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Chunmei Xiao,* Fangye Xu,* Rong Wang, Qi Liang, Kai Shen, Jiali Xu, Lianke Liu Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, People’s Republic of China*These authors contributed equally to this workCorrespondence: Lianke Liu; Jiali XuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, People’s Republic of ChinaTel +86 1395 162 3290Fax +8625-8371-0040Email liulianke@jsph.org.cn; xujiali@jsph.org.cnBackground: Ovarian cancer (OC) is a common malignancy in the gynecological tumor. Standard treatment for ovarian cancer is surgery and chemotherapy based on paclitaxel and platinum. However, traditional chemotherapy for ovarian cancer is limited by drug resistance and systemic side effects. It is imperative to explore effective treatment options for refractory ovarian cancer.Case Presentation: A 52-year-old female initially presented with lower abdominal distension and migratory pain. After the laparoscopic exploration and biopsy, immunohistochemistry showed poorly differentiated adenocarcinoma originated from ovarian (cT3NxM1, stage IV, peritoneal and abdominal wall metastasis). The next generation sequence detected ERRFI1 (T187A, exon4) mutation.Results: The patient received first-line chemotherapy (paclitaxel, nedaplatin plus avastin), followed by maintenance therapy with gefitinib, achieving a 15-month progression-free survival (PFS). After disease progression and second-line treatment failure, endostar plus apatinib was administered for 14 cycles and she obtained a PFS of 14 months without long-term adverse events.Conclusion: We believe that the ERRFI1 gene may be a potential target of gefitinib. Importantly, endostar combined with apatinib is worth recommending for maintenance treatment in refractory ovarian cancer.Keywords: ovarian cancer, antiangiogenic therapy, endostar, apatinib, gefitinib

Additional file 2. Which is entitled with Supplementary Materials and Methods, is a description about protocol revision history for study PCD-DZ650-17-001 (NCT03888092).

Additional file 6. Which is entitled with Preclinical Tissue Distribution Study, describes a preclinical tumor distribution study designed to confirm whether larotinib had a better distribution than other EGFR-TKIs in esophageal tumor tissues.

Additional file 8. Which is entitled with Treatment related adverse events occurring in 10% or more patients, is Table 3 that is cited and indicated within the submitted manuscipt. Since this table is larger than one A4, it is uploaded as an additional file.

Additional file 4. Which is entitled with Progression-free Survival and Overall Survival in Subgroups, is a supplementary table describing subgroup analyses of Progression-free Survival and Overall Survival at different dose levels.

Additional file 7. Which is entitled with Baseline characteristics, is Table 1 that is cited and indicated within the submitted manuscript. Since this table is larger than one A4, it is uploaded as an additional file.

Additional file 5. Which is entitled with Preclinical Kinase Inhibition Assays, is a report describing a preclinical study designed to make comparison of inhibitory activity on EGFR family kinases in the same batch among different first-generation EGFR-TKIs.

Additional file 1. Which is entitled with Preclinical studies on Xenografted Mice Models, is an in vivo assay reporting results regarding the evaluation of antitumor efficacy of larotinib in xenografted mice models, plasma, and tumor tissues.

Additional file 3. Which is entitled with Overall Response Assessed by Independent Radiology Review, is a supplementary table describing confirmed overall response assessed by independent radiology review.

Circular RNAs (circRNAs) are novel noncoding RNAs with a wide range of physiological and pathological activities. However, the expression profile and roles in lung squamous cell carcinoma (LSCC) remain largely unknown. Therefore, we investigated the expression profile of circRNAs in three LSCC and matched adjacent normal tissues using microarray. Total 216 differentially expressed circRNAs were identified, including 135 upregulated and 81 downregulated ones in LSCC tissues. Bioinformatics analysis revealed that these differentially expressed circRNAs were potentially implicated in carcinogenesis using Gene ontology (GO) and KEGG pathway analyses. By constructing miRNA-circRNA interaction network, a total of ten key circRNAs, including 6 upregulated and 4 downregulated circRNAs were further screened and then confirmed using qRT-PCR analysis in another 40 paired of LSCC tissues and adjacent normal tissues. In addition, Kaplan-Meier survival analysis demonstrated that the overall survival time of LSCC patients with high hsa_circRNA_103827 expression and low hsa_circRNA_000122 was significantly shorter (P

Recent studies have indicated that side population (SP) cells, which are an enriched source of cancer stem cells (CSCs), drive and maintain many types of human malignancies. SP cells have distinguishing biological characteristics and are thought to contribute to metastasis, therapy resistance, and tumor recurrence. In the present study, the miRNA expression profiles of SP cells and non-SP cells were compared using miRNA array analysis. Both let-7 and miR-31 were significantly down-regulated in SP cells compared to non-SP cells. The results were confirmed by real-time PCR. Engineered repression of miR-31 caused marked repression of both lung cancer SP cell and non-SP cell growth in vitro. In contrast, engineered repression of let-7 caused marked promotion of both lung cancer SP and non-SP cells growth in vitro. Cell cycle studies further revealed that reduced miR-31 could inhibit SP cell proliferation by a cell cycle arrest in the G0/G1 phase, whereas reduced let-7 induced SP cell proliferation by accelerating G1/S phase transition. Notably, reduced miR-31 prevented SP cell differentiation, whereas reduced let-7 promoted SP cell differentiation under differentiation conditions. These findings indicate that reduced miR-31 and let-7 are involved in maintaining the balance between differentiation and quiescence in SP cells.