{"id":35712,"date":"2025-07-16T02:25:03","date_gmt":"2025-07-16T06:25:03","guid":{"rendered":"https:\/\/www.cancerresearch.org\/?post_type=cri_scientists&p=35712"},"modified":"2025-07-16T02:25:05","modified_gmt":"2025-07-16T06:25:05","slug":"roberta-zappasodi-phd","status":"publish","type":"cri_scientists","link":"https:\/\/www.cancerresearch.org\/es\/cri-funded-scientists\/roberta-zappasodi-phd","title":{"rendered":"Roberta Zappasodi, PhD"},"content":{"rendered":"\n

A common feature of tumors that respond to immunotherapy is the presence of effector T cells (Teff), which help attack cancer. However, Teff often struggle to function in tumors because cancer cells consume key nutrients like glucose that Teff need to function.

Dr. Roberta Zappasodi\u2019s previous research revealed that tumor cells not only deplete glucose rapidly but also disrupt nearby blood vessels, limiting access to oxygen and nutrients. This creates a hostile, nutrient-poor environment that weakens Teff responses. Surprisingly, regulatory T cells (Tregs), which suppress immune activity, thrive under these conditions and accumulate in tumors.

Dr. Zappasodi\u2019s preliminary data show that reducing the amount of glucose used by tumor cells improves immunotherapy responses by converting Tregs into Teff-like cells and restoring functional blood vessels. She will now investigate how this metabolic reprogramming occurs and how the converted Tregs contribute to anti-tumor immunity. These findings could reveal new ways to reprogram suppressive immune cells into cancer-fighting allies, potentially enhancing the effectiveness of immunotherapy.<\/p>\n\n\n\n

Research Focus<\/h2>\n\n\n\n

T cells, metabolism, anti-tumor immunity<\/strong><\/p>\n\n\n\n

Projects and Grants<\/h2>\n\n\n\n

Mechanisms of \u201cfragile\u201d intratumoral regulatory T cells supporting anti-tumor immunity<\/strong><\/p>\n","protected":false},"excerpt":{"rendered":"

A common feature of tumors that respond to immunotherapy is the presence of effector T cells (Teff), which help attack cancer. 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