Ebbesenbaker1009

The era of genetics and precision medicine has been reforming this world. How will plastic surgeons in the field of vascular anomalies conform to the trend? This article systematically reviews the identification of serum biomarkers, risk factors, specific mutations in the angiogenesis-related genes such as GNAQ, RASA1, TEK, and their impact on the diagnosis and treatment of vascular anomalies with preliminary results that have been previously reported and leading the tide. Moreover, a new disease classification for complex vascular malformations based on PIK3CA genetic evidence and various treatment breakthroughs is briefly summarized. With gene sequencing, bioinformatics, and big data, we confront the challenges of research in the vascular anomalies domain and explore possibilities of precision medicine development.

The era of genetics and precision medicine has been reforming this world. How will plastic surgeons in the field of vascular anomalies conform to the trend? This article systematically reviews the identification of serum biomarkers, risk factors, specific mutations in the angiogenesis-related genes such as GNAQ, RASA1, TEK, and their impact on the diagnosis and treatment of vascular anomalies with preliminary results that have been previously reported and leading the tide. Moreover, a new disease classification for complex vascular malformations based on PIK3CA genetic evidence and various treatment breakthroughs is briefly summarized. With gene sequencing, bioinformatics, and big data, we confront the challenges of research in the vascular anomalies domain and explore possibilities of precision medicine development.We aim to describe two cases of creatine phosphokinase (CPK) and liver enzymes elevation occurring as adverse effects of alectinib (Alecensa) treatment for anaplastic lymphoma kinase (ALK)-mutated metastatic nonsmall cell lung cancer (NSCLC). A 56-year-old female and a 59-year-old male diagnosed with NSCLC exhibiting ALK gene rearrangements were treated by alectinib administration. The former had a complete response of widespread metastatic disease within 3 months, and the latter also had a substantial response. Both patients initially experienced an episode of CPK elevation and neither had dose modifications. At the end of the treatment, CPK and liver enzymes returned to normal range despite the continuation of alectinib full dose. A transient elevation of CPK and liver enzymes may take place during the alectinib treatment, indicating a tumor tissue damage thus contributing to a significant response.Many patients with recurrent/metastatic squamous cell cancer of the head and neck (SCCHN) are old or fragile and, despite deserving rapid and deep responses due to symptoms or a high tumor burden, they are not candidates for the current standard in the first-line setting of pembrolizumab plus platinum-5-FU. Other chemoimmunotherapy combinations substituting the 5-FU infusion by a taxane, may allow for less toxic effects without the need for a central venous catheter placement while maintaining efficacy. We present the case of an oral cavity cancer progressing with bulky disease to first-line cetuximab-paclitaxel in a frail and malnourished patient, where second-line treatment with pembrolizumab and reduced-dose 3-weekly carboplatin-paclitaxel achieved a deep and durable response. This is, to our knowledge, the first reported case of such combination being used in the R/M setting of SCCHN. Clinical trials should try to investigate the feasibility of this potentially less toxic and convenient combination in patients with SCCHN.Esophageal cancer is one of the most aggressive malignant cancers in the world. Circular RNA hsa_circ_0000554 (circ_0000554) and Fermitin family members 1 (FERMT1) are rated to the advancement of esophageal cancer. Nevertheless, the regulatory mechanisms between circ_0000554 and FERMT1 in the radioresistance of esophageal cancer are unclear. Quantitative real-time PCR (qRT-PCR) was applied to examine the expression of circ_0000554, FERMT1 mRNA, and miR-485-5p. Western blot analysis was employed to assess the protein expression levels of FERMT1, Ki-67, matrix metalloproteinase (MMP)-9 and MMP-2. Cell colony formation, migration, invasion, radiosensitivity and apoptosis were evaluated by cell colony formation, transwell or flow cytometry assays. The relationship between circ_0000554 or FERMT1 and miR-485-5p was verified with dual-luciferase reporter assay. Circ_0000554 and FERMT1 expression was enhanced in esophageal cancer tissues and radioresistant esophageal cancer tissues. Both circ_0000554 and FERMT1 repression blocked cell colony formation, migration, invasion and elevated cell radiosensitivity and apoptosis in esophageal cancer cells. Importantly, circ_0000554 served as a sponge for miR-485-5p in esophageal cancer cells. And FERMT1 acted as a downstream target for miR-485-5p. Additionally, circ_0000554 modulated FERMT1 expression via miR-485-5p. Furthermore, FERMT1 enhancement reversed circ_0000554 inhibition-mediated effects on the colony formation, migration, invasion, radiosensitivity and apoptosis of esophageal cancer cells. Circ_0000554 silencing repressed EC progression and enhanced cell radiosensitivity through downregulating FERMT1 via sponging miR-485-5p, which provided a possible method for improving the radioresistence of esophageal cancer.Prostate cancer is the most common urinary malignancy in males. Long noncoding RNA small nucleolar RNA host gene 1 (lncRNA SNHG1) has been reported to play a crucial role in the development of various cancers. However, the understanding of SNHG1 in prostate cancer is still limited and needs further investigation. In this study, we found the level of SNHG1 was significantly upregulated in prostate cancer tissues and cells. Knockdown of SNHG1 significantly suppressed proliferation, migration and invasion and promoted cell apoptosis in prostate cancer cells. In addition, knockdown of SNHG1 significantly downregulated proliferating cell nuclear antigen and upregulated cleaved caspase-3. MiR-383-5p was identified to be a target of SNHG1 by bioinformatics analysis, dual-luciferase reporter assay, RNA immunoprecipitation assay and RNA pull-down assay. MiR-383-5p was significantly downregulated in prostate cancer tissues and cells. RP-6306 nmr Inhibition of miR-383-5p could partially restore the effects of SNHG1 knockdown on prostate cancer cell proliferation, apoptosis, migration and invasion.