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      Interrogating open issues in cancer precision medicine with patient-derived xenografts

      Author(s): , , , , , , , , , ,   , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,
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      Journal: Nature Reviews Cancer
      Publisher: Springer Nature

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          Abstract

          This Opinion article discusses progress and challenges in using patient-derived xenograft (PDX) models in cancer precision medicine. It is primarily co-authored by members of the EurOPDX Consortium and as such highlights the merits of shared PDX resources.

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          Dissecting the multicellular ecosystem of metastatic melanoma by single-cell RNA-seq.

          Itay Tirosh, Benjamin Izar, Sanjay M. Prakadan … (2016)
          To explore the distinct genotypic and phenotypic states of melanoma tumors, we applied single-cell RNA sequencing (RNA-seq) to 4645 single cells isolated from 19 patients, profiling malignant, immune, stromal, and endothelial cells. Malignant cells within the same tumor displayed transcriptional heterogeneity associated with the cell cycle, spatial context, and a drug-resistance program. In particular, all tumors harbored malignant cells from two distinct transcriptional cell states, such that tumors characterized by high levels of the MITF transcription factor also contained cells with low MITF and elevated levels of the AXL kinase. Single-cell analyses suggested distinct tumor microenvironmental patterns, including cell-to-cell interactions. Analysis of tumor-infiltrating T cells revealed exhaustion programs, their connection to T cell activation and clonal expansion, and their variability across patients. Overall, we begin to unravel the cellular ecosystem of tumors and how single-cell genomics offers insights with implications for both targeted and immune therapies.
          Article 0 comments Cited 1374 times – based on 0 reviews     Review now
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            Cancer immunoediting: integrating immunity's roles in cancer suppression and promotion.

            Robert D. Schreiber, Lloyd J. Old, Mark J. Smyth (2011)
            Understanding how the immune system affects cancer development and progression has been one of the most challenging questions in immunology. Research over the past two decades has helped explain why the answer to this question has evaded us for so long. We now appreciate that the immune system plays a dual role in cancer: It can not only suppress tumor growth by destroying cancer cells or inhibiting their outgrowth but also promote tumor progression either by selecting for tumor cells that are more fit to survive in an immunocompetent host or by establishing conditions within the tumor microenvironment that facilitate tumor outgrowth. Here, we discuss a unifying conceptual framework called "cancer immunoediting," which integrates the immune system's dual host-protective and tumor-promoting roles.
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              The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups

              Christina Curtis, Sohrab Shah, Suet-Feung Chin … (2012)
              The elucidation of breast cancer subgroups and their molecular drivers requires integrated views of the genome and transcriptome from representative numbers of patients. We present an integrated analysis of copy number and gene expression in a discovery and validation set of 997 and 995 primary breast tumours, respectively, with long-term clinical follow-up. Inherited variants (copy number variants and single nucleotide polymorphisms) and acquired somatic copy number aberrations (CNAs) were associated with expression in ~40% of genes, with the landscape dominated by cis- and trans-acting CNAs. By delineating expression outlier genes driven in cis by CNAs, we identified putative cancer genes, including deletions in PPP2R2A, MTAP and MAP2K4. Unsupervised analysis of paired DNA–RNA profiles revealed novel subgroups with distinct clinical outcomes, which reproduced in the validation cohort. These include a high-risk, oestrogen-receptor-positive 11q13/14 cis-acting subgroup and a favourable prognosis subgroup devoid of CNAs. Trans-acting aberration hotspots were found to modulate subgroup-specific gene networks, including a TCR deletion-mediated adaptive immune response in the ‘CNA-devoid’ subgroup and a basal-specific chromosome 5 deletion-associated mitotic network. Our results provide a novel molecular stratification of the breast cancer population, derived from the impact of somatic CNAs on the transcriptome.
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                Author and article information

                Journal
                Title: Nature Reviews Cancer
                Abbreviated Title: Nat Rev Cancer
                Publisher: Springer Nature
                ISSN (Print): 1474-175X
                ISSN (Electronic): 1474-1768
                Publication date Created: January 20 2017
                Publication date (Print): January 20 2017
                Volume:
                Issue:
                Article
                DOI: 10.1038/nrc.2016.140
                PubMed ID: 28104906
                SO-VID: 6272feca-0684-48ab-94cf-34f5d611537d
                Copyright © © 2017
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