• Targeted therapies, drug resistance, and two recent cancer research publications

  • Dec 10 2021
  • Length: 35 mins
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Targeted therapies, drug resistance, and two recent cancer research publications

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  • In this episode of the TheoryLab podcast, two American Cancer Society grantees discussed key takeaways from their recent publications. In the first part of the conversation, which is intended for a lay audience, Dr. Joshua Andersen and Dr. Bhuminder Singh talked about targeted therapies, treatment side effects, and drug resistance. Then they moved into a more technical discussion of their recent papers. Dr. Andersen recently published findings showing that “TNK1 is a ubiquitin-binding and 14-3-3-regulated kinase that can be targeted to block tumor growth.” https://doi.org/10.1038/s41467-021-25622-3 Dr. Singh published a study recently showing that “Induction of apically mistrafficked epiregulin disrupts epithelial polarity via aberrant EGFR signaling.” https://doi.org/10.1242/jcs.255927 Joshua L. Andersen, PhD, is Associate Professor of Biochemistry at Brigham Young University. He is a two-time American Cancer Society grantee. Bhuminder Singh, PhD, is Assistant Professor of Medicine and Cell and Developmental Biology at Vanderbilt University Medical Center, and he is also a two-time American Cancer Society grantee. 1:25 – Dr. Andersen explains why his lab is focused on improving targeted therapies 2:31 – Dr. Singh describes how his research is focused on addressing drug resistance in colorectal cancer 4:28 – Dr. Andersen dives into his lab’s new Nature Communications paper on a new cancer driver—"it’s been probably the most rewarding project that I’ve been a part of in my career” 8:11 – Dr. Singh asks a few questions about the paper: “Are there any mutations in TNK1 in human cancer?” 10:01 – What ubiquitinated proteins was it binding to? 11:44 – Is TNK1 itself ubiquitinated in certain conditions? 12:49 – Dr. Singh explains takeaways from his paper, “Induction of apically mistrafficked epiregulin disrupts epithelial polarity via aberrant EGFR signaling” 19:16 – Follow-up questions from Dr. Andersen: “How could the mistrafficking of a single ligand affect its localization so dramatically?” 22:04 – “That has to send a signal then to start trafficking the intracellular EGFR out to the apical side of the cell, right?” 27:49 – “As someone who hasn’t really thought about cell polarity very much inside a solid tumor, what would be the effects of mistrafficking in terms of the architecture of a solid tumor?” 31:18 – The impact of American Cancer Society funding on their research
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