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Elsevier
Cancer letters

Elsevier

0304-3835

Cancer letters/Journal Cancer lettersSCIISTP
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    A nomogram based on clinical information, conventional ultrasound and radiomics improves prediction of malignant parotid gland lesions

    Li Q.Jiang T.Zhang C.Zhang Y....
    8页
    查看更多>>摘要：? 2021 Elsevier B.V.Although conventional ultrasound (CUS) allows for clear detection of parotid gland lesions (PGLs), it fails to accurately provide benign-malignant differentiation due to overlapping morphological features. Radiomics is capable of processing large-quantity volume of data hidden in CUS image undiscovered by naked eyes. The aim was to explore the potential of CUS-based radiomics score (Rad-score) in distinguishing benign (BPGLs) and malignant PGLs (MPGLs). A consecutive of 281 PGLs (197 in training set and 84 in test set) with definite pathological confirmation was retrospectively enrolled. 1465 radiomics features were extracted from CUS images and Rad-score was constructed by using Least Absolute Shrinkage and Selection Operator (LASSO) algorithm. Different nomogram models, including clinic-radiomics (Clin + Rad-score), CUS-clinic (CUS + Clin) and combined CUS-clinic-radiomics (CUS + Clin + Rad-score), were built using logistic regression. The diagnostic performance of different models were calculated and compared by area under receiver operating curve (AUC) and corresponding sensitivity and specificity. Finally, 26 radiomics features were independent signatures for predicting MPGLs, with MPGLs having higher Rad-scores in both cohorts (both P < 0.05). In the test population, CUS + Clin + Rad-score obtained an excellent diagnostic result, with significantly higher AUC value (AUC = 0.91) when compared to that of CUS + Clin (AUC = 0.84) and Clin + Rad-score (AUC = 0.74), respectively (both P < 0.05). In addition, the sensitivity of this combined model was higher than that of single Rad-score model (100.00% vs. 71.43%, P = 0.031) without compromising the specificity value (82.86% vs. 88.57%, P = 0.334). The calibration curve and decision curve analysis also indicated the clinical effectiveness of the proposed combined nomogram. The combined CUS-clinic-radiomics model may help improve the discrimination of BPGLs from MPGLs.
      原文链接:
    • NSTL
    • Elsevier

    Innate tumor killers in colorectal cancer

    Zhong F.Lin Y.Jing X.Ye Y....
    12页
    查看更多>>摘要：? 2021 Elsevier B.V.Standard treatment of colorectal cancer (CRC) improves the prognosis of CRC patients, but it is still intractable to control the progression of metastatic CRC. Immune microenvironment and immunotherapies of CRC have received extensive attention in recent years, but present immunotherapies of CRC have mainly focused on T cells and therapeutic response is only observed in a small proportion of patients. Innate immune cells are the first-line of defense in the development of malignancies. Natural killer (NK) cells, NKT cells and γδT cells are three types of innate cells of lymphoid origin and show cytotoxicity against various tumor cells including CRC. Besides, in the development of CRC, they can also be inhibited or express regulatory type, promoting tumor progression. Researches about anti-tumorigenic and pro-tumorigenic mechanisms of these cells are ongoing and regulation of these cells is also being unearthed. Meanwhile, immunotherapies using these cells more or less have shown efficacy in animal models and some of them are under exploration in clinical trials. This review provides an overview of intrinsic properties of NK cell, NKT cell and γδT cell, and summarizes current related promising treatment strategies.
      原文链接:
    • NSTL
    • Elsevier

    Nuclear PD-L1 promotes cell cycle progression of BRAF-mutated colorectal cancer by inhibiting THRAP3

    Ma R.Liu Y.Che X.Li C....
    13页
    查看更多>>摘要：? 2021 Elsevier B.V.Colorectal cancers (CRCs) with the BRAF V600E mutation exhibit upregulation of programmed death ligand 1 (PD-L1) but fail to respond to immunotherapy targeting programmed cell death protein 1 (PD-1)/PD-L1. Recent studies have explored the intracellular functions of PD-L1. Here, we demonstrate that PD-L1 was highly expressed in both the cytoplasm and nucleus of BRAF-mutated CRC tumor cells and tissues. Nuclear PD-L1 (nPD-L1) promoted the growth of tumor cells both in vitro and in vivo. Mechanistic investigations revealed that PD-L1 translocation into the nucleus was facilitated by the binding of p-ERK. Further, nPD-L1 upregulated the expression of cell cycle regulator BUB1 via interactions with thyroid hormone receptor-associated protein 3 (THRAP3), thereby accelerating cell cycle progression and promoting cell proliferation. Moreover, BRAF V600E-mutated CRC cells exhibited upregulation of PD-L1 expression via the transcription factor LEF-1. These findings reveal a novel role of nPD-L1, which promotes cell cycle progression in an immune-independent manner in BRAF V600E-mutated CRC. Our study provides novel insight into the mechanisms underlying BRAF V600E-mutated CRC progression.
      原文链接:
    • NSTL
    • Elsevier

    Drug repositioning: Using psychotropic drugs for the treatment of glioma

    Zhang T.Yu R.Gao S.You F....
    10页
    查看更多>>摘要：? 2021 The AuthorsPsychotropic drugs can penetrate the blood–brain barrier and regulate the levels of neurotransmitters and neuromodulators such as γ-aminobutyric acid, glutamate, serotonin, dopamine, and norepinephrine in the brain, and thus influence neuronal activity. Neuronal activity in the tumor microenvironment can promote the growth and expansion of glioma. There is increasing evidence that in addition to their use in the treatment of mental disorders, antipsychotic, antidepressant, and mood-stabilizing drugs have clinical potential for cancer therapy. These drugs have been shown to inhibit the malignant progression of glioma by targeting signaling pathways related to cell proliferation, apoptosis, or invasion/migration or by increasing the sensitivity of glioma cells to conventional chemotherapy or radiotherapy. In this review, we summarize findings from preclinical and clinical studies investigating the use of antipsychotics, antidepressants, and mood stabilizers in the treatment of various types of cancer, with a focus on glioma; and discuss their presumed antitumor mechanisms. The existing evidence indicates that psychotropic drugs with established pharmacologic and safety profiles can be repurposed as anticancer agents, thus providing new options for the treatment of glioma.
      原文链接:
    • NSTL
    • Elsevier

    SETD8 stabilized by USP17 epigenetically activates SREBP1 pathway to drive lipogenesis and oncogenesis of ccRCC

    Li X.Liu Z.Xia C.Yan K....
    14页
    查看更多>>摘要：? 2021Recently, epigenetic modifications, including DNA methylation, histone modification and noncoding RNA (ncRNA)-associated gene silencing, have received increasing attention from the scientific community. Many studies have demonstrated that epigenetic regulation can render dynamic alterations in the transcriptional potential of a cell, which then affects the cell's biological function. The initiation and development of clear cell renal cell carcinoma (ccRCC), the most common subtype of renal cell cancer (RCC), is also closely related to genomic alterations by epigenetic modification. For ccRCC, lipid accumulation is one of the most typical characteristics. In other words, dysregulation of lipid uptake and synthesis occurs in ccRCC, which inversely promotes cancer proliferation and progression. However, the link among epigenetic alterations, lipid biosynthesis and renal cancer progression remains unclear. SETD8 is a histone methyltransferase and plays pivotal roles in cell cycle regulation and oncogenesis of various cancers, but its role in RCC is not well understood. In this study, we discovered that SETD8 was significantly overexpressed in RCC tumors, which was positively related to lipid storage and correlated with advanced tumor grade and stage and poor patient prognosis. Depletion of SETD8 by siRNAs or inhibitor UNC0379 diminished fatty acid (FA) de novo synthesis, cell proliferation and metastasis in ccRCC cells. Mechanistically, SETD8, which was posttranslationally stabilized by USP17, could transcriptionally modulate sterol regulatory element-binding protein 1 (SREBP1), a key transcription factor in fatty acid biosynthesis and lipogenesis, by monomethylating the 20th lysine of the H4 histone, elevating lipid biosynthesis and accumulation in RCC and further promoting cancer progression and metastasis. Taken together, the USP17/SETD8/SREBP1 signaling pathway plays a pivotal role in promoting RCC progression. SETD8 might be a novel biomarker and potential therapeutic target for treating RCC.
      原文链接:
    • NSTL
    • Elsevier

    Context-dependent transcriptional regulations of YAP/TAZ in cancer

    Guo Y.Luo J.Zou H.Liu C....
    10页
    查看更多>>摘要：? 2021 The AuthorsAs the downstream effectors of Hippo pathway, YAP/TAZ are identified to participate in organ growth, regeneration and tumorigenesis. However, owing to lack of a DNA-binding domain, YAP/TAZ usually act as coactivators and cooperate with other transcription factors or partners to mediate their transcriptional outputs. In this article, we first present an overview of the core components and the upstream regulators of Hippo-YAP/TAZ signaling in mammals, and then systematically summarize the identified transcription factors or partners that are responsible for the downstream transcriptional output of YAP/TAZ in various cancers.
      原文链接:
    • NSTL
    • Elsevier

    Hippo/YAP signaling choreographs the tumor immune microenvironment to promote triple negative breast cancer progression via TAZ/IL-34 axis

    Wang Z.Wang F.Ding X.-Y.Li T.-E....
    17页
    查看更多>>摘要：? 2021 Elsevier B.V.Growing evidence suggests that the bidirectional interactions between cancer cells and their surrounding environment, namely the tumor microenvironment (TME), contribute to cancer progression, metastasis, and resistance to treatment. Intense investigation of the Hippo pathway, which controls multiple central cellular functions in tumorigenesis, was focused on cancer cells. However, the role of the Hippo pathway in modulating tumor–stromal interactions in triple-negative breast cancer remains largely unknown. Therefore, this study focused on revealing the effects of Hippo-YAP/TAZ signaling on the immune microenvironment. Our findings reveal that the activity of the Hippo pathway is associated with worse disease outcomes in TNBC and could increase TAM infiltration through the TAZ/IL-34 axis, leading to an immunosuppressive microenvironment and impairing the treatment efficacy of anti-PD-L1. Thus, the TAZ/IL-34 axis may serve as a novel target for TNBC patients.
      原文链接:
    • NSTL
    • Elsevier

    Letter to the editor regarding “Dual blockade of EGFR and CDK4/6 delays head and neck squamous cell carcinoma progression by inducing metabolic rewiring."

    Liang R.
    2页
      原文链接:
    • NSTL
    • Elsevier

    Reply

    Chaudhary S.Lakshmanan I.Ganti A.K.Macha M.A....
    2页
      原文链接:
    • NSTL
    • Elsevier