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  1. Article: Novel omics technology driving translational research in precision oncology.

    Basu, Anubhav / Budhraja, Anshul / Juwayria / Abhilash, Dasari / Gupta, Ishaan

    Advances in genetics

    2021  Volume 108, Page(s) 81–145

    Abstract: In this review, we summarize the current challenges faced by cancer researchers and motivate the use of novel genomics solutions. We follow this up with a comprehensive overview of three recent genomics technologies: liquid biopsy, single-cell RNA ... ...

    Abstract In this review, we summarize the current challenges faced by cancer researchers and motivate the use of novel genomics solutions. We follow this up with a comprehensive overview of three recent genomics technologies: liquid biopsy, single-cell RNA sequencing and spatial transcriptomics. We discuss a few representative protocols/assays for each technology along with their strengths, weaknesses, optimal use-cases, and their current stage of clinical deployment by summarizing trial data. We focus on how these technologies help us develop a better understanding of cancer as a rapidly evolving heterogeneous genetic disease that modulates its immediate microenvironment leading to systemic macro-level changes in the patient body. We summarize the review with a flowchart that integrates these three technologies in the existing workflows of clinicians and researchers toward robust detection, accurate diagnosis, and precision oncology.
    MeSH term(s) Genomics ; Humans ; Neoplasms/genetics ; Precision Medicine ; Technology ; Translational Research, Biomedical ; Tumor Microenvironment
    Language English
    Publishing date 2021-10-07
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 148-x
    ISSN 0065-2660
    ISSN 0065-2660
    DOI 10.1016/bs.adgen.2021.08.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The polybasic insert, the RBD of the SARS-CoV-2 spike protein, and the feline coronavirus - evolved or yet to evolve.

    Budhraja, Anshul / Pandey, Sakshi / Kannan, Srinivasaraghavan / Verma, Chandra S / Venkatraman, Prasanna

    Biochemistry and biophysics reports

    2021  Volume 25, Page(s) 100907

    Abstract: Recent research on the SARS-CoV-2 pandemic has exploded around the furin-cleavable polybasic insert PRRAR↓S, found within the spike protein. The insert and the receptor-binding domain, (RBD), are vital clues in the Sherlock Holmes-like investigation into ...

    Abstract Recent research on the SARS-CoV-2 pandemic has exploded around the furin-cleavable polybasic insert PRRAR↓S, found within the spike protein. The insert and the receptor-binding domain, (RBD), are vital clues in the Sherlock Holmes-like investigation into the origin of the virus and in its zoonotic crossover. Based on comparative analysis of the whole genome and the sequence features of the insert and the RBD domain, the bat and the pangolin have been proposed as very likely intermediary hosts. In this study, using the various databases, in-house developed tools, sequence comparisons, structure-guided docking, and molecular dynamics simulations, we cautiously present a fresh, theoretical perspective on the SARS-CoV-2 virus activation and its intermediary host. They are a) the SARS-CoV-2 has not yet acquired a fully optimal furin binding site or this seemingly less optimal sequence, PRRARS, has been selected for survival; b) in structural models of furin complexed with peptides, PRRAR↓S binds less well and with distinct differences as compared to the all basic RRKRR↓S; c) these differences may be exploited for the design of virus-specific inhibitors; d) the novel polybasic insert of SARS-CoV-2 may be promiscuous enough to be cleaved by multiple enzymes of the human airway epithelium and tissues which may explain its unexpected broad tropism; e) the RBD domain of the feline coronavirus spike protein carries residues that are responsible for high-affinity binding of the SARS-CoV-2 to the ACE 2 receptor; f)
    Language English
    Publishing date 2021-01-13
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2831046-9
    ISSN 2405-5808 ; 2405-5808
    ISSN (online) 2405-5808
    ISSN 2405-5808
    DOI 10.1016/j.bbrep.2021.100907
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The polybasic insert, the RBD of the SARS-CoV-2 spike protein, and the feline coronavirus – evolved or yet to evolve

    Anshul Budhraja / Sakshi Pandey / Srinivasaraghavan Kannan / Chandra S. Verma / Prasanna Venkatraman

    Biochemistry and Biophysics Reports, Vol 25, Iss , Pp 100907- (2021)

    2021  

    Abstract: Recent research on the SARS-CoV-2 pandemic has exploded around the furin-cleavable polybasic insert PRRAR↓S, found within the spike protein. The insert and the receptor-binding domain, (RBD), are vital clues in the Sherlock Holmes-like investigation into ...

    Abstract Recent research on the SARS-CoV-2 pandemic has exploded around the furin-cleavable polybasic insert PRRAR↓S, found within the spike protein. The insert and the receptor-binding domain, (RBD), are vital clues in the Sherlock Holmes-like investigation into the origin of the virus and in its zoonotic crossover. Based on comparative analysis of the whole genome and the sequence features of the insert and the RBD domain, the bat and the pangolin have been proposed as very likely intermediary hosts. In this study, using the various databases, in-house developed tools, sequence comparisons, structure-guided docking, and molecular dynamics simulations, we cautiously present a fresh, theoretical perspective on the SARS-CoV-2 virus activation and its intermediary host. They are a) the SARS-CoV-2 has not yet acquired a fully optimal furin binding site or this seemingly less optimal sequence, PRRARS, has been selected for survival; b) in structural models of furin complexed with peptides, PRRAR↓S binds less well and with distinct differences as compared to the all basic RRKRR↓S; c) these differences may be exploited for the design of virus-specific inhibitors; d) the novel polybasic insert of SARS-CoV-2 may be promiscuous enough to be cleaved by multiple enzymes of the human airway epithelium and tissues which may explain its unexpected broad tropism; e) the RBD domain of the feline coronavirus spike protein carries residues that are responsible for high-affinity binding of the SARS-CoV-2 to the ACE 2 receptor; f) en route zoonotic transfer, the virus may have passed through the domestic cat whose very human-like ACE2 receptor and furin may have played some role in optimizing the traits required for zoonotic transfer.
    Keywords Spike protein ; Furin ; Host ; Proteases ; SARS-CoV-2 ; Feline CoV ; Biology (General) ; QH301-705.5 ; Biochemistry ; QD415-436
    Language English
    Publishing date 2021-03-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Molecular signature of postmortem lung tissue from COVID-19 patients suggests distinct trajectories driving mortality.

    Budhraja, Anshul / Basu, Anubhav / Gheware, Atish / Abhilash, Dasari / Rajagopala, Seesandra / Pakala, Suman / Sumit, Madhuresh / Ray, Animesh / Subramaniam, Arulselvi / Mathur, Purva / Nambirajan, Aruna / Kumar, Sachin / Gupta, Ritu / Wig, Naveet / Trikha, Anjan / Guleria, Randeep / Sarkar, Chitra / Gupta, Ishaan / Jain, Deepali

    Disease models & mechanisms

    2022  Volume 15, Issue 5

    Abstract: To elucidate the molecular mechanisms that manifest lung abnormalities during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, we performed whole-transcriptome sequencing of lung autopsies from 31 patients with severe COVID-19 and ...

    Abstract To elucidate the molecular mechanisms that manifest lung abnormalities during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, we performed whole-transcriptome sequencing of lung autopsies from 31 patients with severe COVID-19 and ten uninfected controls. Using metatranscriptomics, we identified the existence of two distinct molecular signatures of lethal COVID-19. The dominant 'classical' signature (n=23) showed upregulation of the unfolded protein response, steroid biosynthesis and complement activation, supported by massive metabolic reprogramming leading to characteristic lung damage. The rarer signature (n=8) that potentially represents 'cytokine release syndrome' (CRS) showed upregulation of cytokines such as IL1 and CCL19, but absence of complement activation. We found that a majority of patients cleared SARS-CoV-2 infection, but they suffered from acute dysbiosis with characteristic enrichment of opportunistic pathogens such as Staphylococcus cohnii in 'classical' patients and Pasteurella multocida in CRS patients. Our results suggest two distinct models of lung pathology in severe COVID-19 patients, which can be identified through complement activation, presence of specific cytokines and characteristic microbiome. These findings can be used to design personalized therapy using in silico identified drug molecules or in mitigating specific secondary infections.
    MeSH term(s) Autopsy ; COVID-19 ; Cytokines ; Humans ; Lung/pathology ; SARS-CoV-2
    Chemical Substances Cytokines
    Language English
    Publishing date 2022-06-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.049572
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Molecular signature of postmortem lung tissue from COVID-19 patients suggests distinct trajectories driving mortality

    Anshul Budhraja / Anubhav Basu / Atish Gheware / Dasari Abhilash / Seesandra Rajagopala / Suman Pakala / Madhuresh Sumit / Animesh Ray / Arulselvi Subramaniam / Purva Mathur / Aruna Nambirajan / Sachin Kumar / Ritu Gupta / Naveet Wig / Anjan Trikha / Randeep Guleria / Chitra Sarkar / Ishaan Gupta / Deepali Jain

    Disease Models & Mechanisms, Vol 15, Iss

    2022  Volume 5

    Abstract: To elucidate the molecular mechanisms that manifest lung abnormalities during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, we performed whole-transcriptome sequencing of lung autopsies from 31 patients with severe COVID-19 and ...

    Abstract To elucidate the molecular mechanisms that manifest lung abnormalities during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, we performed whole-transcriptome sequencing of lung autopsies from 31 patients with severe COVID-19 and ten uninfected controls. Using metatranscriptomics, we identified the existence of two distinct molecular signatures of lethal COVID-19. The dominant ‘classical’ signature (n=23) showed upregulation of the unfolded protein response, steroid biosynthesis and complement activation, supported by massive metabolic reprogramming leading to characteristic lung damage. The rarer signature (n=8) that potentially represents ‘cytokine release syndrome’ (CRS) showed upregulation of cytokines such as IL1 and CCL19, but absence of complement activation. We found that a majority of patients cleared SARS-CoV-2 infection, but they suffered from acute dysbiosis with characteristic enrichment of opportunistic pathogens such as Staphylococcus cohnii in ‘classical’ patients and Pasteurella multocida in CRS patients. Our results suggest two distinct models of lung pathology in severe COVID-19 patients, which can be identified through complement activation, presence of specific cytokines and characteristic microbiome. These findings can be used to design personalized therapy using in silico identified drug molecules or in mitigating specific secondary infections.
    Keywords sars-cov-2 ; infectious disease ; metatranscriptomics ; whole-transcriptome sequencing ; lung microbiome ; Medicine ; R ; Pathology ; RB1-214
    Subject code 610
    Language English
    Publishing date 2022-05-01T00:00:00Z
    Publisher The Company of Biologists
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Molecular signature of postmortem lung tissue from COVID-19 patients suggests distinct trajectories driving mortality

    Budhraja, Anshul / Basu, Anubhav / Gheware, Atish / Abhilash, Dasari / Rajagopala, Seesandra / Pakala, Suman / Sumit, Madhuresh / Ray, Animesh / Arulselvi, S / Mathur, Purva / Nambirajan, Aruna / Kumar, Sachin / Gupa, Ritu / Wig, Naveet / Trikha, Anjan / Guleria, Randeep / Sarkar, Chitra / Gupta, Ishaan / Jain, Deepali

    bioRxiv

    Abstract: The precise molecular mechanisms behind severe life-threatening lung abnormalities during severe SARS-CoV-2 infections are still unclear. To address this challenge, we performed whole transcriptome sequencing of lung autopsies from 31 patients suffering ... ...

    Abstract The precise molecular mechanisms behind severe life-threatening lung abnormalities during severe SARS-CoV-2 infections are still unclear. To address this challenge, we performed whole transcriptome sequencing of lung autopsies from 31 patients suffering from severe COVID-19 related complications and 10 uninfected controls. Using a metatranscriptome analysis of lung tissue samples we identified the existence of two distinct molecular signatures of lethal COVID-19. The dominant "classical" signature (n=23) showed upregulation of unfolded protein response, steroid biosynthesis and complement activation supported by massive metabolic reprogramming leading to characteristic lung damage. The rarer signature (n=8) potentially representing "Cytokine Release Syndrome" (CRS) showed upregulation of IL1 cytokines such CCL19 but absence of complement activation and muted inflammation. Further, dissecting expression of individual genes within enriched pathways for patient signature suggests heterogeneity in host response to the primary infection. We found that the majority of patients cleared the SARS-CoV-2 infection, but all suffered from acute dysbiosis with characteristic enrichment of opportunistic pathogens such as Gordonia bronchialis in "classical" patients and Staphylococcus warneri in CRS patients. Our results suggest two distinct models of lung pathology in severe COVID-19 patients that can be identified through the status of the complement activation, presence of specific cytokines and characteristic microbiome. This information can be used to design personalized therapy to treat COVID-19 related complications corresponding to patient signature such as using the identified drug molecules or mitigating specific secondary infections.
    Keywords covid19
    Language English
    Publishing date 2021-11-08
    Publisher Cold Spring Harbor Laboratory
    Document type Article ; Online
    DOI 10.1101/2021.11.08.467705
    Database COVID19

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