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The polycistronic miR‐17‐92 cluster is instrumental in physiological processes commonly dysregulated in cancer, such as proliferation, the cell cycle, apoptosis, and differentiation. MicroRNA‐18a (miR‐18a) is one of the most conserved and multifunctional miRNAs in the cluster and is frequently overexpressed in malignant tumors. Altered miR‐18a expression has been found in various physiological and pathological processes, including cell proliferation, apoptosis, epithelial–mesenchymal transition (EMT), tumorigenesis, cancer invasion and metastasis. In this review, we summarized the molecular basis and regulatory targets of miR‐18a in cancer development. Interestingly, miR‐18a has a dual functional role in either promoting or inhibiting oncogenesis in different human cancers. The differential miRNA expression in cancers of the same organ at different stages or of various subtypes suggests that this dual function of miR‐18a is independent of cancer type and may be attributed to the fundamental differences in tumorigenic mechanisms. Finally, we summarized the current clinical use of miR‐18a and discussed its potential uses in cancer therapy.

The differential diagnosis of primary central nervous system lymphoma from glioblastoma multiforme (GBM) is essential due to the difference in treatment strategies. This study retrospectively reviewed 77 patients (24 with lymphoma and 53 with GBM) to identify the stable and distinguishable characteristics of lymphoma and GBM in 18 F-fluorodeocxyglucose (FDG) positron emission tomography (PET) images using a radiomics approach. Three groups of maps, namely, a standardized uptake value (SUV) map, an SUV map calibrated with the normal contralateral cortex (ncc) activity (SUV/ncc map), and an SUV map calibrated with the normal brain mean (nbm) activity (SUV/nbm map), were generated, and a total of 107 radiomics features were extracted from each SUV map. The margins of the ROI were adjusted to assess the stability of the features, and the area under the curve (AUC) of the receiver operating characteristic curve of each feature was compared with the SUVmax to evaluate the distinguishability of the features. Nighty-five radiomics features from the SUV map were significantly different between lymphoma and GBM, 46 features were numeric stable after marginal adjustment, and 31 features displayed better performance than SUVmax. Features extracted from the SUV map demonstrated higher AUCs than features from the further calibrated maps. Tumors with solid metabolic patterns were also separately evaluated and revealed similar results. Thirteen radiomics features that were stable and distinguishable than SUVmax in every circumstance were selected to distinguish lymphoma from glioblastoma, and they suggested that lymphoma has a higher SUV in most interval segments and is more mathematically heterogeneous than GBM. This study suggested that 18 F-FDG-PET-based radiomics is a reliable noninvasive method to distinguish lymphoma and GBM.

Antiangiogenic therapy is a universal approach to the treatment of malignant gliomas but fails to prolong the overall survival of newly diagnosed or recurrent glioblastoma patients. Imaging biomarkers are quantitative imaging parameters capable of objectively describing biological processes, pathological changes and treatment responses in some situations and have been utilized for outcome predictions of malignant gliomas in anti-angiogenic therapy. Advanced magnetic resonance imaging techniques (including perfusion-weighted imaging and diffusion-weighted imaging), positron emission computed tomography and magnetic resonance spectroscopy are imaging techniques that can be used to acquire imaging biomarkers, including the relative cerebral blood volume (rCBV), Ktrans, and the apparent diffusion coefficient (ADC). Imaging indicators for a better prognosis when treating malignant gliomas with antiangiogenic therapy include the following: a lower pre- or post-treatment rCBV, less change in rCBV during treatment, a lower pre-treatment Ktrans, a higher vascular normalization index during treatment, less change in arterio-venous overlap during treatment, lower pre-treatment ADC values for the lower peak, smaller ADC volume changes during treatment, and metabolic changes in glucose and phenylalanine. The investigation and utilization of these imaging markers may confront challenges, but may also promote further development of anti-angiogenic therapy. Despite considerable evidence, future prospective studies are critically needed to consolidate the current data and identify novel biomarkers.

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Serum and glucocorticoid-inducible kinase 1 (SGK1) is an AGC kinase that has been reported to be involved in a variety of physiological and pathological processes. Recent evidence has accumulated that SGK1 acts as an essential Akt-independent mediator of phosphatidylinositol 3-kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling pathway in cancer. SGK1 is overexpressed in several tumors, including prostate cancer, colorectal carcinoma, glioblastoma, breast cancer, and endometrial cancer. The functions of SGK1 include regulating tumor growth, survival, metastasis, autophagy, immunoregulation, calcium (Ca2+) signaling, cancer stem cells, cell cycle, and therapeutic resistance. In this review, we introduce the pleiotropic role of SGK1 in the development and progression of tumors, summarize its downstream targets, and integrate the knowledge provided by preclinical studies that the prospect of SGK1 inhibition as a potential therapeutic approach.

Background and Objective Parathyroid carcinoma (PC) is a rare malignant neoplasm with a relatively poor prognosis. The loss of parafibromin expression or the presence of CDC73 mutation has been found to be remarkably associated with malignancy in parathyroid tumours. However, the prognostic role of them in PC has not yet been shown due to sampling limitations. We conducted a systematic review and meta‐analysis based on individual patient data to clarify the performance of parafibromin immunohistochemical staining and CDC73 gene sequencing in predicting outcomes for patients PC. Methods Published studies from PubMed/MEDLINE, EMBASE, Cochrane and Scopus Databases were searched using the terms ‘parafibromin’, ‘CDC73’, ‘HRPT2’ and ‘parathyroid’ to identify eligible studies. From the included studies, the survival data of patients with PC were extracted, and a Cox proportional hazards model was used to assess hazard ratio (HR) for disease‐free survival (DFS) and overall survival (OS). Results A total of 193 patients from 9 studies were included in this survival analysis. Negative immunohistochemical staining of parafibromin was shown to be a risk factor for recurrence/metastasis (HR 2.73, P = .002) and death (HR 2.54, P = .004). Patient age ≥ 50 years was significantly related to lower OS (HR 2.37, P = .004) but not to DFS. CDC73 mutation was not statistically related to DFS or OS. Conclusions Negative parafibromin staining indicated a higher risk of recurrence/metastasis and mortality. The immunohistochemical staining of parafibromin seems to be more promising in predicting outcomes for patients with PC than the sequencing of CDC73.

Background MicroRNAs have been reported to participate in tumorigenesis, treatment resistance, and tumor metastasis. Novel microRNAs need to be identified and investigated to guide the clinical prognosis or therapy for breast cancer. Method The copy number variations (CNVs) of MIR3613 from Cancer Genome Atlas (TCGA) or Cancer Cell Line Encyclopedia (CCLE) were analyzed, and its correlation with breast cancer subtypes or prognosis was investigated. The expression level of miR-3613-3p in tumor tissues or serum of breast cancer patients was detected using in situ hybridization and qPCR. Gain-of-function studies were performed to determine the regulatory role of miR-3613-3p on proliferation, apoptosis, and tumor sphere formation of human breast cancer cells MDA-MB-231 or MCF-7. The effects of miR-3613-3p on tumor growth or metastasis in an immunocompromised mouse model of MDA-MB-231-luciferase were explored by intratumor injection of miR-3613-3p analogue. The target genes, interactive lncRNAs, and related signaling pathways of miR-3613-3p were identified by bioinformatic prediction and 3′-UTR assays. Results We found that MIR3613 was frequently deleted in breast cancer genome and its deletion was correlated with the molecular typing, and an unfavorable prognosis in estrogen receptor-positive patients. MiR-3613-3p level was also dramatically lower in tumor tissues or serum of breast cancer patients. Gain-of-function studies revealed that miR-3613-3p could suppress proliferation and sphere formation and promote apoptosis in vitro and impeded tumor growth and metastasis in vivo. Additionally, miR-3613-3p might regulate cell cycle by targeting SMS, PAFAH1B2, or PDK3 to restrain tumor progression. Conclusion Our findings indicate a suppressive role of miR-3613-3p in breast cancer progression, which may provide an innovative marker or treatment for breast cancer patients.