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  1. Book: Epitranscriptomics

    Gupta, Romi / Wajapeyee, Narendra

    methods and protocols

    (Methods in molecular biology ; 1870 ; Springer protocols)

    2019  

    Author's details edited by Narendra Wajapeyee, Romi Gupta
    Series title Methods in molecular biology ; 1870
    Springer protocols
    Collection
    Language English
    Size xii, 298 Seiten, Illustrationen
    Publisher Humana Press
    Publishing place New York, NY
    Publishing country United States
    Document type Book
    HBZ-ID HT019927634
    ISBN 978-1-4939-8807-5 ; 9781493988082 ; 1-4939-8807-7 ; 1493988085
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Zs A 7042 -1870- verfügbar in Königswinter Königswinter

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  2. Book: Eukaryotic transcriptional and post-transcriptional gene expression regulation

    Wajapeyee, Narendra / Gupta, Romi

    (Methods in molecular biology ; 1507 ; Springer protocols)

    2017  

    Author's details edited by Narendra Wajapeyee and Romi Gupta
    Series title Methods in molecular biology ; 1507
    Springer protocols
    Collection
    Keywords eukaryotic cells ; eukaryotic gene expression regulation ; gene expression ; posttranscriptional gene expression regulation ; transcriptional
    Language English
    Size xi, 278 Seiten, Illustrationen, 25.4 cm x 17.8 cm, 0 g
    Publisher Humana Press
    Publishing place New York
    Publishing country United States
    Document type Book
    HBZ-ID HT019124420
    ISBN 978-1-4939-6516-8 ; 1-4939-6516-6 ; 9781493965182 ; 1493965182
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Zs A 7042 -1507- verfügbar in Königswinter Königswinter

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  3. Article ; Online: Epigenetic regulation and targeting of ECM for cancer therapy.

    Gupta, Romi

    American journal of physiology. Cell physiology

    2022  Volume 322, Issue 4, Page(s) C762–C768

    Abstract: The tumor microenvironment (TME) composed of different types of cells embedded in extracellular matrix (ECM) has crucial effects on cancer growth and metastasis. ECM is made of a variety of proteins that provide structural support to the cells and ... ...

    Abstract The tumor microenvironment (TME) composed of different types of cells embedded in extracellular matrix (ECM) has crucial effects on cancer growth and metastasis. ECM is made of a variety of proteins that provide structural support to the cells and regulate biological functions by modulating the cross talk among cells, thus effecting tumor growth and progression. In this mini-review, the author discusses epigenetic modifications that regulate the expression of fibrous ECM proteins and glycoproteins and the prospects of targeting them for cancer therapy.
    MeSH term(s) Epigenesis, Genetic/genetics ; Extracellular Matrix/metabolism ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Tumor Microenvironment/genetics
    Language English
    Publishing date 2022-03-02
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00022.2022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.89: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Roles and therapeutic targeting of ceramide metabolism in cancer.

    Wajapeyee, Narendra / Beamon, Teresa Chiyanne / Gupta, Romi

    Molecular metabolism

    2024  Volume 83, Page(s) 101936

    Abstract: Background: Ceramides are sphingolipids that act as signaling molecules involved in regulating cellular processes including apoptosis, proliferation, and metabolism. Deregulation of ceramide metabolism contributes to cancer development and progression. ... ...

    Abstract Background: Ceramides are sphingolipids that act as signaling molecules involved in regulating cellular processes including apoptosis, proliferation, and metabolism. Deregulation of ceramide metabolism contributes to cancer development and progression. Therefore, regulation of ceramide levels in cancer cells is being explored as a new approach for cancer therapy.
    Scope of the review: This review discusses the multiple roles of ceramides in cancer cells and strategies to modulate ceramide levels for cancer therapy. Ceramides attenuate cell survival signaling and metabolic pathways, while activating apoptotic mechanisms, making them tumor-suppressive. Approaches to increase ceramide levels in cancer cells include using synthetic analogs, inhibiting ceramide degradation, and activating ceramide synthesis. We also highlight combination therapies such as use of ceramide modulators with chemotherapies, immunotherapies, apoptosis inducers, and anti-angiogenics, which offer synergistic antitumor effects. Additionally, we also describe ongoing clinical trials evaluating ceramide nanoliposomes and analogs. Finally, we discuss the challenges of these therapeutic approaches including the complexity of ceramide metabolism, targeted delivery, cancer heterogeneity, resistance mechanisms, and long-term safety.
    Major conclusions: Ceramide-based therapy is a potentially promising approach for cancer therapy. However, overcoming hurdles in pharmacokinetics, specificity, and resistance is needed to optimize its efficacy and safety. This requires comprehensive preclinical/clinical studies into ceramide signaling, formulations, and combination therapies. Ceramide modulation offers opportunities for developing novel cancer treatments, but a deeper understanding of ceramide biology is vital to advance its clinical applications.
    Language English
    Publishing date 2024-04-09
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 2708735-9
    ISSN 2212-8778 ; 2212-8778
    ISSN (online) 2212-8778
    ISSN 2212-8778
    DOI 10.1016/j.molmet.2024.101936
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Identification of the Mutational Landscape of Gynecological Malignancies.

    Chava, Suresh / Gupta, Romi

    Journal of Cancer

    2020  Volume 11, Issue 16, Page(s) 4870–4883

    Abstract: Background: ...

    Abstract Background:
    Language English
    Publishing date 2020-06-08
    Publishing country Australia
    Document type Journal Article
    ZDB-ID 2573318-7
    ISSN 1837-9664
    ISSN 1837-9664
    DOI 10.7150/jca.46174
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Betacellulin promotes tumor development and EGFR mutant lung cancer growth by stimulating the EGFR pathway and suppressing apoptosis.

    Chava, Suresh / Bugide, Suresh / Zhang, Xuchen / Gupta, Romi / Wajapeyee, Narendra

    iScience

    2022  Volume 25, Issue 5, Page(s) 104211

    Abstract: Oncogenic mutations in ... ...

    Abstract Oncogenic mutations in the
    Language English
    Publishing date 2022-04-06
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2022.104211
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Epigenetic Alterations and Mechanisms That Drive Resistance to Targeted Cancer Therapies.

    Wajapeyee, Narendra / Gupta, Romi

    Cancer research

    2021  Volume 81, Issue 22, Page(s) 5589–5595

    Abstract: Cancer is a complex disease and cancer cells typically harbor multiple genetic and epigenetic alterations. Large-scale sequencing of patient-derived cancer samples has identified several druggable driver oncogenes. Many of these oncogenes can be ... ...

    Abstract Cancer is a complex disease and cancer cells typically harbor multiple genetic and epigenetic alterations. Large-scale sequencing of patient-derived cancer samples has identified several druggable driver oncogenes. Many of these oncogenes can be pharmacologically targeted to provide effective therapies for breast cancer, leukemia, lung cancer, melanoma, lymphoma, and other cancer types. Initial responses to these agents can be robust in many cancer types and some patients with cancer experience sustained tumor inhibition. However, resistance to these targeted therapeutics frequently emerges, either from intrinsic or acquired mechanisms, posing a major clinical hurdle for effective treatment. Several resistance mechanisms, both cell autonomous and cell nonautonomous, have been identified in different cancer types. Here we describe how alterations of the transcriptome, transcription factors, DNA, and chromatin regulatory proteins confer resistance to targeted therapeutic agents. We also elaborate on how these studies have identified underlying epigenetic factors that drive drug resistance and oncogenic pathways, with direct implications for the prevention and treatment of drug-resistant cancer.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Biomarkers, Tumor/antagonists & inhibitors ; Biomarkers, Tumor/genetics ; Drug Resistance, Neoplasm ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Molecular Targeted Therapy ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/pathology
    Chemical Substances Antineoplastic Agents ; Biomarkers, Tumor
    Language English
    Publishing date 2021-09-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-21-1606
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.135/5: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: Transcriptional determinants of cancer immunotherapy response and resistance.

    Gupta, Romi / Mehta, Amitkumar / Wajapeyee, Narendra

    Trends in cancer

    2022  Volume 8, Issue 5, Page(s) 404–415

    Abstract: The host immune response is a potent defense mechanism against cancer development and progression. To survive, cancer cells must develop mechanisms to evade the immune response. Based on this knowledge, a series of new therapies collectively referred to ... ...

    Abstract The host immune response is a potent defense mechanism against cancer development and progression. To survive, cancer cells must develop mechanisms to evade the immune response. Based on this knowledge, a series of new therapies collectively referred to as immunotherapies have been developed and translated to the clinic for treating cancer patients. Although some cancer subtypes have shown strong clinical responses, including curative outcomes in some patients, immunotherapies have not worked as desired for some subtypes and forms of cancers. We provide an overview of the transcriptional mechanisms that drive the response and resistance to immunotherapies. We also discuss possible interventions to enhance the outcomes of immunotherapies by targeting dysregulated transcriptional networks in cancer cells.
    MeSH term(s) Humans ; Immunotherapy ; Neoplasms/genetics ; Neoplasms/therapy
    Language English
    Publishing date 2022-02-03
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 2852626-0
    ISSN 2405-8025 ; 2405-8033 ; 2405-8033
    ISSN (online) 2405-8025 ; 2405-8033
    ISSN 2405-8033
    DOI 10.1016/j.trecan.2022.01.008
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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  9. Article ; Online: Co-targeting of specific epigenetic regulators in combination with CDC7 potently inhibit melanoma growth

    Suresh Chava / Suresh Bugide / Parmanand Malvi / Romi Gupta

    iScience, Vol 25, Iss 8, Pp 104752- (2022)

    2022  

    Abstract: Summary: Melanoma is a highly aggressive skin cancer that frequently metastasizes, but current therapies only benefit some patients. Here, we demonstrate that the serine/threonine kinase cell division cycle 7 (CDC7) is overexpressed in melanoma, and ... ...

    Abstract Summary: Melanoma is a highly aggressive skin cancer that frequently metastasizes, but current therapies only benefit some patients. Here, we demonstrate that the serine/threonine kinase cell division cycle 7 (CDC7) is overexpressed in melanoma, and patients with higher expression have shorter survival. Transcription factor ELK1 regulates CDC7 expression, and CDC7 inhibition promotes cell cycle arrest, senescence, and apoptosis, leading to inhibition of melanoma tumor growth and metastasis. Our chemical genetics screen with epigenetic inhibitors revealed stronger melanoma tumor growth inhibition when XL413 is combined with the EZH2 inhibitor GSK343 or BRPF1/2/3 inhibitor OF1. Mechanistically, XL413 with GSK343 or OF1 synergistically altered the expression of tumor-suppressive genes, leading to higher apoptosis than the single agent alone. Collectively, these results identify CDC7 as a driver of melanoma tumor growth and metastasis that can be targeted alone or in combination with EZH2 or BRPF1/2/3 inhibitors.
    Keywords Chemistry ; Epigenetics ; Cell biology ; Cancer ; Science ; Q
    Subject code 610
    Language English
    Publishing date 2022-08-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: Co-targeting of specific epigenetic regulators in combination with CDC7 potently inhibit melanoma growth.

    Chava, Suresh / Bugide, Suresh / Malvi, Parmanand / Gupta, Romi

    iScience

    2022  Volume 25, Issue 8, Page(s) 104752

    Abstract: Melanoma is a highly aggressive skin cancer that frequently metastasizes, but current therapies only benefit some patients. Here, we demonstrate that the serine/threonine kinase cell division cycle 7 (CDC7) is overexpressed in melanoma, and patients with ...

    Abstract Melanoma is a highly aggressive skin cancer that frequently metastasizes, but current therapies only benefit some patients. Here, we demonstrate that the serine/threonine kinase cell division cycle 7 (CDC7) is overexpressed in melanoma, and patients with higher expression have shorter survival. Transcription factor ELK1 regulates CDC7 expression, and CDC7 inhibition promotes cell cycle arrest, senescence, and apoptosis, leading to inhibition of melanoma tumor growth and metastasis. Our chemical genetics screen with epigenetic inhibitors revealed stronger melanoma tumor growth inhibition when XL413 is combined with the EZH2 inhibitor GSK343 or BRPF1/2/3 inhibitor OF1. Mechanistically, XL413 with GSK343 or OF1 synergistically altered the expression of tumor-suppressive genes, leading to higher apoptosis than the single agent alone. Collectively, these results identify CDC7 as a driver of melanoma tumor growth and metastasis that can be targeted alone or in combination with EZH2 or BRPF1/2/3 inhibitors.
    Language English
    Publishing date 2022-07-15
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2022.104752
    Database MEDical Literature Analysis and Retrieval System OnLINE

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