Grantee Impact Archives

Lymphatic Vessels: Enabling Defense on Two Fronts

In a war, first-line troops are essential -- such are resident memory T cells (TRM), standing guard at peripheral sites, ready to fight infections and cancer. The Laboratory for Lymphatic Immunobiology, led by 2022 AACR-Bristol Myers Squibb Midcareer Female Investigator Grant Recipient Amanda Lund, PhD, seeks to understand how transport of TRMs through lymphatic vessels helps facilitate critical peripheral immune responses to antigen, whether presented by infectious agents or cancer cells.

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TTFields: A Potential Treatment of Spinal Metastases

Claudio E. Tatsui, MD, recipient of the 2021 AACR-Novocure Tumor Treating Fields Research Grant, and Christopher A. Alvarez-Breckenridge, MD, PhD, recipient of the 2023 AACR-Novocure Career Development Award for Cancer Research recently uncovered how the emerging treatment modality Tumor Treating Fields (TTFields) could be leveraged as a local therapy in the treatment of spinal metastases.

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Neutrophils Pave the Way for Chronic Stress-Induced Cancer Metastasis

Xue-Yan He, PhD, was awarded the AACR-AstraZeneca Breast Cancer Research Fellowship in 2021. During her postdoctoral fellowship, Dr. He uncovered how neutrophils create a pro-metastatic environment in response to chronic stress. The results of this study highlight the potential of stress reduction as a strategy for cancer patients to improve treatment outcome.

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PARP Inhibitors: Not Just for Solid Tumors

More than half of patients with myelodysplastic syndrome (MDS) have a mutation in an RNA splicing factor gene. In particular, mutations in U2AF1 and SRSF2 splicing factor genes are associated with worse overall survival and increased risk of transformation of MDS to secondary acute myelogenous leukemia. The team led by Hai Dang Nguyen, PhD, recipient of a 2022 AACR Career Development Award to Further Diversity, Equity, and Inclusion in Cancer Research, demonstrated the therapeutic potential of PARP inhibitors in U2AF1- and SRSF2- mutant leukemias.

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A Mechanosensitive Hormone Signaling Pathway Increases Breast Cancer Risk

Jason Northey, PhD, recipient of the 2015 AACR Basic Cancer Research Fellowship and 2017 AACR-Janssen Fellowship in Cancer Interception Research, and his colleagues uncovered how a stiff extracellular matrix, such as that observed in high mammographic density breast tissue, promotes ERK activity, progesterone receptor-dependent RANK signaling, and increased stemness, pointing to a potential benefit of RANK signaling inhibition as an anti-cancer treatment and prevention strategy.

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H. Pylori Infection Alters the Trajectory of Gastric Cancer Beyond Initiation

Valerie O’Brien, PhD, recipient of the 2018 Debbie’s Dream Foundation-AACR Gastric Cancer Research Fellowship, in memory of Sally Mandel, and her colleagues discovered a precancerous gastric epithelium cell type whose expansion is driven by the bacterium Helicobacter pylori (Hp), a bacterium that colonizes the stomach of half the world’s population.

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Remodeling of the Tumor Microenvironment in Ewing Sarcoma

Emma Wrenn, PhD, recipient of the 2022 AACR-QuadW Foundation Sarcoma Research Fellowship, in memory of Willie Tichenor and her colleagues recently uncovered a mechanism by which rare sub-populations of tumor cells expressing low levels of EWS::FLI1 remodel the tumor microenvironment in Ewing Sarcoma.

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Navigating Bladder Cancer: FGFR3 and the Immunotherapy Challenge

More than 80,000 people are diagnosed in the US with bladder cancer each year. 2019 AACR Grant Recipient Joshua Meeks, MD, PhD, sought to define immune checkpoint inhibitor resistance mechanisms in bladder cancer.

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Impacting Community through Community

A growing share of US adult smokers – Hispanic/Latino adults – have been found to be less likely to receive advice to quit and use proven cessation treatments than non-Hispanic white adults. 2021 AACR-Genentech Cancer Disparities Fellow Francisco Cartujano, MD, seeks to address tobacco-related disparities in Latinos by promoting smoking cessation and physical activity using a mobile intervention.

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Targeting TNBC with an MDM2- PROTAC

Triple negative breast cancer (TNBC) is an aggressive cancer with high rates of p53 inactivation and lower survival rates than other breast cancer types due to increased metastasis and relapse (1). Owing to the frequent inactivation of p53, compounds that inhibit p53 from binding to its negative regulator, MDM2, are ineffective in TNBC. In a recent study published in Cancer Discovery, Dr. Eischen and her colleagues used an MDM2-targeted PROteolysis TArgeting Chimera (PROTAC) to reveal the requirement for MDM2 in p53 inactivated TNBC and identify a new therapeutic target for the disease.

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