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Showing 1–12 of 12 results
Advanced filters: Author: Chandan Kumar-Sinha Clear advanced filters

  • Chandan Kumar-Sinha and Arul Chinnaiyan summarize the increasing use of sequencing panels to screen for cancer-associated genes in tumor and germline samples. The authors highlight the increasing appreciation of aberrations in regulatory genes or chromatin-related genes and argue that precision oncology must be considered in the context of adding value to the standard of care, not apart from it.

    • Chandan Kumar-Sinha
    • Arul M Chinnaiyan
    Reviews
    Nature Biotechnology
    Volume: 36, P: 46-60

  • This report identifies oncogenic fusions in individuals with breast cancer involving the genes encoding NOTCH and MAST, recurring in approximately 5–7% of studied cases. The fusions show growth-promoting properties that suggest that they may represent targetable events in a subset of people with breast cancer.

    • Dan R Robinson
    • Shanker Kalyana-Sundaram
    • Arul M Chinnaiyan
    Research
    Nature Medicine
    Volume: 17, P: 1646-1651

  • Gene fusions have long been known to have an important role in leukaemias, but they have recently been identified in a majority of prostate cancers. Understanding their role in this disease could lead to better targeted therapies.

    • Chandan Kumar-Sinha
    • Scott A. Tomlins
    • Arul M. Chinnaiyan
    Reviews
    Nature Reviews Cancer
    Volume: 8, P: 497-511

  • Human telomeres are protected by a specialized shelterin complex composed of six proteins. Here the authors structurally characterize the interaction between the POT1-TPP1 shelterin component and identify mutations associated with genome instability and cancer that disrupt the POT1-TPP1 interaction.

    • Cong Chen
    • Peili Gu
    • Ming Lei
    ResearchOpen Access
    Nature Communications
    Volume: 8, P: 1-15

  • Using a combination of new generation long- and short-read sequencing technologies, this study analyses cancer samples for gene fusion transcripts. The approach uncovers transcripts arising from known gene fusions in leukaemia and prostate cancer, as well as newly discovered ones in prostate cancer.

    • Christopher A. Maher
    • Chandan Kumar-Sinha
    • Arul M. Chinnaiyan
    Research
    Nature
    Volume: 458, P: 97-101

  • Argonaute 2 (AGO2) binds RAS and is required for cellular transformation. Here, the authors establish a KRAS-driven mouse model of pancreatic cancer with conditional loss of AGO2 and show that the early phase of neoplastic lesion initiation is dependent on EGFR/RAS but not AGO2, while AGO2 is required for pancreatic ductal adenocarcinoma progression and metastasis.

    • Sunita Shankar
    • Jean Ching-Yi Tien
    • Arul M. Chinnaiyan
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-17

  • Genetic regulators of cancer are identified by combining data on global gene expression and DNA copy number.

    • Chandan Kumar-Sinha
    • Arul M Chinnaiyan
    News & Views
    Nature Biotechnology
    Volume: 24, P: 524-526

  • Clinical exome and transcriptome sequencing of 500 adult patients with metastatic solid tumours of diverse lineage and biopsy site, as part of the Michigan Oncology Sequencing (MI-ONCOSEQ) Program.

    • Dan R. Robinson
    • Yi-Mi Wu
    • Arul M. Chinnaiyan
    Research
    Nature
    Volume: 548, P: 297-303

  • Tumour growth involves anomalies in cell cycle genes and emergent phenotypes, but the tumour proliferation rate (or mitotic index) is defined by just one marker, Ki-67. A study now integrates expression patterns of several markers to generate spatio-temporal maps of cell proliferation in cancer tissues.

    • Chandan Kumar-Sinha
    • Arul M. Chinnaiyan
    News & Views
    Nature Cell Biology
    Volume: 24, P: 285-287

  • Using pair-end transcriptome sequencing, this study provides the identification of Raf pathway gene rearrangements in a small proportion of prostate and gastric cancers and in melanomas. The fusion proteins show tumorigenic potential and represent a unique activating alteration of this oncogenic pathway, which seems to be mutually exclusive from known cancer-associated Raf mutations. This suggests that therapeutic Raf inhibition can be expanded to this fusion-harboring subset of solid tumors.

    • Nallasivam Palanisamy
    • Bushra Ateeq
    • Arul M Chinnaiyan
    Research
    Nature Medicine
    Volume: 16, P: 793-798