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8 results on '"Ketosugbo, Kwami F'

1. Oral minoxidil for late alopecia in cancer survivors

Author

Kuo, Alyce Mei-Shiuan, Reingold, Rachel E., Ketosugbo, Kwami F., Pan, Alexander, Kraehenbuehl, Lukas, Dusza, Stephen, Gajria, Devika, Lake, Diana E., Bromberg, Jacqueline F., Traina, Tiffany A., Fornier, Monica N., Gucalp, Ayca, D’Alessandro, Brian M., Rotemberg, Veronica, Dauscher, Megan, Shapiro, Jerry, Goldfarb, Shari B., Markova, Alina, and Lacouture, Mario E.

Published
2024
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2. Immunologic Profiling of Immune-Related Cutaneous Adverse Events with Checkpoint Inhibitors Reveals Polarized Actionable Pathways

Author

Lacouture, Mario E., primary, Goleva, Elena, additional, Shah, Neil, additional, Rotemberg, Veronica, additional, Kraehenbuehl, Lukas, additional, Ketosugbo, Kwami F., additional, Merghoub, Taha, additional, Maier, Tara, additional, Bang, Alexander, additional, Gu, Stephanie, additional, Salvador, Trina, additional, Moy, Andrea P., additional, Lyubchenko, Taras, additional, Xiao, Olivia, additional, Hall, Clifton F., additional, Berdyshev, Evgeny, additional, Crooks, James, additional, Weight, Ryan, additional, Kern, Jeffrey A., additional, and Leung, Donald Y.M., additional

Published
2024
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3. Immunologic Profiling of Immune-Related Cutaneous Adverse Events with Checkpoint Inhibitors Reveals Polarized Actionable Pathways

Author

Lacouture, Mario E; https://orcid.org/0000-0002-4818-3710, Goleva, Elena; https://orcid.org/0000-0002-4685-9318, Shah, Neil; https://orcid.org/0000-0001-5752-6212, Rotemberg, Veronica; https://orcid.org/0000-0003-0639-2677, Kraehenbuehl, Lukas; https://orcid.org/0000-0001-5411-5661, Ketosugbo, Kwami F; https://orcid.org/0000-0003-1637-1941, Merghoub, Taha; https://orcid.org/0000-0002-1518-5111, Maier, Tara; https://orcid.org/0009-0001-7691-404X, Bang, Alexander; https://orcid.org/0000-0002-1700-2411, Gu, Stephanie; https://orcid.org/0000-0002-6416-785X, Salvador, Trina; https://orcid.org/0009-0009-2346-0660, Moy, Andrea P; https://orcid.org/0000-0001-5431-6682, Lyubchenko, Taras; https://orcid.org/0000-0001-9466-5916, Xiao, Olivia; https://orcid.org/0000-0002-3869-5894, Hall, Clifton F; https://orcid.org/0000-0002-5180-1014, Berdyshev, Evgeny; https://orcid.org/0000-0002-1376-0098, Crooks, James; https://orcid.org/0000-0002-0021-5701, Weight, Ryan; https://orcid.org/0009-0006-0982-2096, Kern, Jeffrey A; https://orcid.org/0000-0001-9709-9622, Leung, Donald Y M; https://orcid.org/0000-0002-0177-3844, Lacouture, Mario E; https://orcid.org/0000-0002-4818-3710, Goleva, Elena; https://orcid.org/0000-0002-4685-9318, Shah, Neil; https://orcid.org/0000-0001-5752-6212, Rotemberg, Veronica; https://orcid.org/0000-0003-0639-2677, Kraehenbuehl, Lukas; https://orcid.org/0000-0001-5411-5661, Ketosugbo, Kwami F; https://orcid.org/0000-0003-1637-1941, Merghoub, Taha; https://orcid.org/0000-0002-1518-5111, Maier, Tara; https://orcid.org/0009-0001-7691-404X, Bang, Alexander; https://orcid.org/0000-0002-1700-2411, Gu, Stephanie; https://orcid.org/0000-0002-6416-785X, Salvador, Trina; https://orcid.org/0009-0009-2346-0660, Moy, Andrea P; https://orcid.org/0000-0001-5431-6682, Lyubchenko, Taras; https://orcid.org/0000-0001-9466-5916, Xiao, Olivia; https://orcid.org/0000-0002-3869-5894, Hall, Clifton F; https://orcid.org/0000-0002-5180-1014, Berdyshev, Evgeny; https://orcid.org/0000-0002-1376-0098, Crooks, James; https://orcid.org/0000-0002-0021-5701, Weight, Ryan; https://orcid.org/0009-0006-0982-2096, Kern, Jeffrey A; https://orcid.org/0000-0001-9709-9622, and Leung, Donald Y M; https://orcid.org/0000-0002-0177-3844

Abstract

Purpose: Immune-related cutaneous adverse events (ircAEs) occur in ≥50% of patients treated with checkpoint inhibitors (CPI), but mechanisms are poorly understood. Experimental Design: Phenotyping/biomarker analyses were conducted in 200 patients on CPIs (139 with ircAEs, 61 without, control) to characterize their clinical presentation and immunologic endotypes. Cytokines were evaluated in skin biopsies, skin tape strip (STS) extracts and plasma using real-time PCR and Meso Scale Discovery multiplex cytokine assays. Results: Eight ircAE phenotypes were identified: pruritus (26%), maculopapular rash (MPR; 21%), eczema (19%), lichenoid (11%), urticaria (8%), psoriasiform (6%), vitiligo (5%), and bullous dermatitis (4%). All phenotypes showed skin lymphocyte and eosinophil infiltrates. Skin biopsy PCR revealed the highest increase in IFN-gamma mRNA in patients with lichenoid (p<0.0001) and psoriasiform dermatitis (p<0.01) as compared to patients without ircAEs, while the highest IL-13 mRNA levels were detected in the eczema (p<0.0001, compared to control). IL-17A mRNA was selectively increased in psoriasiform (p<0.001), lichenoid (p<0.0001), bullous dermatitis (p<0.05) and MPR (p<0.001), compared to control. Distinct cytokine profiles were confirmed in STS and plasma. Analysis determined increased skin/plasma IL-4 cytokine in pruritus, skin IL-13 in eczema, plasma IL-5 and IL-31 in eczema and urticaria, and mixed-cytokine pathways in MPR. Broad inhibition via corticosteroids or type 2-cytokine targeted inhibition resulted in clinical benefit in these ircAEs. In contrast, significant skin upregulation of type 1/type 17 pathways was found in psoriasiform, lichenoid, bullous dermatitis, and type 1 activation in vitiligo. Conclusions: Distinct immunologic ircAE endotypes suggest actionable targets for precision medicine-based interventions.

Published
2024

5. A screen for E3 ubiquitination ligases that genetically interact with the adaptor protein Cindr during Drosophila eye patterning.

Author

Kwami F Ketosugbo, Henry L Bushnell, and Ruth I Johnson

Subjects
Medicine, Science
Abstract

Ubiquitination is a crucial post-translational modification that can target proteins for degradation. The E3 ubiquitin ligases are responsible for recognizing substrate proteins for ubiquitination, hence providing specificity to the process of protein degradation. Here, we describe a genetic modifier screen that identified E3 ligases that modified the rough-eye phenotype generated by expression of cindrRNAi transgenes during Drosophila eye development. In total, we identified 36 E3 ligases, as well as 4 Cullins, that modified the mild cindrRNA mis-patterning phenotype. This indicates possible roles for these E3s/Cullins in processes that require Cindr function, including cytoskeletal regulation, cell adhesion, cell signaling and cell survival. Three E3 ligases identified in our screen had previously been linked to regulating JNK signaling.

Published
2017
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6. JNK is antagonized to ensure the correct number of interommatidial cells pattern the Drosophila retina

Author

Ruth I. Johnson, Mark B. Hellerman, Kwami F. Ketosugbo, Christina E. Feiler, Valerie L. Nazzaro, and Henry L. Bushnell

Subjects
0301 basic medicine, Programmed cell death, animal structures, Morphogenesis, Apoptosis, Biology, Epithelium, Retina, Article, 03 medical and health sciences, 0302 clinical medicine, medicine, Animals, Drosophila Proteins, Molecular Biology, Body Patterning, Kinase, Microfilament Proteins, JNK Mitogen-Activated Protein Kinases, Pupa, Gene Expression Regulation, Developmental, Cell Biology, biology.organism_classification, Cell biology, ddc, 030104 developmental biology, medicine.anatomical_structure, Drosophila melanogaster, Signal transduction, 030217 neurology & neurosurgery, Drosophila Protein, Developmental Biology, Signal Transduction
Abstract

Apoptosis is crucial during the morphogenesis of most organs and tissues, and is utilized for tissues to achieve their proper size, shape and patterning. Many signaling pathways contribute to the precise regulation of apoptosis. Here we show that Jun N-terminal Kinase (JNK) activity contributes to the coordinated removal of interommatidial cells via apoptosis in the Drosophila pupal retina. This is consistent with previous findings that JNK activity promotes apoptosis in other epithelia. However, we found that JNK activity is repressed by Cindr (the CIN85 and CD2AP ortholog) in order to promote cell survival. Reducing the amount of Cindr resulted in ectopic cell death. Increased expression of the Drosophila JNK basket in the setting of reduced cindr expression was found to result in even more severe apoptosis, whilst ectopic death was found to be reduced if retinas were heterozygous for basket. Hence Cindr is required to properly restrict JNK-mediated apoptosis in the pupal eye, resulting in the correct number of interommatidial cells. A lack of precise control over developmental apoptosis can lead to improper tissue morphogenesis.

Published
2018

7. A screen for E3 ubiquitination ligases that genetically interact with the adaptor protein Cindr during Drosophila eye patterning

Author

Henry L. Bushnell, Kwami F. Ketosugbo, and Ruth I. Johnson

Subjects
0301 basic medicine, Pigments, Genetic Screens, Organogenesis, Gene Identification and Analysis, lcsh:Medicine, Eye, Biochemistry, Ligases, 0302 clinical medicine, Ubiquitin, Medicine and Health Sciences, Drosophila Proteins, lcsh:Science, Phylogeny, Multidisciplinary, biology, Drosophila Melanogaster, Sense Organ Development, Microfilament Proteins, Signal transducing adaptor protein, Eukaryota, Animal Models, Cullin Proteins, Cell biology, Enzymes, Insects, Eye Development, Experimental Organism Systems, Physical Sciences, Drosophila, Drosophila melanogaster, Anatomy, Research Article, Cell signaling, Arthropoda, MAP Kinase Signaling System, Transgene, Ubiquitin-Protein Ligases, Ocular Anatomy, Materials Science, Protein degradation, Research and Analysis Methods, Retina, 03 medical and health sciences, Model Organisms, Ocular System, Genetics, Animals, Cell adhesion, Alleles, Materials by Attribute, Body Patterning, lcsh:R, Ubiquitination, Organisms, Biology and Life Sciences, Proteins, Epistasis, Genetic, Pupil, biology.organism_classification, Invertebrates, 030104 developmental biology, Genetic Loci, biology.protein, Enzymology, Eyes, lcsh:Q, Head, Organism Development, 030217 neurology & neurosurgery, Genetic screen, Developmental Biology
Abstract

Ubiquitination is a crucial post-translational modification that can target proteins for degradation. The E3 ubiquitin ligases are responsible for recognizing substrate proteins for ubiquitination, hence providing specificity to the process of protein degradation. Here, we describe a genetic modifier screen that identified E3 ligases that modified the rough-eye phenotype generated by expression of cindrRNAi transgenes during Drosophila eye development. In total, we identified 36 E3 ligases, as well as 4 Cullins, that modified the mild cindrRNA mis-patterning phenotype. This indicates possible roles for these E3s/Cullins in processes that require Cindr function, including cytoskeletal regulation, cell adhesion, cell signaling and cell survival. Three E3 ligases identified in our screen had previously been linked to regulating JNK signaling.

Published
2017

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