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Trends in Cancer
This journal offers authors two options (open access or subscription) to publish research

Feb 01, 2022

Volume 8Issue 2p81-158, e1-e2
Host microbiota influence both cancer incidence and therapeutic responsiveness, challenging the view that tumors depend on intrinsic properties. In this issue, Sholl et al. evaluate the utility of cancer-associated microbiota in patient diagnosis, prognosis, and treatment by discussing its role in cancer development and its use as a biomarker and therapeutic. Cover image represents the complexity of the microbial ecosystem. Cover image designed by Danielle Loughlin and adapted with permission from Gettyimages/KajaNi, Gettyimages/DivVector, Gettyimages/MariyaII....
Host microbiota influence both cancer incidence and therapeutic responsiveness, challenging the view that tumors depend on intrinsic properties. In this issue, Sholl et al. evaluate the utility of cancer-associated microbiota in patient diagnosis, prognosis, and treatment by discussing its role in cancer development and its use as a biomarker and therapeutic. Cover image represents the complexity of the microbial ecosystem. Cover image designed by Danielle Loughlin and adapted with permission from Gettyimages/KajaNi, Gettyimages/DivVector, Gettyimages/MariyaII.

Spotlight

  • An epigenetic signature in CD19-CAR T cells predicts clinical outcome

    • Federico Simonetta,
    • Francesco Bertoni
    The potential impact of epigenetic profiles on adoptive T cell immunotherapies is currently unknown. In a recent study in the Journal of the National Cancer Institute, Garcia-Prieto et al. show that specific DNA methylation profiles of CD19-CAR T cells are associated with improved clinical outcome of patients with B cell malignancies.

Forum

  • Combination therapies for targeting FGFR2 fusions in cholangiocarcinoma

    • Anna Saborowski,
    • Arndt Vogel,
    • Oreste Segatto
    Fibroblast growth factor receptor 2 (FGFR2) fusion proteins (FFs) are oncogenic drivers in 10–15% of intrahepatic cholangiocarcinoma (iCCA). FGFR-specific inhibitors provide temporary benefit in FF+ unresectable patients. Recent work with mouse iCCA models has documented the necessary role of RAS-ERK downstream to FFs and provided examples of preclinical experimentation aimed at improving FF targeting in iCCA.

Reviews

  • Redrawing therapeutic boundaries: microbiota and cancer

    • Jonathan Sholl,
    • Gregory D. Sepich-Poore,
    • Rob Knight,
    • Thomas Pradeu
    The unexpected roles of the microbiota in cancer challenge explanations of carcinogenesis that focus on tumor-intrinsic properties. Most tumors contain bacteria and viruses, and the host’s proximal and distal microbiota influence both cancer incidence and therapeutic responsiveness. Continuing the history of cancer–microbe research, these findings raise a key question: to what extent is the microbiota relevant for clinical oncology? We approach this by critically evaluating three issues: how the microbiota provides a predictive biomarker of cancer growth and therapeutic responsiveness, the microbiota’s causal role(s) in cancer development, and how therapeutic manipulations of the microbiota improve patient outcomes in cancer.
  • Evolution of metastasis: new tools and insights

    • Philippe Gui,
    • Trever G. Bivona
    Open Access
    Metastasis is an evolutionary process occurring across multiple organs and timescales. Due to its continuous and dynamic nature, this multifaceted process has been challenging to investigate and remains incompletely understood, in part due to the lack of tools capable of probing genomic evolution at high enough resolution. However, technological advances in genetic sequencing and editing have provided new and powerful methods to refine our understanding of the complex series of events that lead to metastatic dissemination.
  • Cancer catecholamine conundrum

    • H. Wackerhage,
    • J.F. Christensen,
    • M. Ilmer,
    • I. von Luettichau,
    • B.W. Renz,
    • M. Schönfelder
    Exercise, psychosocial stress, and drugs such as adrenergic agonists and antagonists increase the concentrations of catecholamines and/or alter adrenergic signaling. Intriguingly, exercise studies universally suggest that catecholamines are cancer-inhibiting whereas cancer stress studies typically report the opposite, whereas β-blocker studies show variable effects. Here, we term variable effects of catecholamines in cancer the cancer catecholamine conundrum. Variable effects of catecholamines can potentially be explained by variable expression of nine adrenergic receptor isoforms and by other factors including catecholamine effects on cancer versus immune or endothelial cells.
  • Exploiting T cell signaling to optimize engineered T cell therapies

    • Haopeng Wang,
    • Xianming Song,
    • Lianjun Shen,
    • Xinxin Wang,
    • Chenqi Xu
    Engineered T cell therapies, mainly chimeric antigen receptor (CAR)-T and T cell receptor (TCR)-T, have become the new frontier of cancer treatment. CAR-T and TCR-T therapies differ in many aspects, including cell persistence and toxicity, leading to different therapeutic outcomes. Both TCR and CAR recognize antigens and trigger T cell mediated antitumor response, but they have distinct molecular structures and signaling properties. TCR represents one of the most complex receptors, while CAR is a single-chain chimera integrating modules from multiple immune receptors.
  • Impact of tissue-agnostic approvals for patients with sarcoma

    • Roberto Carmagnani Pestana,
    • Juliana Rodrigues Beal,
    • Amanda Parkes,
    • Nelson Hamerschlak,
    • Vivek Subbiah
    Tissue-agnostic drug development is a major step forward in offering treatment options for rare tumors. Sarcomas are heterogeneous rare malignancies with more than 100 subtypes. Recent failure of Phase III trials, nonbiomarker-driven clinical trials, and rarity hamper developmental therapeutics in sarcomas. Since a ‘one-size-fits-all’ approach continues to be the standard of care, tissue-agnostic approvals assume significance in sarcomas. In this review, we focus on the clinical evidence of recent drug approvals for neurotrophic tyrosine receptor kinase (NTRK) fusion, microsatellite instability-high (MSI-H) or mismatch repair deficient (dMMR) phenotype, and tumor mutation burden-high (TMB-H) status in the context of sarcomas, and the future landscape of tissue-agnostic targets, such as rearranged during transfection (RET), fibroblast growth factor receptor (FGFR), and neuregulin-1 (NRG1).
  • Antimetastatic defense by CD8+ T cells

    • Paulino Tallón de Lara,
    • Héctor Castañón,
    • Michelle Sterpi,
    • Maries van den Broek
    Metastasis is an intricate process whereby tumor cells migrate from the primary tumor, survive in the circulation, seed distal organs, and proliferate to create metastatic foci. CD8+ T cells can detect and eliminate tumor cells. Research on CD8+ T cell–dependent antitumor immunity has classically focused on its role in the primary tumor. There is increasing evidence, however, that CD8+ T cells have unique antimetastatic functions in various steps of the metastatic cascade. Here, we review the mechanisms whereby CD8+ T cells control metastatic lesions.
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