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Comparing with DL scheme and radiomics scheme (the area under a receiver operating characteristic curve (AUC) 0.83 ± 0.05, 0.87 ± 0.04), our new fusion scheme (AUC 0.90 ± 0.03) significant improves the risk classification performance (p less then 0.05). In a comparison with two radiologists, our new model yields higher accuracy of 80.3%. The kappa value for inter-radiologist agreement is 0.6. It demonstrates that applying AI method is an effective way to improve the invasiveness risk prediction performance of GGNs. In future, fusion of DL and radiomics features may have a potential to handle the classification task with limited dataset in medical imaging. Copyright © 2020 Xia, Gong, Hao, Yang, Lin, Wang and Peng.As a chemotherapeutic agent, bortezomib (BTZ) is used for the treatment of multiple myeloma with adverse effect of painful peripheral neuropathy. Our current study was to determine the inhibitory effects of blocking microRNA-155 (miR-155) signal on BTZ-induced neuropathic pain and the underlying mechanisms. We employed real time RT-PCR and western blot analysis to examine the miR-155 and expression of pro-inflammatory tumor necrosis factor-α receptor (TNFR1) in the dorsal horn of the spinal cord. Its downstream signals p38-MAPK and JNK and transient receptor potential ankyrin 1 (TRPA1) were also determined. Mechanical pain and cold sensitivity were assessed by behavioral test. In result, inhibition of miR-155 significantly attenuated mechanical allodynia and thermal hyperalgesia in BTZ rats, which was accompanied with decreasing expression of TNFR1, p38-MAPK, JNK, and TRPA1. In contrast, miRNA-155 mimics amplified TNFR1-TRPA1 pathway and augmented mechanical pain and cold sensitivity. In addition, mechanical and thermal hypersensitivity induced by miRNA-155 mimics were attenuated after blocking TNFR1, p38-MAPK, JNK, and TRPA1. Overall, we show the key role of miR-155 in modifying BTZ-induced neuropathic pain through TNFR1-TRPA1 pathway, suggesting that miR-155 is a potential target in preventing neuropathic pain development during intervention of BTZ. Copyright © 2020 Duan, Zhang, Li, Pang and Wang.Cancer stem cells (CSCs) are able to promote initiation, survival and maintenance of tumor growth and have been involved in gastrointestinal cancers (GICs) such as esophageal, gastric and colorectal. It is well known that blood supply facilitates cancer progression, recurrence, and metastasis. In this regard, tumor-induced angiogenesis begins with expression of pro-angiogenic molecules such as vascular endothelial growth factor (VEGF), which in turn lead to neovascularization and thus to tumor growth. Another pattern of blood supply is called vasculogenic mimicry (VM). It is a reminiscent of the embryonic vascular network and is carried out by CSCs that have the capability of transdifferentiate and form vascular-tube structures in absence of endothelial cells. In this review, we discuss the role of CSCs in angiogenesis and VM, since these mechanisms represent a source of tumor nutrition, oxygenation, metabolic interchange and facilitate metastasis. Identification of CSCs mechanisms involved in angiogenesis and VM could help to address therapeutics for GICs. Copyright © 2020 Lizárraga-Verdugo, Avendaño-Félix, Bermúdez, Ramos-Payán, Pérez-Plasencia and Aguilar-Medina.[This corrects the article DOI 10.3389/fonc.2020.00176.]. Copyright © 2020 Li, Huang, Hsieh, Chen, Cheng, Chen, Liu, Chen, Huang, Lo and Chang.Oropharyngeal cancer (OPC) caused by human papillomavirus (HPV) is a rising global concern. Early lesions are small and are often located in difficult to access areas (such as the crypts of the tonsils or base of tongue). Unlike cervical cancer, there is no standard or routine screening program for HPV-driven OPC. HPV DNA from OPC tumors may shed directly into saliva, and this can be used as a biomarker for early diagnosis. In this study, we report the first-ever clinically occult OPC in an asymptomatic patient discovered through a saliva test. This case relied upon serial measurements of HPV-16 DNA in saliva, which fell to undetectable levels following low morbidity, curative treatment. Copyright © 2020 Tang, Vasani, Taheri, Walsh, Hughes, Kenny and Punyadeera.Background Dipeptidyl peptidase-4 (DPP4), a cell surface protein, exhibits a crucial role in tumor biology and regulation of the immune system. We aim to study the impact of DPP4 inhibitors (DPP4i) in patients with prostate cancer (PRC), pancreatic cancer (PC) and breast cancer (BC). Methods Using the SEER and Medicare linked database, we identified patients with PRC or PC or BC with coexisting type II diabetes mellitus between 2007 and 2015. Patients were classified into four groups (1) not on either DPP4i or metformin (reference group), this group included patient that were on anti-diabetic agents other than metformin or DPP4i (2) metformin only, (3) DPP4i only, and (4) DPP4i along with metformin (combination group). Selleck RU58841 Overall survival (OS) analyses were performed using SAS®, version 9.4. Results We identified 15,330 patients with PRC, 5,359 patients with PC and 16,085 patients with BC. In PRC cohort, patients on DPP4i had significant survival advantage with HR 0.77 (95% CI 0.64-0.93), P = 0.005 when compared to the reference group. Patients taking metformin also had significant OS benefit with HR 0.87 (95% CI 0.81-0.93), P less then 0.0001 when compared to the reference group. However, in BC cohort, OS did not favor the patients taking DPP4i with HR 1.07 (95% CI 0.93-1.25, P = 0.33). Similarly, in PC cohort, OS was indifferent for the patients on DPP4i with HR 1.07 (95% CI 0.93-1.24, P = 0.68). Upon subgroup analyses of PRC patients, the survival favored the group taking DPP4i, irrespective of stage, use of chemotherapy, androgen-deprivation therapy, and prostatectomy or radiation therapy. Conclusions DPP4i seems to improve survival in PRC patients; however, not in PC or BC patients. While the exact mechanism involved remains to be elucidated, a prospective clinical trial would help to confirm these findings. Copyright © 2020 Shah, Hong, Bishnoi, Ali, Skelton, Dang, Huo and Dang.Sialic acids (SA), negatively charged nine-carbon sugars, have long been implicated in cancer metastasis since 1960's but its detailed functional roles remain elusive. We present a computational analysis of transcriptomic data of cancer vs. control tissues of eight types in TCGA, aiming to elucidate the possible reason for the increased production and utilization of SAs in cancer and their possible driving roles in cancer migration. Our analyses have revealed for all cancer types (1) the synthesis and deployment enzymes of SAs are persistently up-regulated throughout the progression for all but one cancer type; and (2) gangliosides, of which SAs are part, tend to converge to specific types that allow SAs to pack at high densities on cancer cell surface as a cancer advances. Statistical and modeling analyses suggest that (i) a highly plausible reason for the increased syntheses of SAs is to produce net protons, used for neutralizing the OH- persistently generated by elevated intracellular iron metabolism coupled with chronic inflammation in cancer tissues; (ii) the level of SA accumulation on cancer cell surface strongly correlates with the stage of cancer migration, as well as multiple migration-related characteristics such as altered cell-cell adhesion, mechanical stress, cell protrusion, and contraction; and (iii) the pattern of SA deployment correlates with the 5-year survival rate of a cancer type. Overall, our study provides strong evidence for that the continuous accumulation of SAs on cancer cell surface gives rise to increasingly stronger cell-cell repulsion due to their negative charges, leading to cell deformation by electrostatic force-induced mechanical compression, which is known to be able to drive cancer cell migration established by recent studies. Copyright © 2020 Sun, Zhou, Jiang and Xu.Background This study aims to compare survival outcome after receiving radiofrequency ablation (RFA) and surgical resection (SR) for solitary hepatocellular carcinoma (HCC) with size large as 5 cm. Methods The SEER database was queried for patients with HCC tumors who were treated with RFA or SR between 2004 and 2015. Univariate and multivariate Cox analysis was used to assess the influence of potential variables on the patients' outcome. Additionally, propensity score matching (PSM) and multiple imputations (MI) were used as sensitivity analyses. Results Of 1,985 cases, 934 patients received RFA treatment, while the rest underwent surgical resection. The patients in the RFA group had poorer overall survival (OS) and cancer-specific survival (CSS) than those in the SR group regardless of the tumor size before matching and MI. By using PSM analysis at a 11 ratio, 1,302 cases were paired and we have found that SR had a positive impact on OS and CSS of patients with tumors measuring from 3.1 to 5 cm. However, when the tumor size was less then 3 cm, patients undergoing SR had similar survival benefit with those after RFA. The above results were confirmed after performing PSM analysis at a 12 and 13 ratio. Conclusion By applying several effective sensitivity analyses, we demonstrated that OS and CSS were similar between the patients with tumors smaller than 3 cm receiving RFA and SR. But SR may be a superior treatment option with better long-term outcome than RFA in patients with tumor measuring 3.1-5 cm. Copyright © 2020 Zheng, Zhang, Lin, Song, Qi and Luo.Acute myeloid leukemia is a heterogeneous disease with a 5-year survival rate of 28.3%, and current treatment options constrained by dose-limiting toxicities. One of the key signaling pathways known to be frequently activated and dysregulated in AML is PI3K/AKT. Its dysregulation is associated with aggressive cell growth and drug resistance. We investigated the activity of Phenybutyl isoselenocyanate (ISC-4) in primary cells obtained from newly diagnosed AML patients, diverse AML cell lines, and normal cord blood cells. ISC-4 significantly inhibited survival and clonogenicity of primary human AML cells without affecting normal cells. We demonstrated that ISC-4-mediated p-Akt inhibition caused apoptosis in primary AML (CD34+) stem cells and enhanced efficacy of cytarabine. ISC-4 impeded leukemia progression with improved overall survival in a syngeneic C1498 mouse model with no obvious toxic effects on normal myelopoiesis. In U937 xenograft model, bone marrow cells exhibited significant reduction in human CD45+ cells in ISC-4 (~87%) or AraC (~89%) monotherapy groups compared to control. Notably, combination treatment suppressed the leukemic infiltration significantly higher than the single-drug treatments (~94%). Together, the present findings suggest that ISC-4 might be a promising agent for AML treatment. Copyright © 2020 Annageldiyev, Tan, Thakur, Dhanyamraju, Ramisetti, Bhadauria, Schick, Zeng, Sharma, Dunton, Dovat, Desai, Zheng, Feith, Loughran, Amin, Sharma, Claxton and Sharma.The homeobox A cluster (HOXA) gene family, comprising 11 members, is involved in a wide spectrum of biological functions in human cancers. However, there is little research on the expression profile and prognostic values of HOXA genes in laryngeal squamous cell cancer (LSCC). Based on updated public resources and integrative bioinformatics analysis, we assessed the expression profile and prognostic values of the HOXA family members. Expression and methylation data on HOXA family members were obtained from The Cancer Genome Atlas (TCGA). The prognostic values of HOXA members and clinical features were identified. A gene set enrichment analysis (GSEA) was conducted to explore the mechanism underlying the involvement of HOXA members in LSCC. The associations between tumor immune infiltrating cells (TIICs) and the HOXA family members were evaluated using the Tumor Immune Estimation Resource (TIMER) database. HOXA2 and HOXA4 were downregulated and HOXA7 and HOXA9-13 were upregulated in LSCC. Upregulation of HOXA10, HOXA11, and HOXA13, along with two clinical characteristics (M stage and gender), were associated with a poor LSCC prognosis based on the results of univariate and multivariate Cox proportional hazards regression analyses.
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