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Sex Differences in the Response to Lung Cancer and Its Relation to Programmed Cell Death Protein-1/Programmed
Morgan Puglisi1, Lauren May1, Thusna Gardiyehewa1
1Department of Human and Molecular Genetics, VCU Institute of Molecular Medicine, Massey Cancer Center, VCU School of Medicine, Richmond, VA 23298, USA.
Abstract:
Background/Objectives: Tumor cells exploit a variety of mechanisms to inhibit the immune response to lung cancer. The programmed cell death protein-1/programmed death-ligand-1 (PD-1/PD-L1) axis is frequently dysregulated in lung cancers with significant impacts on tumor growth. A sex difference has been observed in lung cancer progression and the response to PD-1/PD-L1 therapy, with the extent of benefits differing between men and women. The mechanism underlying these differences has not been fully established. Methods: In an attempt to better understand the nature of these differences, we searched the available literature for reports connecting sex specific bioactive molecules-including estrogens, progesterone, testosterone, follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin, leptin, and activin/inhibin-to sex differences in lung cancer and the response to PD-1/PDL-1 therapies. We then condensed this information to help generate testable hypotheses to explain the observed sex differences in lung cancer and its immunotherapies. Conclusions: From these efforts, we discovered potential roles for sex steroids, FSH, LH, prolactin, leptin, and activin/inhibin in both immune cell activity and cancer cell survival and in the response to PD-1/PD-L1 therapies.
Insights
Sex hormones and other bioactive molecules may explain why lung cancer and immunotherapy responses differ between men and women. Further research into these factors could improve treatments for programmed cell death protein-1/programmed death-ligand-1 (PD-1/PD-L1) therapies.
Area of Science:
- Immunology
- Oncology
- Endocrinology
Background:
- Lung cancer progression and response to PD-1/PD-L1 therapy show observed sex differences.
- The mechanisms driving these sex-based disparities in lung cancer remain unclear.
- The programmed cell death protein-1/programmed death-ligand-1 (PD-1/PD-L1) pathway is crucial in regulating anti-tumor immunity.
Purpose of the Study:
- To investigate the role of sex-specific bioactive molecules in sex differences in lung cancer.
- To explore the connection between these molecules and responses to PD-1/PD-L1 immunotherapies.
- To generate hypotheses explaining observed sex disparities in lung cancer and its treatment.
Main Methods:
- Literature review of studies linking sex hormones (estrogens, progesterone, testosterone) and other molecules (FSH, LH, prolactin, leptin, activin/inhibin) to lung cancer.
- Analysis of existing data on sex differences in lung cancer progression and PD-1/PD-L1 therapy outcomes.
- Synthesis of findings to formulate testable hypotheses.
Main Results:
- Identified potential roles for sex steroids, FSH, LH, prolactin, leptin, and activin/inhibin.
- These molecules appear to influence immune cell activity and cancer cell survival.
- Evidence suggests involvement in the response to PD-1/PD-L1 therapies.
Conclusions:
- Sex-specific bioactive molecules are implicated in lung cancer sex differences.
- These molecules may modulate immune responses and cancer cell behavior.
- Understanding these roles could refine PD-1/PD-L1 immunotherapy strategies for different sexes.
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