Recommendations suggest that seminoma patients with a residual disease in the retroperitoneum larger than 3 cm should be subjected for PET scanning with 18-fluorodeoxyglucose. Relatively high sensitivity, specificity and a negative predictive value (80-95%) may guide clinical decision to spare these patients of high morbidity of an unnecessary surgery. However, a positive predictive value of around 50% renders PET scanning difficult to interpret in the case of positive finding. These patients often require extremely difficult surgical procedures with the high risk of post-operative morbidity. Therefore, seminoma patients with PET positive residual masses larger than 3 cm still remain a serious challenge in the decision making of nuclear medicine specialist, oncologists, and urologic surgeons. In this article, we aim to summarize data on controversial dilemmas in staging procedures, active surveillance, and post-chemotherapy assessment of GCTs based on the available published literature. The purpose of this study was to establish a nomogram combining classical parameters and immunohistochemical markers to predict the recurrence of patients with stage I-II endometrial cancer (EC). 419 patients with stage I-II endometrial cancer who received primary surgical treatment at the First Affiliated Hospital of Chongqing Medical University were involved in this study as a training cohort. Univariate and multivariate Cox regression analysis of screening prognostic factors were performed in the training cohort to develop a nomogram model, which was further validated in 248 patients (validation cohort) from the Second Affiliated Hospital of Chongqing Medical University. The calibration curve was used for internal and external verification of the model, and the C-index was used for comparison among different models. There were 51 recurrent cases in the training cohort while 31 cases in the validation cohort. Univariate analysis showed that age, histological type, histological grade, myometrial invasion, cervical stromal invasion, postoperative adjuvant treatment, and four immunohistochemical makers (Ki67, estrogen receptor, progesterone receptor, P53) were the related factors for recurrence of EC. Multivariate analysis demonstrated that histological type (P = 0.029), myometrial invasion (P = 0.003), cervical stromal invasion (P = 0.001), Ki67 (P < 0.001), ER (P = 0.009) and P53 expression (P = 0.041) were statistically correlated with recurrence of EC. Recurrence-free survival was better predicted by the proposed nomogram with a C-index of 0.832 (95% CI, 0.752-0.912) in the training cohort, and the validation set confirmed the finding with a C-index of 0.861 (95% CI, 0.755-0.967). The nomogram model combining classical parameters and immunohistochemical markers can better predict the recurrence in patients with FIGO stage I-II EC.The nomogram model combining classical parameters and immunohistochemical markers can better predict the recurrence in patients with FIGO stage I-II EC.Osteosarcoma (OS), a type of malignant bone tumor, is commonly found in children and adolescents. Although previous studies have identified that long non-coding RNAs (lncRNAs) regulate OS, it is unclear whether lncRNAs impact the progression of OS. Here, we identified LINC00607, a lncRNA that facilitates OS proliferation, migration, and invasion. Based on the RNA-sequencing results, LINC00607 expression was significantly upregulated in pulmonary metastasis within OS. Functional experiments revealed that LINC00607 promoted migration and invasion of endothelial cells to exacerbate epithelial-mesenchymal transition (EMT). PCI-32765 Furthermore, the results of RNA pull-down assay and invasion assay suggested that the binding between LINC00607 and miR-607 promoted OS invasion. Bioinformatic analysis and rescue experiments demonstrated that E2F6, a transcriptional factor, functioned downstream of LINC00607/miR-607. Finally, we found that LINC00607 promoted OS progression in vivo. This work revealed that LINC00607 worked as an miR-607 sponge to upregulate E2F6 expression, which promoted tumor proliferation in OS. These results identified a novel therapeutic target for treating OS.[This corrects the article DOI 10.3389/fonc.2020.00488.].Positive Regulatory Domain (PRDM) gene family members commonly express two main molecular variants, the PR-plus isoform usually acting as tumor suppressor and the PR-minus one functioning as oncogene. Accordingly, PRDM2/RIZ encodes for RIZ1 (PR-plus) and RIZ2 (PR-minus). In human cancers, genetic or epigenetic modifications induce RIZ1 silencing with an expression level imbalance in favor of RIZ2 that could be relevant for tumorigenesis. Additionally, in estrogen target cells and tissues, estradiol increases RIZ2 expression level with concurrent increase of cell proliferation and survival. Several attempts to study RIZ2 function in HeLa or MCF-7 cells by its over-expression were unsuccessful. Thus, we over-expressed RIZ2 in HEK-293 cells, which are both RIZ1 and RIZ2 positive but unresponsive to estrogens. The forced RIZ2 expression increased cell viability and growth, prompted the G2-to-M phase transition and organoids formation. Accordingly, microarray analysis revealed that RIZ2 regulates several genes involved in mitosis. Consistently, RIZ silencing in both estrogen-responsive MCF-7 and -unresponsive MDA-MB-231 cells induced a reduction of cell proliferation and an increase of apoptosis rate. Our findings add novel insights on the putative RIZ2 tumor-promoting functions, although additional attempts are warranted to depict the underlying molecular mechanism.Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infects humans through the angiotensin converting enzyme-2 (ACE-2) receptor expressed on many cells, including lymphocytes. In Covid-19 patients IL-6 is overexpressed, and hyperactivated plasmacytoid lymphocytes are detected in peripheral blood film. We hypothesize that, due to the unpredictable interaction between the new virus and the B cell lineage of infected patients, a cascade of out of control events can ensue, capable of determining unexpected pathologic disorders involving such lineage. Here we report two cases of autoimmune hemolytic anemia (AIHA) and two cases of B-cell hematological malignancies developed or reactivated during acute SARS-CoV-2 infection. The temporal relationship of the events may suggest a potential causal relationship between SARS-CoV-2 infection and the hematopoietic disorders. We suggest that special attention should be paid to COVID-19 patients with underlining B cell lineage disorders.