Home / Journals / OR / Vol.29, No.4, 2021
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  • Open AccessOpen Access

    VIEWPOINT

    Biobanking in the digital pathology era

    GIUSEPPINA BONIZZI, LORENZO ZATTONI, NICOLA FUSCO*
    Oncology Research, Vol.29, No.4, pp. 229-233, 2021, DOI:10.32604/or.2022.024892
    Abstract Digital Pathology is becoming more and more important to achieve the goal of precision medicine. Advances in whole-slide imaging, software integration, and the accessibility of storage solutions have changed the pathologists’ clinical practice, not only in terms of laboratory workflow but also for diagnosis and biomarkers analysis. In parallel with the pathology setting advancement, translational medicine is approaching the unprecedented opportunities unrevealed by artificial intelligence (AI). Indeed, the increased usage of biobanks’ datasets in research provided new challenges for AI applications, such as advanced algorithms, and computer-aided techniques. In this scenario, machine learning-based approaches are being propose in order to… More >

  • Open AccessOpen Access

    REVIEW

    PI3K/AKT signaling pathway as a critical regulator of Cisplatin response in tumor cells

    ZAHRA NASRPOUR NAVAEI1, GHAZALEH KHALILI-TANHA1, AMIR SADRA ZANGOUEI2, MOHAMMAD REZA ABBASZADEGAN3, MEYSAM MOGHBELI1,3,*
    Oncology Research, Vol.29, No.4, pp. 235-250, 2021, DOI:10.32604/or.2022.025323
    Abstract Chemotherapy is one of the main therapeutic modalities for cancer patients. Cisplatin (CDDP), as one of the first-line drugs, is of great importance in the chemotherapy of various tumors. However, a significant percentage of cancer patients are resistant to CDDP treatment. Due to the CDDP side effects on normal tissues, the diagnosis of CDDP resistance is required to suggest the most efficient therapeutic strategies for cancer patients. Several molecular mechanisms and signaling pathways are associated with CDDP response. The PI3K/AKT signaling pathway has a pivotal role in the transmission of extracellular signals into the cells to regulate various pathophysiological processes… More >

  • Open AccessOpen Access

    ARTICLE

    Long noncoding RNA PPP1R14B-AS1 imitates microRNA-134-3p to facilitate breast cancer progression by upregulating LIM and SH3 protein 1

    LIMIN ZHOU1, LIANBO ZHANG2, XIN GUAN3, YI DONG1, TAO LIU1,*
    Oncology Research, Vol.29, No.4, pp. 251-262, 2021, DOI:10.32604/or.2022.03582
    Abstract Long noncoding RNA PPP1R14B antisense RNA 1 (PPP1R14B-AS1) has emerged as a critical modulator of liver cancer and lung adenocarcinoma progression. However, the functional importance and biological relevance of PPP1R14B-AS1 in breast cancer remain unclear. Therefore, this study was designed to detect PPP1R14B-AS1 levels in breast cancer cells using qRT–PCR and elucidate the influence of PPP1R14B-AS1 on aggressive phenotypes. Furthermore, molecular events mediating the action of PPP1R14B-AS1 were characterized in detail. Functional experiments addressed the impacts of PPP1R14B-AS1 knockdown on breast cancer cells. In this study, PPP1R14B-AS1 was found to be overexpressed in breast cancer, exhibiting a close correlation with… More >

  • Open AccessOpen Access

    ARTICLE

    Long noncoding RNA TMEM147-AS1 serves as a microRNA-326 sponge to aggravate the malignancy of gastric cancer by upregulating SMAD5

    XUFU QIN1,#, ZIYE JIANG1,#, YONGCUI ZHU1,*, HONGPENG XUE1, CHENGQUN WEI2
    Oncology Research, Vol.29, No.4, pp. 263-273, 2021, DOI:10.32604/or.2022.03568
    Abstract The abnormal expression of long noncoding RNAs (lncRNAs) is frequently observed in gastric cancer (GC) and considered an important driving force in GC progression. However, little is known regarding the involvement of TMEM147-AS1 in GC. Therefore, we examined TMEM147-AS1 expression in GC and determined its prognostic value. In addition, TMEM147-AS1 expression was depleted to identify the functional changes in response to TMEM147-AS1 deficiency. Using the cancer genome atlas dataset and our own cohort, we identified a strong expression of TMEM147-AS1 in GC. Increased TMEM147-AS1 levels in GC showed a significant association with poor prognosis. TMEM147-AS1 interference resulted in the inhibition… More >

  • Open AccessOpen Access

    ARTICLE

    PRPF6 promotes metastasis and paclitaxel resistance of ovarian cancer via SNHG16/CEBPB/GATA3 axis

    HAN WANG, YINGYING ZHOU, SIYANG ZHANG, YA QI, MIN WANG*
    Oncology Research, Vol.29, No.4, pp. 275-289, 2021, DOI:10.32604/or.2022.03561
    Abstract Metastasis and paclitaxel (PTX) resistance are the main reason for the poor prognosis of ovarian cancer (OC). Evidence showed that RNA-binding proteins (RBPs) and long noncoding RNAs (lncRNAs) can modulate post-transcriptional regulation. The aim of this study was to determine the relationship among RBP, lncRNA and OC and to further guide clinical therapy. Immunohistochemistry revealed that pre-mRNA processing factor 6 (PRPF6) was upregulated in OC chemoresistant tissues and was closely related to advanced (Federation of International of Gynecologists and Obstetricians) FIGO stages and chemo-resistance. PRPF6 promoted progression, and PTX resistance in vitro and in vivo. And the transcripts of small… More >

  • Open AccessOpen Access

    ARTICLE

    Long noncoding RNA LINC02568 sequesters microRNA-874-3p to facilitate malignancy in breast cancer cells via cyclin E1 overexpression

    YI DONG1, LIANBO ZHANG2, XIN GUAN3, TAO LIU1, LIMIN ZHOU1,*
    Oncology Research, Vol.29, No.4, pp. 291-303, 2021, DOI:10.32604/or.2022.025172
    Abstract Increasing numbers of long noncoding RNAs (lncRNAs) are implicated in breast cancer oncogenicity. However, the contribution of LINC02568 toward breast cancer progression remains unclear and requires further investigation. Herein, we evaluated LINC02568 expression in breast cancer and clarified its effect on disease malignancy. We also investigated the mechanisms underlying the pro-oncogenic role of LINC02568. Consequently, LINC02568 was upregulated in breast cancer samples, with a notable association with worse overall survival. Functionally, depleted LINC02568 suppressed cell proliferation, colony formation, and metastasis, whereas LINC02568 overexpression exerted the opposite effects. Our mechanistic investigations suggested that LINC02568 was physically bound to and sequestered microRNA-874-3p… More >

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