2025 Forbeck Foundation Spring Newsletter

BECK SCHOLARS

FUSION ONCOGENE

Ilaria Gritti, PhD Massachusetts General Hospital AVAILABLE FOR SPONSORSHIP

Derek Janssens, PhD Fred Hutch Cancer Center SPONSORED BY: BILL KINZER

Fibrolamellar carcinoma (FLC) is a rare liver cancer in young adults caused by a gene fusion (DNAJB1-PRKACA). This fusion turns on a pathway that helps the cancer grow. My research focuses on blocking this pathway with treatments and understanding how it affects the cell’s energy centers (mitochondria)

Derek is developing new genomics technologies to study how cells commit to specific fates in diverse human tissues, focusing on DNA-binding proteins at the single-cell level. Many cancer- related fusion proteins bind to DNA, and changes in this binding may contribute to tumors’ ability to resist treatment.

MEET THE 2025 SPRING FORBECK SCHOLARS

HARNESSING STROMA-IMMUNE INTERACTIONS FOR ANTI-CANCER THERAPY

Anna-Maria Globig, MD Allen Institute for Immunology SPONSORED BY: THE LEINEBERG FOUNDATION My lab studies how nerve signals in tumors affect T cell exhaustion and immune responses in cancers like pancreatic cancer. By understanding the interactions between nerves, immune cells, and tumor cells, we aim to develop new strategies to enhance cancer treatments and overcome current therapy limitations.

Alex Papachristodoulou, PhD Columbia University Irving Medical Center SPONSORED BY: THE LEINEBERG FOUNDATION My research explores how mitochondrial DNA (mtDNA) changes, often overlooked in cancer studies, drive prostate cancer. I study how mtDNA mutations and NKX3.1 loss fuel cancer progression, using unique models to uncover links between mitochondrial stress, aging, and cancer. Zhangli Su, PhD University of Alabama at Birmingham SPONSORED BY: BILL & HELEN JOHNSON My research combines experimental lab work and bioinformatics to understand how RNA modifications contribute to cancer. I study how these modifications respond to environmental and internal signals and their role in regulating RNA metabolism and signaling in cancer development. Shruthy Suresh, PhD Institute of Genomics & Integrative Biology SPONSORED BY: THE SPEDALE FAMILY My lab studies how cancer cells change their metabolism to spread and evade the immune system. We found that disrupted cholesterol transport in melanoma weakens T cell responses. We’re exploring how this reshapes the tumor environment and testing if blocking a cholesterol byproduct can boost immunotherapy.

MITOCHONDRIAL STRESS IN CANCER

Emma Guilbaud, PhD Fox Chase Cancer Center SPONSORED BY: THE LEINEBERG FOUNDATION My research focuses on boosting immune responses in breast cancer (BC) after radiation therapy (RT). Since BC often resists immunotherapy, I study how targeting mitochondrial stress—like blocking mitophagy and enhancing immune signals—can strengthen RT’s anticancer effects.

RNA MODIFICATIONS IN MRNA TRANSLATION AND CANCER Steffen Fuchs, MD Charité-University Medicine Berlin SPONSORED BY: THE LEINEBERG FOUNDATION

My research focuses on how RNA molecules drive therapy resistance in childhood neuroblastoma. I study circular RNAs (circRNAs) and their role in cancer progression, explore their potential as biomarkers in liquid biopsies, and use advanced sequencing to uncover RNA changes.

TARGETING MITOCHONDRIA IN CANCER (IMMUNO)THERAPY Hannah Bell, PhD University of Michigan SPONSORED BY: THE ECKLAND FAMILY

SPONSOR A SCHOLAR Forbeck Scholars are selected through a highly competitive process. With your pledge of $1,000 a year for three years ($3,000 commitment), you are supporting a specific candidate, of your choice, to attend these meetings and to follow his/her progress over the years. Many of our scholars have become highly acclaimed researchers, directors of institutions; they are the future of cancer research.

I discovered that perforin, a T cell protein crucial for anti-tumor immunity, damages mitochondria by disrupting iron uptake. This leads to mitochondrial dysfunction. My goal is to develop therapies to enhance perforin’s effects and improve immunotherapy.

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