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  • Open Access

    ARTICLE

    Knockdown of HE4 suppresses tumor growth and invasiveness in lung adenocarcinoma through regulation of EGFR signaling

    YUE ZHANG1,#, WENYU YANG1,#, XIAOWANG HAN1,#, YUE QIAO1, HAITAO WANG2, TING CHEN1, TIANYING LI1, WEN-BIN OU1,*

    Oncology Research, Vol.32, No.6, pp. 1119-1128, 2024, DOI:10.32604/or.2024.045025 - 23 May 2024

    Abstract It has been shown that the high expression of human epididymis protein 4 (HE4) in most lung cancers is related to the poor prognosis of patients, but the mechanism of pathological transformation of HE4 in lung cancer is still unclear. The current study is expected to clarify the function and mechanism of HE4 in the occurrence and metastasis of lung adenocarcinoma (LUAD). Immunoblotting evaluated HE4 expression in lung cancer cell lines and biopsies, and through analysis of The Cancer Genome Atlas (TCGA) dataset. Frequent HE4 overexpression was demonstrated in LUAD, but not in lung squamous… More >

  • Open Access

    REVIEW

    Opportunities and challenges of CD47-targeted therapy in cancer immunotherapy

    QIUQIANG CHEN1,*, XUEJUN GUO2, WENXUE MA3,*

    Oncology Research, Vol.32, No.1, pp. 49-60, 2024, DOI:10.32604/or.2023.042383 - 15 November 2023

    Abstract Cancer immunotherapy has emerged as a promising strategy for the treatment of cancer, with the tumor microenvironment (TME) playing a pivotal role in modulating the immune response. CD47, a cell surface protein, has been identified as a crucial regulator of the TME and a potential therapeutic target for cancer therapy. However, the precise functions and implications of CD47 in the TME during immunotherapy for cancer patients remain incompletely understood. This comprehensive review aims to provide an overview of CD47’s multifaced role in TME regulation and immune evasion, elucidating its impact on various types of immunotherapy… More > Graphic Abstract

    Opportunities and challenges of CD47-targeted therapy in cancer immunotherapy

  • Open Access

    VIEWPOINT

    DNA polymerase θ (POLQ): A druggable DNA polymerase for homologous recombination-deficient cancer cells

    MERAN KESHAWA EDIRIWEERA*

    BIOCELL, Vol.47, No.3, pp. 441-444, 2023, DOI:10.32604/biocell.2023.025747 - 03 January 2023

    Abstract Irregularities in the DNA repair pathways are frequently observed in cancer. Dysregulated DNA repair pathways support growth advantages to tumor cells. DNA polymerase-theta (POLQ) is an error-prone DNA polymerase involved in double-strand break repair through microhomology-mediated end joining (MMEJ). POLQ also mediates translesion DNA synthesis and it is largely not expressed in normal cells. POLQ is overexpressed in a range of cancer cells, including homologous recombination (HR) deficient cancer cells. In HR deficient cells, MMEJ is crucial as a backup DNA repair pathway, indicating the indispensable role of POLQ-mediated MMEJ in HR deficient cancer cells. More >

  • Open Access

    REVIEW

    Frizzled Receptors in Tumors, Focusing on Signaling, Roles, Modulation Mechanisms, and Targeted Therapies

    Yu Sun, Wei Wang, Chenghai Zhao

    Oncology Research, Vol.28, No.6, pp. 661-674, 2020, DOI:10.3727/096504020X16014648664459

    Abstract Wnt molecules play crucial roles in development and adult homeostasis through their receptors Frizzled proteins (Fzds). Fzds mediate canonical b-catenin pathway and various noncanonical b-catenin-independent pathways. Aberrant Fzd signaling is involved in many diseases including cancer. Wnt/b-catenin is a well-established oncogenic pathway involved in almost every aspect of tumor development. However, Fzd-mediated noncanonical Wnt pathways function as both tumor promoters and tumor suppressors depending on cellular context. Fzd-targeted therapies have proven to be effective on cultured tumor cells, tumor cell xenografts, mouse tumor models, and patient-derived xenografts (PDX). Moreover, Fzd-targeted therapies synergize with chemotherapy in More >

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