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  1. Article: Chromosome 7 to the rescue: overcoming chromosome 10 loss in gliomas.

    Nair, Nishanth Ulhas / Schäffer, Alejandro A / Gertz, E Michael / Cheng, Kuoyuan / Zerbib, Johanna / Sahu, Avinash Das / Leor, Gil / Shulman, Eldad D / Aldape, Kenneth D / Ben-David, Uri / Ruppin, Eytan

    bioRxiv : the preprint server for biology

    2024  

    Abstract: The co-occurrence of chromosome 10 loss and chromosome 7 gain in gliomas is the most frequent loss-gain co-aneuploidy pair in human cancers, a phenomenon that has been investigated without resolution since the late 1980s. Expanding beyond previous gene- ... ...

    Abstract The co-occurrence of chromosome 10 loss and chromosome 7 gain in gliomas is the most frequent loss-gain co-aneuploidy pair in human cancers, a phenomenon that has been investigated without resolution since the late 1980s. Expanding beyond previous gene-centric studies, we investigate the co-occurrence in a genome-wide manner taking an evolutionary perspective. First, by mining large tumor aneuploidy data, we predict that the more likely order is 10 loss followed by 7 gain. Second, by analyzing extensive genomic and transcriptomic data from both patients and cell lines, we find that this co-occurrence can be explained by functional rescue interactions that are highly enriched on 7, which can possibly compensate for any detrimental consequences arising from the loss of 10. Finally, by analyzing transcriptomic data from normal, non-cancerous, human brain tissues, we provide a plausible reason why this co-occurrence happens preferentially in cancers originating in certain regions of the brain.
    Language English
    Publishing date 2024-01-22
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.01.17.576103
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Synthetic lethality across normal tissues is strongly associated with cancer risk, onset, and tumor suppressor specificity.

    Cheng, Kuoyuan / Nair, Nishanth Ulhas / Lee, Joo Sang / Ruppin, Eytan

    Science advances

    2021  Volume 7, Issue 1

    Abstract: Various characteristics of cancers exhibit tissue specificity, including lifetime cancer risk, onset age, and cancer driver genes. Previously, the large variation in cancer risk across human tissues was found to strongly correlate with the number of stem ...

    Abstract Various characteristics of cancers exhibit tissue specificity, including lifetime cancer risk, onset age, and cancer driver genes. Previously, the large variation in cancer risk across human tissues was found to strongly correlate with the number of stem cell divisions and abnormal DNA methylation levels. Here, we study the role of synthetic lethality in cancer risk. Analyzing normal tissue transcriptomics data in the Genotype-Tissue Expression project, we quantify the extent of co-inactivation of cancer synthetic lethal (cSL) gene pairs and find that normal tissues with more down-regulated cSL gene pairs have lower and delayed cancer risk. Consistently, more cSL gene pairs become up-regulated in cells treated by carcinogens and throughout premalignant stages in vivo. We also show that the tissue specificity of numerous tumor suppressor genes is associated with the expression of their cSL partner genes across normal tissues. Overall, our findings support the possible role of synthetic lethality in tumorigenesis.
    MeSH term(s) Cell Transformation, Neoplastic/genetics ; DNA Methylation ; Genes, Tumor Suppressor ; Humans ; Neoplasms/genetics ; Synthetic Lethal Mutations
    Language English
    Publishing date 2021-01-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.abc2100
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Author Correction: A systematic genome-wide mapping of oncogenic mutation selection during CRISPR-Cas9 genome editing.

    Sinha, Sanju / Barbosa, Karina / Cheng, Kuoyuan / Leiserson, Mark D M / Jain, Prashant / Deshpande, Anagha / Wilson, David M / Ryan, Bríd M / Luo, Ji / Ronai, Ze'ev A / Lee, Joo Sang / Deshpande, Aniruddha J / Ruppin, Eytan

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 2828

    Language English
    Publishing date 2022-05-16
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-30475-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Using a Recently Approved Tumor Mutational Burden Biomarker to Stratify Patients for Immunotherapy May Introduce a Sex Bias.

    Sinha, Neelam / Sinha, Sanju / Cheng, Kuoyuan / Madan, Sanna / Erez, Ayelet / Ryan, Bríd M / Schäffer, Alejandro A / Aldape, Kenneth / Ruppin, Eytan

    JCO precision oncology

    2021  Volume 5, Page(s) 1147–1150

    MeSH term(s) Biomarkers, Tumor/genetics ; Female ; Humans ; Immune Checkpoint Inhibitors/therapeutic use ; Immunotherapy ; Male ; Mutation ; Neoplasms/genetics ; Neoplasms/therapy ; Patient Selection ; Sexism
    Chemical Substances Biomarkers, Tumor ; Immune Checkpoint Inhibitors
    Language English
    Publishing date 2021-06-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural
    ISSN 2473-4284
    ISSN (online) 2473-4284
    DOI 10.1200/PO.21.00168
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Synthetic lethality-based prediction of anti-SARS-CoV-2 targets.

    Pal, Lipika R / Cheng, Kuoyuan / Nair, Nishanth Ulhas / Martin-Sancho, Laura / Sinha, Sanju / Pu, Yuan / Riva, Laura / Yin, Xin / Schischlik, Fiorella / Lee, Joo Sang / Chanda, Sumit K / Ruppin, Eytan

    iScience

    2022  Volume 25, Issue 5, Page(s) 104311

    Abstract: Novel strategies are needed to identify drug targets and treatments for the COVID-19 pandemic. The altered gene expression of virus-infected host cells provides an opportunity to specifically inhibit viral propagation via targeting the synthetic lethal ... ...

    Abstract Novel strategies are needed to identify drug targets and treatments for the COVID-19 pandemic. The altered gene expression of virus-infected host cells provides an opportunity to specifically inhibit viral propagation via targeting the synthetic lethal and synthetic dosage lethal (SL/SDL) partners of such altered host genes. Pursuing this disparate antiviral strategy, here we comprehensively analyzed multiple
    Language English
    Publishing date 2022-04-27
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2022.104311
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Author Correction

    Sanju Sinha / Karina Barbosa / Kuoyuan Cheng / Mark D. M. Leiserson / Prashant Jain / Anagha Deshpande / David M. Wilson / Bríd M. Ryan / Ji Luo / Ze’ev A. Ronai / Joo Sang Lee / Aniruddha J. Deshpande / Eytan Ruppin

    Nature Communications, Vol 13, Iss 1, Pp 1-

    A systematic genome-wide mapping of oncogenic mutation selection during CRISPR-Cas9 genome editing

    2022  Volume 1

    Keywords Science ; Q
    Language English
    Publishing date 2022-05-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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  7. Article ; Online: Cross-species identification of cancer resistance-associated genes that may mediate human cancer risk.

    Nair, Nishanth Ulhas / Cheng, Kuoyuan / Naddaf, Lamis / Sharon, Elad / Pal, Lipika R / Rajagopal, Padma S / Unterman, Irene / Aldape, Kenneth / Hannenhalli, Sridhar / Day, Chi-Ping / Tabach, Yuval / Ruppin, Eytan

    Science advances

    2022  Volume 8, Issue 31, Page(s) eabj7176

    Abstract: Cancer is a predominant disease across animals. We applied a comparative genomics approach to systematically characterize genes whose conservation levels correlate positively (PC) or negatively (NC) with cancer resistance estimates across 193 vertebrates. ...

    Abstract Cancer is a predominant disease across animals. We applied a comparative genomics approach to systematically characterize genes whose conservation levels correlate positively (PC) or negatively (NC) with cancer resistance estimates across 193 vertebrates. Pathway analysis reveals that NC genes are enriched for metabolic functions and PC genes in cell cycle regulation, DNA repair, and immune response, pointing to their corresponding roles in mediating cancer risk. We find that PC genes are less tolerant to loss-of-function (LoF) mutations, are enriched in cancer driver genes, and are associated with germline mutations that increase human cancer risk. Their relevance to cancer risk is further supported via the analysis of mouse functional genomics and cancer mortality of zoo mammals' data. In sum, our study describes a cross-species genomic analysis pointing to candidate genes that may mediate human cancer risk.
    MeSH term(s) Animals ; Genomics ; Humans ; Loss of Function Mutation ; Mammals ; Mice ; Neoplasms/genetics
    Language English
    Publishing date 2022-08-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.abj7176
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: In vitro and in vivo identification of clinically approved drugs that modify ACE2 expression

    Sanju Sinha / Kuoyuan Cheng / Alejandro A Schäffer / Kenneth Aldape / Eyal Schiff / Eytan Ruppin

    Molecular Systems Biology, Vol 16, Iss 7, Pp n/a-n/a (2020)

    2020  

    Abstract: Abstract The COVID‐19 pandemic caused by SARS‐CoV‐2 has been a global health challenge. Angiotensin‐converting enzyme 2 (ACE2) is the host receptor for SARS‐CoV‐2 entry. Recent studies have suggested that patients with hypertension and diabetes treated ... ...

    Abstract Abstract The COVID‐19 pandemic caused by SARS‐CoV‐2 has been a global health challenge. Angiotensin‐converting enzyme 2 (ACE2) is the host receptor for SARS‐CoV‐2 entry. Recent studies have suggested that patients with hypertension and diabetes treated with ACE inhibitors (ACEIs) or angiotensin receptor blockers have a higher risk of COVID‐19 infection as these drugs could upregulate ACE2, motivating the study of ACE2 modulation by drugs in current clinical use. Here, we mined published datasets to determine the effects of hundreds of clinically approved drugs on ACE2 expression. We find that ACEIs are enriched for ACE2‐upregulating drugs, while antineoplastic agents are enriched for ACE2‐downregulating drugs. Vorinostat and isotretinoin are the top ACE2 up/downregulators, respectively, in cell lines. Dexamethasone, a corticosteroid used in treating severe acute respiratory syndrome and COVID‐19, significantly upregulates ACE2 both in vitro and in vivo. Further top ACE2 regulators in vivo or in primary cells include erlotinib and bleomycin in the lung and vancomycin, cisplatin, and probenecid in the kidney. Our study provides leads for future work studying ACE2 expression modulators.
    Keywords angiotensin I‐converting enzyme 2 ; coronavirus disease 2019 ; dexamethasone ; drug‐modifying ACE2 expression ; severe acute respiratory syndrome coronavirus 2 ; Biology (General) ; QH301-705.5 ; Medicine (General) ; R5-920
    Subject code 610
    Language English
    Publishing date 2020-07-01T00:00:00Z
    Publisher Wiley
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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  9. Article ; Online: In vitro and in vivo identification of clinically approved drugs that modify ACE2 expression.

    Sinha, Sanju / Cheng, Kuoyuan / Schäffer, Alejandro A / Aldape, Kenneth / Schiff, Eyal / Ruppin, Eytan

    Molecular systems biology

    2020  Volume 16, Issue 7, Page(s) e9628

    Abstract: The COVID-19 pandemic caused by SARS-CoV-2 has is a global health challenge. Angiotensin-converting enzyme 2 (ACE2) is the host receptor for SARS-CoV-2 entry. Recent studies have suggested that patients with hypertension and diabetes treated with ACE ... ...

    Abstract The COVID-19 pandemic caused by SARS-CoV-2 has is a global health challenge. Angiotensin-converting enzyme 2 (ACE2) is the host receptor for SARS-CoV-2 entry. Recent studies have suggested that patients with hypertension and diabetes treated with ACE inhibitors (ACEIs) or angiotensin receptor blockers have a higher risk of COVID-19 infection as these drugs could upregulate ACE2, motivating the study of ACE2 modulation by drugs in current clinical use. Here, we mined published datasets to determine the effects of hundreds of clinically approved drugs on ACE2 expression. We find that ACEIs are enriched for ACE2-upregulating drugs, while antineoplastic agents are enriched for ACE2-downregulating drugs. Vorinostat and isotretinoin are the top ACE2 up/downregulators, respectively, in cell lines. Dexamethasone, a corticosteroid used in treating severe acute respiratory syndrome and COVID-19, significantly upregulates ACE2 both in vitro and in vivo. Further top ACE2 regulators in vivo or in primary cells include erlotinib and bleomycin in the lung and vancomycin, cisplatin, and probenecid in the kidney. Our study provides leads for future work studying ACE2 expression modulators.
    MeSH term(s) A549 Cells ; Angiotensin Receptor Antagonists/pharmacology ; Angiotensin-Converting Enzyme 2 ; Angiotensin-Converting Enzyme Inhibitors/pharmacology ; Betacoronavirus ; Bleomycin/pharmacology ; COVID-19 ; Coronavirus Infections/drug therapy ; Dexamethasone/pharmacology ; Drug Design ; Drug Evaluation, Preclinical ; Erlotinib Hydrochloride/pharmacology ; Fluphenazine/pharmacology ; HEK293 Cells ; Humans ; Kidney/drug effects ; Lung/drug effects ; MCF-7 Cells ; Pandemics ; Peptidyl-Dipeptidase A ; Pneumonia, Viral/drug therapy ; SARS-CoV-2 ; Systems Biology ; Up-Regulation ; Vemurafenib/pharmacology ; COVID-19 Drug Treatment
    Chemical Substances Angiotensin Receptor Antagonists ; Angiotensin-Converting Enzyme Inhibitors ; Bleomycin (11056-06-7) ; Vemurafenib (207SMY3FQT) ; Dexamethasone (7S5I7G3JQL) ; Erlotinib Hydrochloride (DA87705X9K) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; Fluphenazine (S79426A41Z)
    Keywords covid19
    Language English
    Publishing date 2020-07-28
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2193510-5
    ISSN 1744-4292 ; 1744-4292
    ISSN (online) 1744-4292
    ISSN 1744-4292
    DOI 10.15252/msb.20209628
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Synthetic lethality-based prediction of anti-SARS-CoV-2 targets.

    Pal, Lipika R / Cheng, Kuoyuan / Nair, Nishanth Ulhas / Martin-Sancho, Laura / Sinha, Sanju / Pu, Yuan / Riva, Laura / Yin, Xin / Schischlik, Fiorella / Lee, Joo Sang / Chanda, Sumit K / Ruppin, Eytan

    bioRxiv : the preprint server for biology

    2021  

    Abstract: Novel strategies are needed to identify drug targets and treatments for the COVID-19 pandemic. The altered gene expression of virus-infected host cells provides an opportunity to specifically inhibit viral propagation via targeting the synthetic lethal ( ... ...

    Abstract Novel strategies are needed to identify drug targets and treatments for the COVID-19 pandemic. The altered gene expression of virus-infected host cells provides an opportunity to specifically inhibit viral propagation via targeting the synthetic lethal (SL) partners of such altered host genes. Pursuing this antiviral strategy, here we comprehensively analyzed multiple
    Language English
    Publishing date 2021-09-15
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2021.09.14.460408
    Database MEDical Literature Analysis and Retrieval System OnLINE

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