1.ER71/ETV2 Promotes Hair Regeneration from Chemotherapeutic Drug-Induced Hair Loss by Enhancing Angiogenesis
Tae-Jin LEE ; Hee-Kyoung KANG ; Jeffrey C. BERRY ; Hong-Gu JOO ; Changwon PARK ; Mark J. MILLER ; Kyunghee CHOI
Biomolecules & Therapeutics 2021;29(5):545-550
Chemotherapy-induced alopecia and hair loss can be stressful in patients with cancer. The hair grows back, but sometimes the hair tends to stay thin. Therefore, understanding mechanisms regulating hair regeneration may improve the management of chemotherapy-induced alopecia. Previous studies have revealed that chemotherapeutic agents induce a hair follicle vascular injury. As hair growth is associated with micro-vessel regeneration, we postulated that the stimulation of angiogenesis might enhance hair regeneration. In particular, mice treated with 5-fluorouracil (5-FU) showed delayed anagen initiation and reduced capillary density when compared with untreated controls, suggesting that the retardation of anagen initiation by 5-FU treatment may be attributed to the loss of perifollicular micro-vessels. We investigated whether the ETS transcription factor ETV2 (aka ER71), critical for vascular development and regeneration, can promote angiogenesis and hair regrowth in a 5-FU-induced alopecia mouse model. Tie2-Cre; Etv2 conditional knockout (CKO) mice, which lack Etv2 in endothelial cells, presented similar hair regrowth rates as the control mice after depilation. Following 5-FU treatment, Tie2-Cre; Etv2 CKO mice revealed a significant reduction in capillary density, anagen induction, and hair restoration when compared with controls. Mice receiving lentiviral Etv2 injection after 5-FU treatment showed significantly improved anagen induction and hair regrowth. Two-photon laser scanning microscopy revealed that enforced Etv2 expression restored normal vessel morphology after 5-FU mediated vessel injury. Our data suggest that vessel regeneration strategies may improve hair regrowth after chemotherapeutic treatment.
2.ER71/ETV2 Promotes Hair Regeneration from Chemotherapeutic Drug-Induced Hair Loss by Enhancing Angiogenesis
Tae-Jin LEE ; Hee-Kyoung KANG ; Jeffrey C. BERRY ; Hong-Gu JOO ; Changwon PARK ; Mark J. MILLER ; Kyunghee CHOI
Biomolecules & Therapeutics 2021;29(5):545-550
Chemotherapy-induced alopecia and hair loss can be stressful in patients with cancer. The hair grows back, but sometimes the hair tends to stay thin. Therefore, understanding mechanisms regulating hair regeneration may improve the management of chemotherapy-induced alopecia. Previous studies have revealed that chemotherapeutic agents induce a hair follicle vascular injury. As hair growth is associated with micro-vessel regeneration, we postulated that the stimulation of angiogenesis might enhance hair regeneration. In particular, mice treated with 5-fluorouracil (5-FU) showed delayed anagen initiation and reduced capillary density when compared with untreated controls, suggesting that the retardation of anagen initiation by 5-FU treatment may be attributed to the loss of perifollicular micro-vessels. We investigated whether the ETS transcription factor ETV2 (aka ER71), critical for vascular development and regeneration, can promote angiogenesis and hair regrowth in a 5-FU-induced alopecia mouse model. Tie2-Cre; Etv2 conditional knockout (CKO) mice, which lack Etv2 in endothelial cells, presented similar hair regrowth rates as the control mice after depilation. Following 5-FU treatment, Tie2-Cre; Etv2 CKO mice revealed a significant reduction in capillary density, anagen induction, and hair restoration when compared with controls. Mice receiving lentiviral Etv2 injection after 5-FU treatment showed significantly improved anagen induction and hair regrowth. Two-photon laser scanning microscopy revealed that enforced Etv2 expression restored normal vessel morphology after 5-FU mediated vessel injury. Our data suggest that vessel regeneration strategies may improve hair regrowth after chemotherapeutic treatment.
3.YPED:An Integrated Bioinformatics Suite and Database for Mass Spectrometry-based Proteomics Research
Colangelo M. CHRISTOPHER ; Shifman MARK ; Cheung KEI-HOI ; Stone L. KATHRYN ; Carriero J. NICHOLAS ; Gulcicek E. EROL ; Lam T. TUKIET ; Wu TERENCE ; Bjornson D. ROBERT ; Bruce CAN ; Nairn C. ANGUS ; Rinehart JESSE ; Miller L. PERRY ; Williams R. KENNETH
Genomics, Proteomics & Bioinformatics 2015;(1):25-35
We report a significantly-enhanced bioinformatics suite and database for proteomics research called Yale Protein Expression Database (YPED) that is used by investigators at more than 300 institutions worldwide. YPED meets the data management, archival, and analysis needs of a high-throughput mass spectrometry-based proteomics research ranging from a single laboratory, group of laboratories within and beyond an institution, to the entire proteomics com-munity. The current version is a significant improvement over the first version in that it contains new modules for liquid chromatography–tandem mass spectrometry (LC–MS/MS) database search results, label and label-free quantitative proteomic analysis, and several scoring outputs for phosphopeptide site localization. In addition, we have added both peptide and protein comparative analysis tools to enable pairwise analysis of distinct peptides/proteins in each sample and of overlapping peptides/proteins between all samples in multiple datasets. We have also implemented a targeted proteomics module for automated multiple reaction monitoring (MRM)/selective reaction monitoring (SRM) assay development. We have linked YPED’s database search results and both label-based and label-free fold-change analysis to the Skyline Panorama repository for online spectra visualization. In addition, we have built enhanced functionality to curate peptide identifications into an MS/MS peptide spectral library for all of our protein database search identification results.
4.Meeting Report: Translational Advances in Cancer Prevention Agent Development Meeting
Mark Steven MILLER ; Peter J. ALLEN ; Powel H. BROWN ; Andrew T. CHAN ; Margie L. CLAPPER ; Roderick H. DASHWOOD ; Shadmehr DEMEHRI ; Mary L. DISIS ; Raymond N. DUBOIS ; Robert J. GLYNN ; Thomas W. KENSLER ; Seema A. KHAN ; Bryon D. JOHNSON ; Karen T. LIBY ; Steven M. LIPKIN ; Susan R. MALLERY ; Emmanuelle J. MEUILLET ; Richard B.S. RODEN ; Robert E. SCHOEN ; Zelton D. SHARP ; Haval SHIRWAN ; Jill M. SIEGFRIED ; Chinthalapally V. RAO ; Ming YOU ; Eduardo VILAR ; Eva SZABO ; Altaf MOHAMMED
Journal of Cancer Prevention 2021;26(1):71-82
The Division of Cancer Prevention of the National Cancer Institute (NCI) and the Office of Disease Prevention of the National Institutes of Health co-sponsored the Translational Advances in Cancer Prevention Agent Development Meeting on August 27 to 28, 2020. The goals of this meeting were to foster the exchange of ideas and stimulate new collaborative interactions among leading cancer prevention researchers from basic and clinical research; highlight new and emerging trends in immunoprevention and chemoprevention as well as new information from clinical trials; and provide information to the extramural research community on the significant resources available from the NCI to promote prevention agent development and rapid translation to clinical trials. The meeting included two plenary talks and five sessions covering the range from pre-clinical studies with chemo/immunopreventive agents to ongoing cancer prevention clinical trials. In addition, two NCI informational sessions describing contract resources for the preclinical agent development and cooperative grants for the Cancer Prevention Clinical Trials Network were also presented.
5.Meeting Report: Translational Advances in Cancer Prevention Agent Development Meeting
Mark Steven MILLER ; Peter J. ALLEN ; Powel H. BROWN ; Andrew T. CHAN ; Margie L. CLAPPER ; Roderick H. DASHWOOD ; Shadmehr DEMEHRI ; Mary L. DISIS ; Raymond N. DUBOIS ; Robert J. GLYNN ; Thomas W. KENSLER ; Seema A. KHAN ; Bryon D. JOHNSON ; Karen T. LIBY ; Steven M. LIPKIN ; Susan R. MALLERY ; Emmanuelle J. MEUILLET ; Richard B.S. RODEN ; Robert E. SCHOEN ; Zelton D. SHARP ; Haval SHIRWAN ; Jill M. SIEGFRIED ; Chinthalapally V. RAO ; Ming YOU ; Eduardo VILAR ; Eva SZABO ; Altaf MOHAMMED
Journal of Cancer Prevention 2021;26(1):71-82
The Division of Cancer Prevention of the National Cancer Institute (NCI) and the Office of Disease Prevention of the National Institutes of Health co-sponsored the Translational Advances in Cancer Prevention Agent Development Meeting on August 27 to 28, 2020. The goals of this meeting were to foster the exchange of ideas and stimulate new collaborative interactions among leading cancer prevention researchers from basic and clinical research; highlight new and emerging trends in immunoprevention and chemoprevention as well as new information from clinical trials; and provide information to the extramural research community on the significant resources available from the NCI to promote prevention agent development and rapid translation to clinical trials. The meeting included two plenary talks and five sessions covering the range from pre-clinical studies with chemo/immunopreventive agents to ongoing cancer prevention clinical trials. In addition, two NCI informational sessions describing contract resources for the preclinical agent development and cooperative grants for the Cancer Prevention Clinical Trials Network were also presented.