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  1. Article: MicroRNAs as promising biomarkers in cancer diagnostics.

    Mishra, Prasun J

    Biomarker research

    2014  Volume 2, Page(s) 19

    Abstract: Cumulating data suggest that small noncoding-RNAs such as microRNAs (miRNAs) can be utilized as potential biomarkers for the diagnosis and prognosis of a variety of diseases such as cancer, neurological disorders, cardiovascular disease and Type-II ... ...

    Abstract Cumulating data suggest that small noncoding-RNAs such as microRNAs (miRNAs) can be utilized as potential biomarkers for the diagnosis and prognosis of a variety of diseases such as cancer, neurological disorders, cardiovascular disease and Type-II diabetes, etc. MiRNAs can be utilized not only for monitoring of treatments but also for patient stratifications. The Tenth Annual miRNA as Biomarkers and Diagnostics conference, 2014, organized in Boston, MA, was primarily focused on recent advancements in the field of miRNA in the early detection of disease, monitoring tumor growth/progression and its potential for precision medicine. This article summarizes findings presented in the miRNA biomarker as cancer diagnostics session. The overarching projections from this and other sessions were that miRNAs are now well established as regulators of tumorigenesis and can be utilized not only as potential biomarkers for the diagnosis and prognosis of a disease but also are useful in patient stratifications and treatment response.
    Language English
    Publishing date 2014-10-22
    Publishing country England
    Document type Journal Article
    ZDB-ID 2699926-2
    ISSN 2050-7771
    ISSN 2050-7771
    DOI 10.1186/2050-7771-2-19
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  2. Article ; Online: Non-coding RNAs as clinical biomarkers for cancer diagnosis and prognosis.

    Mishra, Prasun J

    Expert review of molecular diagnostics

    2014  Volume 14, Issue 8, Page(s) 917–919

    Abstract: Developing more precise diagnostics approaches to predict cancer progression and prognosis is the key to precision medicine. Overwhelming evidence now suggests that small non-coding RNAs such as miRNAs can be useful tools as biomarkers for molecular ... ...

    Abstract Developing more precise diagnostics approaches to predict cancer progression and prognosis is the key to precision medicine. Overwhelming evidence now suggests that small non-coding RNAs such as miRNAs can be useful tools as biomarkers for molecular diagnostics. miRNAs can serve as biomarkers in a variety of diseases, such as neurological disorders, cardiovascular disease, Type II diabetes, cancer and so on. miRNAs can not only be utilized for monitoring treatment but also for patient stratification and hence are promising predictive biomarkers in cancer progression and prognosis, as well as in predicting drug response. This article focuses on some of the recent findings in the field of miRNA biomarkers and discusses its implications for cancer diagnostics and precision medicine.
    MeSH term(s) Biomarkers, Tumor ; Humans ; Neoplasms/diagnosis ; Neoplasms/genetics ; Polymorphism, Genetic ; Prognosis ; RNA, Untranslated/genetics
    Chemical Substances Biomarkers, Tumor ; RNA, Untranslated
    Language English
    Publishing date 2014-10-21
    Publishing country England
    Document type Editorial ; Research Support, N.I.H., Intramural
    ZDB-ID 2112530-2
    ISSN 1744-8352 ; 1473-7159
    ISSN (online) 1744-8352
    ISSN 1473-7159
    DOI 10.1586/14737159.2014.971761
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The miRNA-drug resistance connection: a new era of personalized medicine using noncoding RNA begins.

    Mishra, Prasun J

    Pharmacogenomics

    2012  Volume 13, Issue 12, Page(s) 1321–1324

    MeSH term(s) Drug Resistance/genetics ; Genome, Human ; Humans ; MicroRNAs/genetics ; Precision Medicine/methods ; RNA, Untranslated/genetics
    Chemical Substances MicroRNAs ; RNA, Untranslated
    Language English
    Publishing date 2012-09-11
    Publishing country England
    Document type Editorial
    ZDB-ID 2019513-8
    ISSN 1744-8042 ; 1462-2416
    ISSN (online) 1744-8042
    ISSN 1462-2416
    DOI 10.2217/pgs.12.121
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  4. Article: MicroRNA polymorphisms: a giant leap towards personalized medicine.

    Mishra, Prasun J

    Personalized medicine

    2010  Volume 6, Issue 2, Page(s) 119–125

    Abstract: An individual's genetic inheritance of microRNA polymorphisms associated with disease progression, prognosis and treatment holds the key to create safer and more personalized drugs and can be a giant leap towards personalized medicine." ...

    Abstract "An individual's genetic inheritance of microRNA polymorphisms associated with disease progression, prognosis and treatment holds the key to create safer and more personalized drugs and can be a giant leap towards personalized medicine."
    Language English
    Publishing date 2010-02-18
    Publishing country England
    Document type Journal Article
    ZDB-ID 2299146-3
    ISSN 1744-828X ; 1741-0541
    ISSN (online) 1744-828X
    ISSN 1741-0541
    DOI 10.2217/17410541.6.2.119
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  5. Article: Keratinocyte Induced Differentiation of Mesenchymal Stem Cells into Dermal Myofibroblasts: A Role in Effective Wound Healing.

    Mishra, Pravin J / Mishra, Prasun J / Banerjee, Debabrata

    International journal of translational science

    2016  Volume 2016, Issue 1, Page(s) 5–32

    Abstract: We have previously demonstrated that human mesenchymal stem cells (hMSCs) migrate toward human keratinocytes as well as toward conditioned medium from cultured human keratinocytes (KCM) indicating that the hMSCs respond to signals from keratinocytes [1]. ...

    Abstract We have previously demonstrated that human mesenchymal stem cells (hMSCs) migrate toward human keratinocytes as well as toward conditioned medium from cultured human keratinocytes (KCM) indicating that the hMSCs respond to signals from keratinocytes [1]. Using fluorescently labeled cells we now show that
    Language English
    Publishing date 2016-05-24
    Publishing country Denmark
    Document type Journal Article
    ISSN 2246-8765
    ISSN 2246-8765
    DOI 10.13052/ijts2246-8765.2016.002
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  6. Article ; Online: Integrated Genomics Identifies miR-32/MCL-1 Pathway as a Critical Driver of Melanomagenesis

    Prasun J Mishra / Pravin J Mishra / Glenn Merlino

    PLoS ONE, Vol 11, Iss 11, p e

    Implications for miR-Replacement and Combination Therapy.

    2016  Volume 0165102

    Abstract: Cutaneous malignant melanoma is among the deadliest human cancers, broadly resistant to most clinical therapies. A majority of patients with BRAFV600E melanomas respond well to inhibitors such as vemurafenib, but all ultimately relapse. Moreover, there ... ...

    Abstract Cutaneous malignant melanoma is among the deadliest human cancers, broadly resistant to most clinical therapies. A majority of patients with BRAFV600E melanomas respond well to inhibitors such as vemurafenib, but all ultimately relapse. Moreover, there are no viable treatment options available for other non-BRAF melanoma subtypes in the clinic. A key to improving treatment options lies in a better understanding of mechanisms underlying melanoma progression, which are complex and heterogeneous.In this study we integrated gene and microRNA (miRNA) expression data from genetically engineered mouse models of highly and poorly malignant melanocytic tumors, as well as available human melanoma databases, and discovered an important role for a pathway centered on a tumor suppressor miRNA, miR-32.Malignant tumors frequently exhibited poor expression of miR-32, whose targets include NRAS, PI3K and notably, MCL-1. Accordingly, MCL-1 was often highly expressed in melanomas, and when knocked down diminished oncogenic potential. Forced MCL-1 overexpression transformed immortalized primary mouse melanocytes, but only when also expressing activating mutations in BRAF, CRAF or PI3K. Importantly, both miR-32 replacement therapy and the MCL-1-specific antagonist sabutoclax demonstrated single-agent efficacy, and acted synergistically in combination with vemurafenib in preclinical melanoma models.We here identify miR-32/MCL-1 pathway members as key early genetic events driving melanoma progression, and suggest that their inhibition may be an effective anti-melanoma strategy irrespective of NRAS, BRAF, and PTEN status.
    Keywords Medicine ; R ; Science ; Q
    Subject code 570
    Language English
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Integrated Genomics Identifies miR-32/MCL-1 Pathway as a Critical Driver of Melanomagenesis

    Prasun J Mishra / Pravin J Mishra / Glenn Merlino

    PLoS ONE, Vol 11, Iss 11, p e

    Implications for miR-Replacement and Combination Therapy.

    2016  Volume 0165102

    Abstract: Cutaneous malignant melanoma is among the deadliest human cancers, broadly resistant to most clinical therapies. A majority of patients with BRAFV600E melanomas respond well to inhibitors such as vemurafenib, but all ultimately relapse. Moreover, there ... ...

    Abstract Cutaneous malignant melanoma is among the deadliest human cancers, broadly resistant to most clinical therapies. A majority of patients with BRAFV600E melanomas respond well to inhibitors such as vemurafenib, but all ultimately relapse. Moreover, there are no viable treatment options available for other non-BRAF melanoma subtypes in the clinic. A key to improving treatment options lies in a better understanding of mechanisms underlying melanoma progression, which are complex and heterogeneous.In this study we integrated gene and microRNA (miRNA) expression data from genetically engineered mouse models of highly and poorly malignant melanocytic tumors, as well as available human melanoma databases, and discovered an important role for a pathway centered on a tumor suppressor miRNA, miR-32.Malignant tumors frequently exhibited poor expression of miR-32, whose targets include NRAS, PI3K and notably, MCL-1. Accordingly, MCL-1 was often highly expressed in melanomas, and when knocked down diminished oncogenic potential. Forced MCL-1 overexpression transformed immortalized primary mouse melanocytes, but only when also expressing activating mutations in BRAF, CRAF or PI3K. Importantly, both miR-32 replacement therapy and the MCL-1-specific antagonist sabutoclax demonstrated single-agent efficacy, and acted synergistically in combination with vemurafenib in preclinical melanoma models.We here identify miR-32/MCL-1 pathway members as key early genetic events driving melanoma progression, and suggest that their inhibition may be an effective anti-melanoma strategy irrespective of NRAS, BRAF, and PTEN status.
    Keywords Medicine ; R ; Science ; Q
    Subject code 570
    Language English
    Publishing date 2016-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Integrated Genomics Identifies miR-32/MCL-1 Pathway as a Critical Driver of Melanomagenesis: Implications for miR-Replacement and Combination Therapy.

    Mishra, Prasun J / Mishra, Pravin J / Merlino, Glenn

    PloS one

    2016  Volume 11, Issue 11, Page(s) e0165102

    Abstract: Aims: Cutaneous malignant melanoma is among the deadliest human cancers, broadly resistant to most clinical therapies. A majority of patients with BRAFV600E melanomas respond well to inhibitors such as vemurafenib, but all ultimately relapse. Moreover, ... ...

    Abstract Aims: Cutaneous malignant melanoma is among the deadliest human cancers, broadly resistant to most clinical therapies. A majority of patients with BRAFV600E melanomas respond well to inhibitors such as vemurafenib, but all ultimately relapse. Moreover, there are no viable treatment options available for other non-BRAF melanoma subtypes in the clinic. A key to improving treatment options lies in a better understanding of mechanisms underlying melanoma progression, which are complex and heterogeneous.
    Methods: In this study we integrated gene and microRNA (miRNA) expression data from genetically engineered mouse models of highly and poorly malignant melanocytic tumors, as well as available human melanoma databases, and discovered an important role for a pathway centered on a tumor suppressor miRNA, miR-32.
    Results: Malignant tumors frequently exhibited poor expression of miR-32, whose targets include NRAS, PI3K and notably, MCL-1. Accordingly, MCL-1 was often highly expressed in melanomas, and when knocked down diminished oncogenic potential. Forced MCL-1 overexpression transformed immortalized primary mouse melanocytes, but only when also expressing activating mutations in BRAF, CRAF or PI3K. Importantly, both miR-32 replacement therapy and the MCL-1-specific antagonist sabutoclax demonstrated single-agent efficacy, and acted synergistically in combination with vemurafenib in preclinical melanoma models.
    Conclusions: We here identify miR-32/MCL-1 pathway members as key early genetic events driving melanoma progression, and suggest that their inhibition may be an effective anti-melanoma strategy irrespective of NRAS, BRAF, and PTEN status.
    MeSH term(s) Animals ; Carcinogenesis/genetics ; Carcinogenesis/pathology ; Cell Line, Tumor ; Cell Transformation, Neoplastic/drug effects ; Cell Transformation, Neoplastic/pathology ; Drug Synergism ; Drug Therapy, Combination ; Gene Expression Regulation, Neoplastic/drug effects ; Genes, Tumor Suppressor ; Genomics ; Gossypol/analogs & derivatives ; Gossypol/pharmacology ; Indoles/pharmacology ; Melanoma/genetics ; Melanoma/pathology ; Mice ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Myeloid Cell Leukemia Sequence 1 Protein/antagonists & inhibitors ; Myeloid Cell Leukemia Sequence 1 Protein/metabolism ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Oncogenes ; Proteasome Endopeptidase Complex/metabolism ; Proteolysis ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Signal Transduction/genetics ; Sulfonamides/pharmacology
    Chemical Substances 1,1',6,6',7,7'-hexahydroxy-3,3'-dimethyl-N5-(2-phenylpropyl)-N5'-(2-phenylpropyl)-2,2'-binaphthyl-5,5'-dicarboxamide ; Indoles ; MIRN32 microRNA, mouse ; MicroRNAs ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasm Proteins ; RNA, Messenger ; Sulfonamides ; vemurafenib (207SMY3FQT) ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Gossypol (KAV15B369O)
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0165102
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Elucidating the Drug Repurposing Spectra of COVID-19 with its Analogues SARS and MERS.

    Mishra, Jayanti / Prasun, Chakrawarti / Sahoo, Pravat K / Nair, Maya S

    Mini reviews in medicinal chemistry

    2021  Volume 21, Issue 20, Page(s) 3191–3202

    Abstract: Corona Virus Disease-2019 (COVID-19), caused by the SARS CoV-2 virus, has been announced as a pandemic by the World Health Organization. COVID-19 has affected people globally, infecting more than 39.8 million people and claiming up to 1.11 million lives, ...

    Abstract Corona Virus Disease-2019 (COVID-19), caused by the SARS CoV-2 virus, has been announced as a pandemic by the World Health Organization. COVID-19 has affected people globally, infecting more than 39.8 million people and claiming up to 1.11 million lives, yet there is no effective treatment strategy to cure this disease. As vaccine development is a time-consuming process, currently, efforts are being made to develop alternative plans for the timely and effective management of this disease. Drug repurposing always fascinated researchers and can be utilized as the most acceptable alternative to develop the therapeutics for COVID-19 using the pre-approved drugs. Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has shown resemblance with distinctive enzyme targets, such as 3CLpro/Mpro, RdRp, Cathepsin L, and TMPRSS2 present in SARS CoV and MERS CoV. Therefore, the drugs that have shown efficacy in these viruses can also be used for the treatment of COVID-19. This review focuses on why repurposing could provide a better alternative in COVID- 19 treatment. The similarity in the structure and progression of infection of SARS CoV and MERS viruses offers a direction and validation to evaluate the drugs approved for SARS and MERS against COVID-19. It has been indicated that multiple therapeutic options that demonstrate efficacy against SARS CoV 2 are available to mitigate the potential emergence of COVID-19 infection.
    MeSH term(s) Antiviral Agents/pharmacology ; Antiviral Agents/therapeutic use ; COVID-19/drug therapy ; Coronavirus Infections/drug therapy ; Drug Repositioning ; Humans ; Middle East Respiratory Syndrome Coronavirus/drug effects ; Middle East Respiratory Syndrome Coronavirus/enzymology ; SARS Virus/drug effects ; SARS Virus/enzymology ; SARS-CoV-2/drug effects ; SARS-CoV-2/enzymology ; Severe Acute Respiratory Syndrome/drug therapy
    Chemical Substances Antiviral Agents
    Language English
    Publishing date 2021-02-22
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 2104081-3
    ISSN 1875-5607 ; 1389-5575
    ISSN (online) 1875-5607
    ISSN 1389-5575
    DOI 10.2174/1389557521666210225114733
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    Zs.A 5891: Show issues Location:
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  10. Article ; Online: A traitor in our midst: mesenchymal stem cells contribute to tumor progression and metastasis.

    Mishra, Prasun J / Merlino, Glenn

    Future oncology (London, England)

    2008  Volume 4, Issue 6, Page(s) 745–749

    MeSH term(s) Cytokines/metabolism ; Disease Progression ; Humans ; Mesenchymal Stromal Cells/metabolism ; Mesenchymal Stromal Cells/pathology ; Neoplasm Metastasis/pathology ; Neoplasms/metabolism ; Neoplasms/pathology
    Chemical Substances Cytokines
    Language English
    Publishing date 2008-12
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2184533-5
    ISSN 1744-8301 ; 1479-6694
    ISSN (online) 1744-8301
    ISSN 1479-6694
    DOI 10.2217/14796694.4.6.745
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