The fusion product of FIP1-like-1 (FIP1L1) and platelet-derived growth factor receptor α (PDGFRA) gene rearrangement is a tyrosine kinase oncoprotein sensitive to imatinib. This gene rearrangement characterizes a novel clinico-biological class of myeloid and lymphoid neoplasms with eosinophilia and PDGFRA abnormalities. The DEK proto-oncogene (DEK) and nucleoporin 214 (NUP214) rearrangement is rare in patients with acute myeloid leukemia (AML); therefore, the coexistence of DEK-NUP214 and FIP1L1-PDGFRA rearrangements in patients with AML is extremely rare. The present study presents a rare relapse case of a patient with AML with DEK-NUP214 and FIP1L1-PDGFRA rearrangements, without marked eosinophilia in the peripheral blood or bone marrow. Low-dose imatinib monotherapy without intensive chemotherapy was used to achieve complete hematological remission. Copyright © 2020, Spandidos Publications.Non-small cell lung cancer (NSCLC) is one of the leading causes of global cancer-associated mortality. Aberrant microRNAs (miRs) have been reported to be involved in the pathogenesis of various cancer types. The present study aimed to investigate the expression profile and prognostic value of miR-665 in patients with NSCLC, and to analyze its functional role in tumor progression using NSCLC cells. Reverse transcription-quantitative PCR was used to estimate the expression levels of miR-665. Kaplan-Meier survival curves and Cox regression analysis were performed to evaluate the prognostic value of miR-665. The effects of miR-665 on NSCLC cell proliferation, migration and invasion were examined by cell transfection, and the target gene of miR-665 was explored. CBR-470-1 Nrf2 activator miR-665 expression was elevated in the tissue and cell samples of NSCLC. This increased miR-665 expression was associated with lymph node metastasis and TNM stage. An independent association between miR-665 and overall survival was identified in patients with NSCLC. When regulating the expression levels of miR-665 in vitro, NSCLC cell proliferation, migration and invasion were enhanced by overexpression of miR-665, but were inhibited by knockdown of miR-665. The luciferase activity results indicated that the protein tyrosine phosphatase receptor type B (PTPRB) was a direct target of miR-665 in NSCLC cells. The present study provided evidence for the clinical significance of a decreased expression of miR-665 in the prognosis of NSCLC. Upregulation of miR-665 contributed to tumor cell proliferation, migration and invasion by targeting PTPRB, suggesting the potential of miR-665 as a candidate therapeutic target for NSCLC treatment. Copyright © Xia et al.ATP binding cassette subfamily D member 3 (ABCD3) is a member of the superfamily of ATP-binding cassette (ABC) transporters, which serve crucial roles in the process of tumor cell resistance to chemotherapy. The present study investigated the diagnostic and prognostic capabilities of ABCD3 in colorectal cancer (CRC) by bioinformatics analysis. Gene expression data and corresponding clinical information of patients with CRC were collected from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. The results demonstrated that ABCD3 mRNA level was decreased in CRC tissues compared with normal tissues following Wilcoxon test analysis. Furthermore, ABCD3 protein expression was significantly higher in normal colon tissues compared with colon adenocarcinoma tissues according to the Human Protein Atlas. In addition, the area under the Receiver Operating Characteristic curve based on comparison between the tumor and normal groups derived from TCGA and GEO databases demonstrated that the use of Afindings from this study demonstrated that ABCD3 mRNA expression may be considered as a potential diagnostic and prognostic biomarker in patients with CRC. ABCD3 expression levels may participate in the regulation of cell apoptosis and cell cycle. In addition, GSEA analysis identified Kyoto Encyclopaedia of Genes and Genomes pathways for renal cell carcinoma, thyroid cancer and CRC involving ABCD3. Copyright © Zhang et al.Metastasis remains a notable issue in patients with newly diagnosed colorectal carcinomas (CRC). Although anti-angiogenic therapies target metastatic diseases, hypoxia-inducible factor-1 α (HIF-1α) and vascular endothelial growth factor (VEGF) status are routinely evaluated in primary tumors as metastatic sites are infrequently biopsied. The present study aimed to investigate the expression and significance of HIF-1α, VEGF and microvascular density (MVD) in primary tumors and corresponding metastatic CRC tissues. HIF-1α, VEGF and CD34 status were analyzed via immunohistochemistry analysis in 46 patients who underwent surgical resection of primary CRC (35 colon and 11 rectum) and matched metastases (lymph node and liver metastases) in Shandong Cancer Hospital. The association between selected biomarker status and clinicopathological characteristics was analyzed, and expression levels in primary tumors and corresponding metastases were compared. A total of 46 paired colorectal primary tumor and synchronous metat varied from that exhibited in MVD. The current analysis will improve the current understanding of the metastasis models and provide further evidence for evaluating the response to HIF-1α and VEGF inhibitors. Copyright © Yin et al.In a previous study, 2′,4′-dihydroxy-6′-methoxy-3′,5′-dimethylchalcone (ChalcEA) isolated from the leaves of Eugenia aquea was reported to inhibit proliferation of the breast adenocarcinoma MCF7 cell line and to promote apoptosis via activation of poly(adenosine diphosphate-ribose) polymerase protein. The present study aimed to evaluate the inhibitory effect of ChalcEA on the proliferation of A549 lung cancer cells using a 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxylmethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay, and to examine the ability of ChalcEA to induce apoptosis through activation of the caspase cascade signaling pathway in a western blotting assay. The results revealed that ChalcEA inhibited proliferation of the A549 lung cancer cell lines in a time- and dose-dependent manner with IC50 values of 25.36 and 19.60 µM for 24 and 48 h treatments, respectively. Western blot analysis indicated that ChalcEA exerted its anti-proliferative effects by promoting apoptosis via the activation of caspase-9 and caspase-3.