About

Charles Chang is an Assistant Professor of Environment at Duke Kunshan University, a position he has held since 2020. He earned his Ph.D. from the University of Wisconsin, Madison in 2016. His professional profile is hosted on Scholars@Duke, where his academic credentials and current appointments are listed. Recent news highlights include his involvement in incorporating climate and sustainability topics into classes across Duke University, as reported in July 2024. Further detailed information about his research focus, background, and key contributions is not provided in the available page text.

Research topics

• Genetics
• Endocrinology
• Biology
• Cancer research
• Internal medicine
• Medicine
• Chemistry
• Immunology
• Biochemistry
• Cell biology

Selected publications

• Single-cell transcriptomics reveals immune landscape dynamics in metastatic hormone receptor-positive breast cancer treated with abemaciclib and endocrine therapy

  Clinical Cancer Research · 2026-05-13

  article

  PURPOSE: In advanced estrogen receptor-positive (ER+), human epidermal growth factor receptor 2-negative (HER2-) breast cancer, the combination of cyclin-dependent kinase 4 and 6 inhibitors (CDK4/6i) with endocrine therapy (ET) is the standard of care for treatment in the first-line setting. While CDK4/6i were initially developed to induce cell cycle arrest, it is evident that CDK4/6i also have the potential to regulate the tumor immune microenvironment. Here, we characterize the baseline immune landscape and the immunomodulatory effects of abemaciclib and ET in advanced breast cancer tumors. METHODS: We used single-cell RNA-sequencing of CD45-enriched cells to investigate the impact of the CDK4/6i, abemaciclib, and ET on the transcriptome of immune cell populations in 13 matched-pair advanced and metastatic ER+/HER2- breast tumor biopsies. We tested the association of immune cell population gene signatures with survival in publicly available datasets. RESULTS: We profiled 170,798 cells from bone, breast, lymph node, and liver biopsies. We find that expression of genes associated with interferon response are downregulated in many T cell populations. Expression of genes associated with antigen presentation were upregulated in tumor-associated macrophages (TAMs) and dendritic cells following treatment. The relative proportion of TREM2+ TAMs decreases following treatment with abemaciclib and ET in late progressors and lower expression of the TREM2+ TAM signature is associated with improved overall survival in breast cancer patients. CONCLUSIONS: Our data reveal heterogeneous lymphoid and myeloid subpopulations in advanced and metastatic breast tumors that are associated with late progression on abemaciclib and ET and overall survival in breast cancer patients.

  PublisherDOI

• Supplementary Video 4 from Targeting CaMKK2 Inhibits Actin Cytoskeletal Assembly to Suppress Cancer Metastasis

  2025-11-24

  articleOpen access

  <p>Supplementary Video 4</p>

  PublisherDOI

• Dietary methionine restriction primes T cell metabolism for activation and tumor inhibition and enhances the efficacy of immune checkpoint blockade

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-09-21

  preprintOpen access

  The proliferation of many cancer cells is methionine dependent and dietary methionine restriction (MR) has shown anti-tumor effects in a wide variety of immunodeficiency preclinical models. Yet, whether MR exerts an anti-tumor effect in the presence of an immune-competent background remains inconclusive. Accumulating evidence has shown an essential role of methionine in immune cell differentiation and function. Thus, competition for methionine between tumor cells and immune cells in the tumor microenvironment may drive tumor growth and tumor response to therapy. Here, we aim to define the impact of MR on tumor growth and associated immunity. We first assessed the effect of MR in a series of immunocompetent mouse models of melanoma, colorectal cancer, breast cancer, and lung. MR led to a broad tumor inhibition effect across these models and such tumor inhibition was not sex-or genetic background-dependent but appears to be fully or partially immune-dependent. Through flow cytometry analysis, we found a consistent increase in intratumoral activated CD8 + T cells across different tumor models and depletion of CD8 + T cells partially or completely reversed MR-induced tumor inhibition in a model dependent manner. Interestingly in young healthy non-tumor-bearing mice, MR increased spleen CD3 + and CD8 + T cell populations. Metabolomics and RNAseq analysis of spleen-derived CD8 + T cells revealed significant increase in purine metabolism and amino acid metabolism and that are in line with the metabolic feature of activated T cells. Furthermore, MR improved the efficacy of anti-PD1 immune checkpoint blockade. Together, MR primes T cell metabolism for its anti-tumor effect and improves the efficacy of anti-PD1 checkpoint blockade.

  PublisherOA PDFDOI

• Supplementary Video 3 from Targeting CaMKK2 Inhibits Actin Cytoskeletal Assembly to Suppress Cancer Metastasis

  2025-11-24

  articleOpen access

  <p>Supplementary Video 3</p>

  PublisherDOI

• Supplementary Data from Increased CaMKK2 Expression Is an Adaptive Response That Maintains the Fitness of Tumor-Infiltrating Natural Killer Cells

  2025-11-26

  articleOpen access

  <p>Supplementary Figures and Tables: 5 figures, 3 tables</p>

  PublisherOA PDFDOI

• Supplementary Video 1 from Targeting CaMKK2 Inhibits Actin Cytoskeletal Assembly to Suppress Cancer Metastasis

  2025-11-24

  articleOpen access

  <p>Supplementary Video 1</p>

  PublisherDOI

• Supplementary Video 2 from Targeting CaMKK2 Inhibits Actin Cytoskeletal Assembly to Suppress Cancer Metastasis

  2025-11-24

  articleOpen access

  <p>Supplementary Video 2</p>

  PublisherDOI

• Supplementary Figures 1-4 and Tables 1-2 from Targeting CaMKK2 Inhibits Actin Cytoskeletal Assembly to Suppress Cancer Metastasis

  2025-11-24

  articleOpen access

  <p>Contains Supplementary Figures 1-4, Supplementary Tables 1-2 and legends for Supplementary Videos 1-4</p>

  PublisherDOI

• Supplementary Video 1 from Targeting CaMKK2 inhibits actin cytoskeletal assembly to suppress cancer metastasis

  2024-09-16

  preprintOpen access

  <p>Supplementary Video 1</p>

  PublisherDOI

• Estrogen signaling suppresses tumor-associated tissue eosinophilia to promote breast tumor growth

  Science Advances · 2024-09-27 · 24 citations

  articleOpen access

  Estrogens regulate eosinophilia in asthma and other inflammatory diseases. Further, peripheral eosinophilia and tumor-associated tissue eosinophilia (TATE) predicts a better response to immune checkpoint blockade (ICB) in breast cancer. However, how and if estrogens affect eosinophil biology in tumors and how this influences ICB efficacy has not been determined. Here, we report that estrogens decrease the number of peripheral eosinophils and TATE, and this contributes to increased tumor growth in validated murine models of breast cancer and melanoma. Moreover, estrogen signaling in healthy female mice also suppressed peripheral eosinophil prevalence by decreasing the proliferation and survival of maturing eosinophils. Inhibiting estrogen receptor (ER) signaling decreased tumor growth in an eosinophil-dependent manner. Further, the efficacy of ICBs was increased when administered in combination with anti-estrogens. These findings highlight the importance of ER signaling as a regulator of eosinophil biology and TATE and highlight the potential near-term clinical application of ER modulators to increase ICB efficacy in multiple tumor types.

  PublisherDOI

Recent grants

• NIH Grant K01CA095094

  NIH · $379k · 2007

Frequent coauthors

• Donald P. McDonnell

  Duke University

  190 shared

• Sandeep Artham

  Duke University

  43 shared

• Dmitri Kazmin

  Stanford University

  39 shared

• Rachid Safi

  Duke University

  39 shared

• Debarati Mukherjee

  Duke University

  38 shared

• Patrick K. Juras

  Duke University

  35 shared

• John D. Norris

  33 shared

• Binita Chakraborty

  32 shared