+ progenitor state. Furthermore, SOX2+ MICs entering a slow-cycling state in response to dormancy signals remain sensitive to killing by targeted KRAS inhibitors but contain a subpopulation that survives and resumes growth upon the removal of KRAS inhibition and dormancy signals. To expand on these findings, I will integrate models of metastatic dormancy both in vitro and in vivo, with strategies to trace and fate-map SOX2+ progenitor cells. Moreover, I will characterize the effect of current targeted and immune checkpoint inhibitors in dormant MICs. In this project I aim to define (1) the dependence of MICs on oncogenic signaling, the (2) effect of targeted therapy and immunotherapy on latent MICs, and (3) strategies to overcome potential resistance mechanisms in MICs. My ultimate goal is to delineate strategies to clear latent MICs and prevent LUAD recurrence.
GMTEC Metastasis Scholars Fellows
Kaden Southard
Mentor: Thomas Norman
Project Title: Drivers of stromal and epithelial transitions in ovarian cancer peritoneal metastasis
High-grade serous ovarian cancer (HGSOC) exhibits a distinctive pattern of metastasis in which cancer cells shed directly into the peritoneal cavity, form heterotypic spheroids with cancer-associated fibroblasts (CAFs), and ultimately implant at distant peritoneal sites. This process requires two critical phenotypic transitions: the progression of fallopian cells from benign p53-mutant precursors to a state capable of anchorage-independent growth, and the emergence of specialized fibroblast states that support cancer cell survival in suspension. Despite their clinical importance, the genetic drivers of these transitions remain poorly understood. This project aims to synthetically recapitulate and thereby mechanistically understand these transitions using a combination of novel genetics techniques and Perturb-seq, a single-cell screening technique that can link engineered genetic changes to their phenotypic impacts at scale.
Philipp Weiler
Mentors: Dana Pe’er & Adrienne Boire
Project Title: Uncovering the regulatory mechanisms leading to leptomeningeal metastasis through multimodal single-cell sequencing across time and space
Systemic cancer spread to the central nervous system (CNS) - leptomeningeal metastasis (LM) - is a devastating diagnosis, entailing disproportionate morbidity and short survival. The limited existing treatment options are merely palliative since cancer invasion into the CNS entails irreparable damage, while the incidence of LM increases with improved treatment options that prolong patient survival, but the mechanisms leading to LM are unknown. The leptomeninges differ from the parenchyma of other metastatic sites as their tissues and fluids are unique in the body; the cerebrospinal fluid (CSF) is a nutrient-depleted environment that has - under normal conditions - traditionally been perceived as isolated from the rest of the body through epithelial cells in the choroid plexus (CP) that form the blood-CSF barrier and produce CSF. Yet, during LM, the epithelial barrier loosens to allow passage of molecules and cells from the CP stroma into the CSF as they pass fibroblasts. Our current understanding of disease progression leads me to a provocative hypothesis that we will study using custom-developed mouse models, high-resolution and multimodal spatial sequencing technologies, and novel computational tools: CNS fibroblast actively remodel their niche in anticipation of LM to recruit, select, and ultimately help administer cancer cells into the CNS.
Shulamit Katzman Endowed Postdoctoral Research Fellow
The Shulamit Katzman Endowed Postdoctoral Research fellowship is awarded to an individual studying the mechanics of metastasis. This highly competitive recognition is set up through a generous gift from the Katzman family specifically for this purpose.
GMTEC’s 2025-2027 Shulamit Katzman Endowed Postdoctoral Research Fellow is Ziad El Bakouny.
Mentors: Craig Thompson and Ed Reznik
Project: Mitochondrial DNA Mutations as Key Drivers of Renal Cell Carcinoma and Modulators of Anti-Tumor Immune Response.
Truncating somatic mutations involving protein-coding genes in mitochondrial DNA (mtDNA) occur in 10% of all cancers, and in up to 20-30% of kidney cancers (Gorelick et al., 2021). The 13 protein-coding genes of the mitochondrial genome encode for key components of the electron transport chain (ETC). Homoplasmic germline mtDNA mutations involving the ETC genes profoundly disrupt mitochondrial oxidative phosphorylation and are universally lethal. Heteroplasmic germline mtDNA mutations lead to mitochondrial disease phenotypes in cells dependent on efficient ATP production, with a significant proportion of patients having renal dysfunction (Gorman et al., 2016; Govers et al., 2021). Paradoxically, somatic mtDNA mutations in cancer involving these genes appear to be under positive selection, despite disrupting the key pathway of ATP generation (Gorelick et al., 2021; Kim et al., 2022). mtDNA research in cancer has been hampered by the limited availability of dedicated mtDNA sequencing and the lack of tools to experimentally model mtDNA variants. Crucially, while mtDNA mutations have been extensively studied in the context of inherited diseases, their role in cancer remains largely unexplored.
We will leverage novel computational advances in mtDNA mutation calling and new methods of mtDNA engineering to study the effect of these somatic mutations on metabolic rewiring, the development of selective dependencies, and the modulation of immune checkpoint inhibitor (ICI) response. Renal cell carcinoma (RCC) represents the ideal tumor to study mtDNA mutations given the high frequency of mtDNA mutations, extensive metabolic disruptions, and responsiveness to ICI. Our overarching hypothesis is that mtDNA mutations cooperate with hypoxia to rewire tumors to a Warburg-like phenotype, which in turn reshapes the immune microenvironment of tumors and can be leveraged to induce synthetic lethalities by inhibiting glycolysis, inducing ferroptosis, or exposure to hyperoxia.