About

Mark T. Hughes, MD, MA, is an Assistant Professor of Medicine at the Johns Hopkins University School of Medicine and a faculty member at the Johns Hopkins Berman Institute of Bioethics. He holds a BA in philosophy with a minor in biology from the University of Virginia, an MD from SUNY at Stony Brook, and a master's degree in philosophy (bioethics) from Georgetown University, where his thesis explored the notion of comfort in the healing relationship. Dr. Hughes's research and teaching focus on ethics in clinical practice, research ethics, and medical education. He is involved in developing and delivering curricula on research ethics and clinical ethics for medical students and residents, and he co-developed an internet-based curriculum utilized by residency programs nationwide. Additionally, he serves as co-chair of the Johns Hopkins Hospital Ethics Committee and Consultation Service, and he helps coordinate the Ethics for Lunch monthly panel discussions. His work includes studying ethical issues in daily medical practice, designing ethics curricula, and teaching clinical skills and ethics to medical trainees.

Research topics

• Medicine
• Nursing
• Computer Science
• Family medicine
• Economics
• Business
• Economic growth

Selected publications

• Supplemental legend from Epithelial-to-Mesenchymal Transition Antagonizes Response to Targeted Therapies in Lung Cancer by Suppressing BIM

  2023-03-31

  preprintOpen access

  <p>Supplemental legend</p>

  PublisherDOI

• Supplementary Figures 1-8 from Epithelial-to-Mesenchymal Transition Antagonizes Response to Targeted Therapies in Lung Cancer by Suppressing BIM

  2023-03-31

  preprintOpen access

  <p>We have developed several models of EMT-mediated resistance to EGFR inhibitors in EGFR mutant lung cancers. Figure S1. Expression of EMT-related genes are inversely correlated with BCL2L11 expression; Figure S2. EMT induced by TGF-β results in depressed BIM and apoptotic resistance to EGFR inhibitors in EGFR mutant lung cancer. Figure S3. EGFRi resistant models that underwent an EMT have suppressed BIM levels. Figure S4. ZEB1 binding site located within the BCL2L11 (BIM) promoter. Figure S5. ZEB1 is an EMT marker associated with resistance to EGFRi in lung cancer and its depletion leads to BIM de-repression. Figure S6. BIM can be liberated with BCL-xL inhibition in mesenchymal EGFR mutant lung cancers to restore EGFRi-induced apoptosis. Figure S7. ABT-263 + EGFRi treatment is effective in EGFRi resistant cancers that have undergone an EMT. Figure S8. ER-TWIST phenotype in vivo and mesenchymal KRAS mutant lung cancers downregulate BIM upon EMT induction.</p>

  PublisherDOI

• Emerging Experiences with Virtual Clinical Ethics Consultation: Case Studies from the United States and Malaysia

  The Journal of Clinical Ethics · 2023-03-01 · 2 citations

  articleOpen access

  AbstractThe COVID-19 pandemic has inspired numerous opportunities for telehealth implementation to meet diverse healthcare needs, including the use of virtual communication platforms to facilitate the growth of and access to clinical ethics consultation (CEC) services across the globe. Here we discuss the conceptualization and implementation of two different virtual CEC services that arose during the COVID-19 pandemic: the Clinical Ethics Malaysia COVID-19 Consultation Service and the Johns Hopkins Hospital Ethics Committee and Consultation Service. A common strength experienced by both platforms during virtual delivery included improved ability for local practitioners to address consultation needs for patient populations otherwise unable to access CEC services in their respective locations. Additionally, virtual platforms allowed for enhanced collaboration and sharing of expertise among ethics consultants. Both contexts encountered numerous challenges related to patient care delivery during the pandemic. The use of virtual technologies resulted in decreased personalization of patient-provider communication. We discuss these challenges with respect to contextual differences specific to each service and setting, including differences in CEC needs, sociocultural norms, resource availability, populations served, consultation service visibility, healthcare infrastructure, and funding disparities. Through lessons learned from a health system in the United States and a national service in Malaysia, we provide key recommendations for health practitioners and clinical ethics consultants to leverage virtual communication platforms to mitigate existing inequities in patient care delivery and increase capacity for CEC globally.

  PublisherOA PDFDOI

• SI Table 1 from Epithelial-to-Mesenchymal Transition Antagonizes Response to Targeted Therapies in Lung Cancer by Suppressing BIM

  2023-03-31

  preprintOpen access

  <p>Top 10 correlated genes to BIM (BCL2L11)</p>

  PublisherDOI

• Data from Epithelial-to-Mesenchymal Transition Antagonizes Response to Targeted Therapies in Lung Cancer by Suppressing BIM

  2023-03-31

  preprintOpen access

  <div>Abstract<p><b>Purpose:</b> Epithelial-to-mesenchymal transition (EMT) confers resistance to a number of targeted therapies and chemotherapies. However, it has been unclear why EMT promotes resistance, thereby impairing progress to overcome it.</p><p><b>Experimental Design:</b> We have developed several models of EMT-mediated resistance to EGFR inhibitors (EGFRi) in <i>EGFR</i>-mutant lung cancers to evaluate a novel mechanism of EMT-mediated resistance.</p><p><b>Results:</b> We observed that mesenchymal <i>EGFR</i>-mutant lung cancers are resistant to EGFRi-induced apoptosis via insufficient expression of BIM, preventing cell death despite potent suppression of oncogenic signaling following EGFRi treatment. Mechanistically, we observed that the EMT transcription factor ZEB1 inhibits BIM expression by binding directly to the BIM promoter and repressing transcription. Derepression of BIM expression by depletion of ZEB1 or treatment with the BH3 mimetic ABT-263 to enhance “free” cellular BIM levels both led to resensitization of mesenchymal <i>EGFR</i>-mutant cancers to EGFRi. This relationship between EMT and loss of BIM is not restricted to <i>EGFR</i>-mutant lung cancers, as it was also observed in <i>KRAS</i>-mutant lung cancers and large datasets, including different cancer subtypes.</p><p><b>Conclusions:</b> Altogether, these data reveal a novel mechanistic link between EMT and resistance to lung cancer targeted therapies. <i>Clin Cancer Res; 24(1); 197–208. ©2017 AACR</i>.</p></div>

  PublisherDOI

• How to “Do Ethics” in Pediatrics Practice

  Pediatric Clinics of North America · 2023-11-14

  review1st authorCorresponding
  PublisherDOI

• Data from Epithelial-to-Mesenchymal Transition Antagonizes Response to Targeted Therapies in Lung Cancer by Suppressing BIM

  2023-03-31

  preprintOpen access

  <div>Abstract<p><b>Purpose:</b> Epithelial-to-mesenchymal transition (EMT) confers resistance to a number of targeted therapies and chemotherapies. However, it has been unclear why EMT promotes resistance, thereby impairing progress to overcome it.</p><p><b>Experimental Design:</b> We have developed several models of EMT-mediated resistance to EGFR inhibitors (EGFRi) in <i>EGFR</i>-mutant lung cancers to evaluate a novel mechanism of EMT-mediated resistance.</p><p><b>Results:</b> We observed that mesenchymal <i>EGFR</i>-mutant lung cancers are resistant to EGFRi-induced apoptosis via insufficient expression of BIM, preventing cell death despite potent suppression of oncogenic signaling following EGFRi treatment. Mechanistically, we observed that the EMT transcription factor ZEB1 inhibits BIM expression by binding directly to the BIM promoter and repressing transcription. Derepression of BIM expression by depletion of ZEB1 or treatment with the BH3 mimetic ABT-263 to enhance “free” cellular BIM levels both led to resensitization of mesenchymal <i>EGFR</i>-mutant cancers to EGFRi. This relationship between EMT and loss of BIM is not restricted to <i>EGFR</i>-mutant lung cancers, as it was also observed in <i>KRAS</i>-mutant lung cancers and large datasets, including different cancer subtypes.</p><p><b>Conclusions:</b> Altogether, these data reveal a novel mechanistic link between EMT and resistance to lung cancer targeted therapies. <i>Clin Cancer Res; 24(1); 197–208. ©2017 AACR</i>.</p></div>

  PublisherDOI

• SI Table 1 from Epithelial-to-Mesenchymal Transition Antagonizes Response to Targeted Therapies in Lung Cancer by Suppressing BIM

  2023-03-31

  preprintOpen access

  <p>Top 10 correlated genes to BIM (BCL2L11)</p>

  PublisherDOI

• “They Would Lift My Spirits”

  Journal of Hospice and Palliative Nursing · 2023-03-11 · 3 citations

  articleOpen access

  Surrogate decision-makers make critical decisions for loved ones at the end of life, and some experience lasting negative psychological outcomes. Understanding whom they rely on for support and the types of support they value may inform nursing care and that of other health team members who work with surrogates. The purpose of the study was to explore decision support and other types of support provided to surrogate decision-makers at the end of life of their loved one and perceived usefulness of the support. This secondary analysis of data from a mixed-methods study involved the examination of the transcripts of qualitative interviews with 13 surrogate decision-makers in the United States, conducted between 2010 and 2014. A constant comparative method was used to identify common themes surrounding surrogate decision support at the end of life. Surrogates valued advance directives and conversations with their loved one about treatment preferences. Surrogates described involving many different types of people in decision-making and other types of support. Finally, surrogates appreciated being reassured that they were doing a good job in making decisions and seemed to seek out this type of affirmation from various sources including the health care team, family, and friends. Nurses are well-positioned to provide this affirmation because of the time that they spend caring for the patient and family. Future research should further explore the concept of affirmation of surrogates in their role as a means of support as they make decisions for a loved one.

  PublisherOA PDFDOI

• SI Table 2 from Epithelial-to-Mesenchymal Transition Antagonizes Response to Targeted Therapies in Lung Cancer by Suppressing BIM

  2023-03-31

  preprintOpen access

  <p>ZEB1 binding sites found in 1975R2 cells compared to 1975 parental cells</p>

  PublisherDOI

Frequent coauthors

• Marie T. Nolan

  Emory University

  38 shared

• Daniel P. Sulmasy

  Georgetown University

  36 shared

• Sherita Hill Golden

  Johns Hopkins University

  33 shared

• Joseph A. Carrese

  Johns Hopkins Medicine

  33 shared

• Allen Kachalia

  Johns Hopkins University

  29 shared

• Joan Kub

  Johns Hopkins University

  28 shared

• Peter B. Terry

  26 shared

• Cynda Hylton Rushton

  Johns Hopkins Berman Institute of Bioethics

  24 shared

Awards & honors

• Blaustein Scholarship in the Ethics of Clinical Practice at…