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Network rewiring,adaptive resistance and combating strategies in breast cancer

Cancer Drug resistance 2019年第4期2卷 1106-1126页

作者： Constance Gaya Cremers Lan K.Nguyen Department of Biochemistry and Molecular Biology School of Biomedical SciencesMonash UniversityClaytonVictoria 3800Australia Biomedicine Discovery Institute Monash UniversityClaytonVictoria 3800Australia

resistance to targeted anti-cancer drugs is a complex phenomenon and a major challenge in cancer *** is becoming increasingly evident that a form of acquired drug resistance known as“adaptive resistance”is a common cause of treatment failure and patient relapse in many *** classical resistance mechanisms that are acquired via genomic alterations,adaptive resistance is instead driven by non-genomic changes involving rapid and dynamic rewiring of signalling and/or transcriptional networks following therapy,enabled by complex pathway crosstalk and feedback *** network rewiring allows tumour cells to adapt to the drug treatment,circumvent the initial drug challenge and continue to survive in the presence of the *** its great clinical importance,adaptive resistance remains largely under-studied and poorly *** review is focused on recent findings which provide new insights into the mechanisms underlying adaptive resistance in breast cancer,highlighting how breast tumour cells rewire intracellular signalling pathways to overcome the stress of initial targeted *** particular,we investigate adaptive resistance to targeted inhibition of two major oncogenic signalling axes frequently dysregulated in breast cancer,the PI3K-AKT-mTOR and RAS-MAPK signalling pathways;and discuss potential combination treatment strategies that overcome such *** addition,we highlight application of quantitative and computational modelling as a novel integrative and powerful approach to gain network-level understanding of network rewiring,and rationally identify and prioritise effective drug combinations.

关键词： Network rewiring adaptive resistance PI3K signalling MAPK signalling breast cancer mathematical modelling systems analysis

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Therapeutics to harness the immune microenvironment in multiple myeloma

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Cancer Drug resistance 2022年第3期5卷 647-661页

作者： James J.Ignatz-Hoover James J.Driscoll University Hospitals Seidman Cancer CenterClevelandOH 44106USA Department of Biochemistry Case Western Reserve UniversityClevelandOH 44106USA Hematopoietic and Immune Cancer Biology Program Case Comprehensive Cancer CenterCase Western Reserve UniversityClevelandOH 44106USA

Multiple myeloma(MM)remains an incurable,genetically heterogeneous disease characterized by the uncontrolled proliferation of transformed plasma cells nurtured within a permissive bone marrow(BM)*** therapies leverage the unique biology of MM cells and target the immune microenvironment that drives tumor growth and facilitates immune *** inhibitors and immunomodulatory drugs were initially introduced to complement and have now supplanted cytotoxic chemotherapy as frontline anti-myeloma ***,monoclonal antibodies,bispecific antibodies,and chimeric antigen receptor T cells were developed to revamp the immune system to overcome immune suppression and improve patient *** current MM therapies have markedly extended patient survival,acquired drug resistance inevitably emerges and drives disease *** logical progression for the next generation of MM therapies would be to design and validate agents that prevent and/or overcome acquired resistance to *** complex BM microenvironment promotes resistance to both current anti-myeloma agents and emerging *** cells are intertwined with a complex BM immune microenvironment that contributes to the development of adaptive drug ***,we describe recently FDA-approved and investigational anti-myeloma agents that directly or indirectly target the BM microenvironment to prevent or overcome drug *** effects of anti-myeloma agents may foster the development of rationally-designed drug cocktails that prevent BM-mediated resistance to immunotherapies.

关键词： Multiple myeloma drug resistance proteasome inhibitors immunomodulators immunotherapeutics adaptive resistance bone marrow microenvironment

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Mechanisms of PD-1 Ligand Induction and the Implications for Cancer Immunotherapy:A Literature Review

Mechanisms of PD-1 Ligand Induction and the Implications for...

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浙江省免疫学会第十次学术大会

作者： Ying Zheng Central Lab The First Hospital of Jiaxing

With the great success of anti-PD-1 therapy in patients with metastatic melanoma,non-small-cell lung cancer and renal cell cancer,cancer immunotherapy targeting the PD-1/PD-L1 pathway has become a hot research ***,the mechanisms underneath remain poorly understood.A key finding that encouraged the development of drugs blocking the PD-1 pathway for cancer immunotherapy was that PD-1 ligands are upregulated in many human cancers,whereas PD-1 is highly expressed on tumor-infiltrating *** solid tumors,PD-L1,rather than PD-L2,appears to be the major ligand *** the initial works,PDL1 mRNA was found to be broadly expressed in various ***,normal human tissues seldom express PD-L1 protein on their cell surface,with the exception of tonsil,placenta,and a small fraction of macrophage-like cells in lung and liver,suggesting that,under normal physiological conditions,PDL1 mRNA is under tight posttranscriptional *** sharp contrast,PD-L1 protein is abundantly expressed on the cell surface in various human ***,the pattern of PD-L1 expression indicated by immunohistochemistry in frozen human tumor section was found to be focal rather than diffuse in most human ***,the majority of in vitro-cultured tumor lines of both human and mouse origin are PD-L1-negative on the cells surface,despite overwhelming PD-L1 signal in specimens that are freshly isolated from patients with *** of the phenomenon as a central process by which cancers resist elimination by endogenous tumor-specific T cells revealed a mechanism for PD-1 ligand upregulation in cancer,known as "adaptive resistance".adaptive resistance refers to the induction of PD-L1 expression on tumor cells in response to specific cytokines,in particular *** IFN-γ is only produced by activated TH1 helper CD4 cells,activated CD8 cells and NK cells,this mechanism represents an adaption of tumor cells upon "sensing" an inflammatory immu

关键词： PD-1 ligation immunotherapy adaptive resistance IFN-γ

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