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  1. Book ; Online ; E-Book: Melanoma in clinical practice

    Alani, Rhoda M. / Sahni, Debjani

    2021  

    Author's details Rhoda M. Alani, Debjani Sahni, editors
    Keywords Melanoma ; Dermatology ; Internal medicine ; Dermatologia
    Subject code 616.99477
    Language English
    Size 1 online resource (354 pages)
    Publisher Springer
    Publishing place Cham, Switzerland
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    ISBN 3-030-82639-2 ; 9783030826383 ; 978-3-030-82639-0 ; 3030826384
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article: p300 KAT regulates SOX10 stability and function in human melanoma.

    Waddell, Aaron / Grbic, Nicole / Leibowitz, Kassidy / Wyant, W Austin / Choudhury, Sabah / Park, Kihyun / Collard, Marianne / Cole, Philip A / Alani, Rhoda M

    bioRxiv : the preprint server for biology

    2024  

    Abstract: SOX10 is a lineage-specific transcription factor critical for melanoma tumor growth, while SOX10 loss-of-function drives the emergence of therapy-resistant, invasive melanoma phenotypes. A major challenge has been developing therapeutic strategies ... ...

    Abstract SOX10 is a lineage-specific transcription factor critical for melanoma tumor growth, while SOX10 loss-of-function drives the emergence of therapy-resistant, invasive melanoma phenotypes. A major challenge has been developing therapeutic strategies targeting SOX10's role in melanoma proliferation, while preventing a concomitant increase in tumor cell invasion. Here, we report that the lysine acetyltransferase (KAT)
    Language English
    Publishing date 2024-02-23
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.02.20.581224
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Epigenetics and cutaneous neoplasms: from mechanism to therapy.

    Gibson, Frederick / Hanly, Ailish / Fisher, Robert / Wyant, W Austin / Wu, Muzhou / Collard, Marianne / Alani, Rhoda M

    Epigenomics

    2023  Volume 15, Issue 3, Page(s) 167–187

    Abstract: Epigenetics encompasses heritable, reversible gene expression patterns that do not arise from mutations in genomic DNA but, rather, are regulated by DNA methylation, histone modifications, RNA modifications and ncRNAs; and epigenetic dysregulation is ... ...

    Abstract Epigenetics encompasses heritable, reversible gene expression patterns that do not arise from mutations in genomic DNA but, rather, are regulated by DNA methylation, histone modifications, RNA modifications and ncRNAs; and epigenetic dysregulation is increasingly recognized as a mechanism of neoplastic disease progression as well as resistance to cancer therapy. This review article focuses on epigenetic modifications implicated in the progression and therapeutic resistance of common cutaneous malignancies, including basal cell carcinoma, squamous cell carcinoma, T-cell lymphoma and malignant melanoma, with an emphasis on therapeutic strategies that may be used to target such disease-associated alterations.
    MeSH term(s) Humans ; Skin Neoplasms/genetics ; Skin Neoplasms/therapy ; Skin Neoplasms/pathology ; Melanoma/genetics ; Epigenesis, Genetic ; Carcinoma, Basal Cell/genetics ; Carcinoma, Basal Cell/pathology ; DNA Methylation
    Language English
    Publishing date 2023-04-05
    Publishing country England
    Document type Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
    ZDB-ID 2537199-X
    ISSN 1750-192X ; 1750-1911
    ISSN (online) 1750-192X
    ISSN 1750-1911
    DOI 10.2217/epi-2023-0016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Gut Microbiome Perturbations in Patients with Hidradenitis Suppurativa: A Case Series.

    Kam, Sarah / Collard, Marianne / Lam, Jimmy / Alani, Rhoda M

    The Journal of investigative dermatology

    2020  Volume 141, Issue 1, Page(s) 225–228.e2

    MeSH term(s) Female ; Gastrointestinal Microbiome ; Hidradenitis Suppurativa/microbiology ; Humans ; Male ; Middle Aged ; Pilot Projects
    Language English
    Publishing date 2020-05-16
    Publishing country United States
    Document type Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80136-7
    ISSN 1523-1747 ; 0022-202X
    ISSN (online) 1523-1747
    ISSN 0022-202X
    DOI 10.1016/j.jid.2020.04.017
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Assessment of lipid and pigment content in suspicious melanocytic lesions to improve melanoma detection.

    Amara, Shivkar V / Grbic, Nicole / Melson, Gabriella / Brem, Candice E / Almier, Nedaa / Bhawan, Jag / Alani, Rhoda M / Collard, Marianne

    Melanoma research

    2023  Volume 33, Issue 4, Page(s) 283–292

    Abstract: Melanoma is a highly aggressive form of skin cancer and the most frequent lethal malignancy diagnosed by dermatologists. Although there have been advances for predicting melanoma prognosis, there are few highly sensitive and specific diagnostic tools for ...

    Abstract Melanoma is a highly aggressive form of skin cancer and the most frequent lethal malignancy diagnosed by dermatologists. Although there have been advances for predicting melanoma prognosis, there are few highly sensitive and specific diagnostic tools for clinically evaluating suspicious melanocytic lesions prior to biopsy. We have recently determined that alterations in cellular lipid and pigment content are associated with tumor progression and melanoma metastasis. Here, we seek to determine if lipid droplet and pigment content assessments near the skin's surface are able to distinguish benign from malignant melanocytic lesions. We obtained 14 benign melanocytic lesions, classified as Melanocytic Pathology Assessment Tool and Hierarchy for Diagnosis (MPATH-Dx) class 1, and 22 malignant melanomas, classified as MPATH-Dx class 4 or 5, from Boston Medical Center. The malignant melanomas had an average greatest thickness of 1.8 ± 2.1 mm with 7/22 biopsies showing the presence of ulceration. Tissues were stained with the Fontana Masson stain to detect pigment or immunohistochemically stained for adipophilin, the main protein component of lipid droplets, to detect lipid droplets. Pigment and lipid droplets were quantified using ImageJ and CellProfiler, respectively. We found no significant difference in total pigment area between benign melanocytic lesions and malignant melanoma, and a 66% decrease in lipid content and 68% reduction in lipid/pigment content between benign melanocytic lesions and malignant melanoma ( P  < 0.05). Our results suggest that lipid content and lipid/pigment content ratios may distinguish benign and malignant melanocytic lesions, which may be useful as a diagnostic tool for histopathologically challenging pigmented lesions.
    MeSH term(s) Humans ; Melanoma/diagnosis ; Melanoma/pathology ; Skin Neoplasms/diagnosis ; Skin Neoplasms/pathology ; Melanocytes/pathology ; Prognosis ; Lipids
    Chemical Substances Lipids
    Language English
    Publishing date 2023-06-05
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1095779-0
    ISSN 1473-5636 ; 0960-8931
    ISSN (online) 1473-5636
    ISSN 0960-8931
    DOI 10.1097/CMR.0000000000000902
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Multimodal Metabolic Imaging Reveals Pigment Reduction and Lipid Accumulation in Metastatic Melanoma.

    Lee, Hyeon Jeong / Chen, Zhicong / Collard, Marianne / Chen, Fukai / Chen, Jiaji G / Wu, Muzhou / Alani, Rhoda M / Cheng, Ji-Xin

    BME frontiers

    2021  Volume 2021, Page(s) 9860123

    Abstract: Objective and Impact ... ...

    Abstract Objective and Impact Statement
    Language English
    Publishing date 2021-10-08
    Publishing country United States
    Document type Journal Article
    ISSN 2765-8031
    ISSN (online) 2765-8031
    DOI 10.34133/2021/9860123
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Drugging the Epigenome: Overcoming Resistance to Targeted and Immunotherapies in Melanoma.

    Hanly, Ailish / Gibson, Frederick / Nocco, Sarah / Rogers, Samantha / Wu, Muzhou / Alani, Rhoda M

    JID innovations : skin science from molecules to population health

    2021  Volume 2, Issue 2, Page(s) 100090

    Abstract: This past decade has seen tremendous advances in understanding the molecular pathogenesis of melanoma and the development of novel effective therapies for melanoma. Targeted therapies and immunotherapies that extend survival of patients with advanced ... ...

    Abstract This past decade has seen tremendous advances in understanding the molecular pathogenesis of melanoma and the development of novel effective therapies for melanoma. Targeted therapies and immunotherapies that extend survival of patients with advanced disease have been developed; however, the vast majority of patients experience relapse and therapeutic resistance over time. Moreover, cellular plasticity has been demonstrated to be a driver of therapeutic resistance mechanisms in melanoma and other cancers, largely functioning through epigenetic mechanisms, suggesting that targeting of the cancer epigenetic landscape may prove a worthwhile endeavor to ensure durable treatment responses and cures. Here, we review the epigenetic alterations that characterize melanoma development, progression, and resistance to targeted therapies as well as epigenetic therapies currently in use and under development for melanoma and other cancers. We further assess the landscape of epigenetic therapies in clinical trials for melanoma and provide a framework for future advances in epigenetic therapies to circumvent the development of therapeutic resistance in melanoma.
    Language English
    Publishing date 2021-12-13
    Publishing country Netherlands
    Document type Journal Article ; Review
    ISSN 2667-0267
    ISSN (online) 2667-0267
    DOI 10.1016/j.xjidi.2021.100090
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Epigenetic Dysregulation in Autoimmune and Inflammatory Skin Diseases.

    Gibson, Frederick / Hanly, Ailish / Grbic, Nicole / Grunberg, Noah / Wu, Muzhou / Collard, Marianne / Alani, Rhoda M

    Clinical reviews in allergy & immunology

    2022  Volume 63, Issue 3, Page(s) 447–471

    Abstract: Epigenetics is the study of heritable, reversible gene expression patterns that do not originate from alterations in the DNA sequence. Epigenetic modifications influence gene expression patterns and include DNA methylation, histone modifications, and ... ...

    Abstract Epigenetics is the study of heritable, reversible gene expression patterns that do not originate from alterations in the DNA sequence. Epigenetic modifications influence gene expression patterns and include DNA methylation, histone modifications, and gene regulation via non-coding RNAs. While the study of epigenetics has been most broadly applied to neoplastic diseases, the role of the epigenome in a wide range of disease processes including autoimmune, allergic, and inflammatory processes is increasingly being recognized. Recent advances in the study of the epigenome have led to novel insights into the pathogenesis and potential therapeutic targets of various pathologic entities including inflammatory diseases. In this review, we examine the nature of epigenetic modifications in several well-studied autoimmune, allergic, and/or inflammatory disorders of the skin including systemic lupus erythematosus, vitiligo, systemic sclerosis, alopecia areata, pemphigus, psoriasis, atopic dermatitis, keloidal scarring, and hidradenitis suppurativa with the aim to determine how such epigenetic changes may be targeted for therapeutic benefit.
    MeSH term(s) Humans ; Epigenomics ; Epigenesis, Genetic ; Skin ; Psoriasis/genetics ; Alopecia Areata
    Language English
    Publishing date 2022-11-08
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1239045-8
    ISSN 1559-0267 ; 1080-0549
    ISSN (online) 1559-0267
    ISSN 1080-0549
    DOI 10.1007/s12016-022-08956-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: The CoREST repressor complex mediates phenotype switching and therapy resistance in melanoma.

    Wu, Muzhou / Hanly, Ailish / Gibson, Frederick / Fisher, Robert / Rogers, Samantha / Park, Kihyun / Zuger, Angelina / Kuang, Kevin / Kalin, Jay H / Nocco, Sarah / Cole, Matthew / Xiao, Amy / Agus, Filisia / Labadorf, Adam / Beck, Samuel / Collard, Marianne / Cole, Philip A / Alani, Rhoda M

    The Journal of clinical investigation

    2024  Volume 134, Issue 6

    Abstract: Virtually all patients with BRAF-mutant melanoma develop resistance to MAPK inhibitors largely through nonmutational events. Although the epigenetic landscape is shown to be altered in therapy-resistant melanomas and other cancers, a specific targetable ... ...

    Abstract Virtually all patients with BRAF-mutant melanoma develop resistance to MAPK inhibitors largely through nonmutational events. Although the epigenetic landscape is shown to be altered in therapy-resistant melanomas and other cancers, a specific targetable epigenetic mechanism has not been validated. Here, we evaluated the corepressor for element 1-silencing transcription factor (CoREST) epigenetic repressor complex and the recently developed bivalent inhibitor corin within the context of melanoma phenotype plasticity and therapeutic resistance. We found that CoREST was a critical mediator of the major distinct melanoma phenotypes and that corin treatment of melanoma cells led to phenotype reprogramming. Global assessment of transcript and chromatin changes conferred by corin revealed specific effects on histone marks connected to epithelial-mesenchymal transition-associated (EMT-associated) transcription factors and the dual-specificity phosphatases (DUSPs). Remarkably, treatment of BRAF inhibitor-resistant (BRAFi-R) melanomas with corin promoted resensitization to BRAFi therapy. DUSP1 was consistently downregulated in BRAFi-R melanomas, which was reversed by corin treatment and associated with inhibition of p38 MAPK activity and resensitization to BRAFi therapies. Moreover, this activity was recapitulated by the p38 MAPK inhibitor BIRB 796. These findings identify the CoREST repressor complex as a central mediator of melanoma phenotype plasticity and resistance to targeted therapy and suggest that CoREST inhibitors may prove beneficial for patients with BRAFi-resistant melanoma.
    MeSH term(s) Humans ; Melanoma/drug therapy ; Melanoma/genetics ; Proto-Oncogene Proteins B-raf/genetics ; Co-Repressor Proteins/genetics ; Drug Resistance, Neoplasm/genetics ; Cell Line, Tumor ; Protein Kinase Inhibitors/pharmacology ; Phenotype ; p38 Mitogen-Activated Protein Kinases
    Chemical Substances Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Co-Repressor Proteins ; Protein Kinase Inhibitors ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2024-02-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI171063
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Book: Promise and progress

    Alani, Rhoda M

    melanoma therapy for 2014 and beyond

    (CC grand rounds, contemporary clinical medicine, great teachers)

    2014  

    Title variant Melanoma therapy for 2014 and beyond
    Institution National Institutes of Health (U.S.),
    Author's details Rhoda M. Alani
    Series title CC grand rounds, contemporary clinical medicine, great teachers
    MeSH term(s) Melanoma/therapy ; Immunotherapy ; Molecular Targeted Therapy ; Precision Medicine ; Proto-Oncogene Proteins B-raf/therapeutic use
    Language English
    Size 1 online resource (1 streaming video file (49 min.)) :, color, sound
    Document type Book
    Note Closed-captioned. ; Title from title screen.
    Database Catalogue of the US National Library of Medicine (NLM)

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