Treatment patterns and clinical outcomes of patients with resectable non-small cell lung cancer receiving neoadjuvant immunochemotherapy: A large-scale, multicenter, real-world study (NeoR-World).

BACKGROUND: Neoadjuvant immunotherapy has ushered in a new era of perioperative treatment for resectable non-small cell lung cancer (NSCLC). However, large-scale data for verifying the efficacy and optimizing the therapeutic strategies of neoadjuvant immunochemotherapy in routine clinical practice are scarce. METHODS: NeoR-World (NCT05974007) was a multicenter, retrospective cohort study involving patients who received neoadjuvant immunotherapy plus chemotherapy or chemotherapy alone in routine clinical practice from 11 medical centers in China between January 2010 and March 2022. Propensity score matching was performed to address indication bias. RESULTS: A total of 408 patients receiving neoadjuvant immunochemotherapy and 684 patients receiving neoadjuvant chemotherapy were included. The pathologic complete response (pCR) and major pathologic response (MPR) rates of the real-world neoadjuvant immunochemotherapy cohort were 32.8% and 58.1%, respectively. Notably, patients with squamous cell carcinoma exhibited significantly higher pCR and MPR rates than those with adenocarcinoma (pCR, 39.2% vs 16.5% [P < .001]; MPR, 66.6% vs 36.5% [P < .001]), whereas pCR and MPR rates were comparable among patients receiving different neoadjuvant cycles. In addition, the 2-year rates of disease-free survival (DFS) and overall survival (OS) rate were 82.0% and 93.1%, respectively. Multivariate analyses identified adjuvant therapy as an independent prognostic factor for DFS (hazard ratio [HR], 0.51; 95% confidence interval [CI], 0.29-0.89; P = .018) and OS (HR, 0.28; 95% CI, 0.13-0.58; P < .001). A significantly longer DFS with adjuvant therapy was observed in patients with non-pCR or 2 neoadjuvant cycles. We observed significant benefits in pCR rate (32.4% vs 6.4%; P < .001), DFS (HR, 0.50; 95% CI, 0.38-0.68; P < .001) and OS (HR, 0.61; 95% CI, 0.40-0.94; P = .024) with immunotherapy plus chemotherapy compared to chemotherapy alone both in the primary propensity-matched cohort and across most key subgroups. CONCLUSIONS: The study validates the superior efficacy of neoadjuvant immunochemotherapy over chemotherapy alone for NSCLC. Adjuvant therapy could prolong DFS in patients receiving neoadjuvant immunochemotherapy, and patients with non-pCR or those who underwent 2 neoadjuvant cycles were identified as potential beneficiaries of adjuvant therapy.

High FN1 expression is associated with poor survival in esophageal squamous cell carcinoma.

Esophageal cancer (EC) is a serious threat to human health. The expression of fibronectin 1 (FN1) in esophageal squamous cell carcinoma (ESCC) remains controversial. The purpose of this study was to elucidate the expression of FN1 in ESCC and to assess the value of FN1 in the prognosis of ESCC patients. 100 ESCC patients from January 2015 to March 2016 were recruited in this study. qRT-PCR and immunohistochemistry (IHC) were used to detect FN1 mRNA and protein expression. The correlation between FN1 expression levels and prognosis of ESCC patients was analyzed. The qRT-PCR results showed that the expression of FN1 mRNA was significantly higher in ESCC tumor tissues than in adjacent esophageal tissues (P < .01). IHC results showed that FN1 protein was expressed in both tumor cells and stroma. High expression of FN1 mRNA and FN1 protein in ESCC tumor tissues was significantly correlated with the depth of tumor invasion, lymph node metastasis and clinical stage of the tumor (P < .05). Survival analysis revealed that patients with higher FN1 mRNA and protein expression had significantly lower survival rates than those with lower FN1 mRNA or protein expression (P < .01). Multivariate cox regression analysis showed that high FN1 protein expression in ESCC tumor tissues was an independent risk factor for low survival in ESCC patients (P < .05). High expression of FN1 protein in ESCC tumor tissue is an independent poor prognostic factor. FN1 protein could be a potential target for the treatment of ESCC.

Exosome-mediated lnc-ABCA12-3 promotes proliferation and glycolysis but inhibits apoptosis by regulating the toll-like receptor 4/nuclear factor kappa-B signaling pathway in esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) is a kind of malignant tumor with high incidence and mortality in the digestive system. The aim of this study is to explore the function of lnc-ABCA12-3 in the development of ESCC and its unique mechanisms. RT-PCR was applied to detect gene transcription levels in tissues or cell lines like TE-1, EC9706, and HEEC cells. Western blot was conducted to identify protein expression levels of mitochondrial apoptosis and toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) signaling pathway. CCK-8 and EdU assays were carried out to measure cell proliferation, and cell apoptosis was examined by flow cytometry. ELISA was used for checking the changes in glycolysis-related indicators. Lnc-ABCA12-3 was highly expressed in ESCC tissues and cells, which preferred it to be a candidate target. The TE-1 and EC9706 cells proliferation and glycolysis were obviously inhibited with the downregulation of lnc-ABCA12-3, while apoptosis was promoted. TLR4 activator could largely reverse the apoptosis acceleration and relieved the proliferation and glycolysis suppression caused by lnc-ABCA12-3 downregulation. Moreover, the effect of lnc-ABCA12-3 on ESCC cells was actualized by activating the TLR4/NF-κB signaling pathway under the mediation of exosome. Taken together, the lnc-ABCA12-3 could promote the proliferation and glycolysis of ESCC, while repressing its apoptosis probably by regulating the TLR4/NF-κB signaling pathway under the mediation of exosome.

Preoperative bowel preparation promotes intestinal functional recovery after esophagectomy.

Background: Patients are prone to intestinal dysfunction after esophagectomy. The value of preoperative bowel preparation before esophagectomy is controversial. There is a lack of evidence as to whether preoperative bowel preparation can help patients improve bowel function and shorten the recovery time of bowel function. Objectives: The objectives of this study were to explore whether preoperative bowel preparation can promote the recovery of intestinal function after esophagectomy. Methods: We analysed 139 patients who underwent elective radical esophagectomy in the Department of Thoracic Surgery at the Second Affiliated Hospital of Xi'an Jiaotong University from May 2016 to December 2018. The enrolled patients were divided into the study group (bowel preparation group) and the control group (no bowel preparation group) of 71 cases and 68 cases. Patients in the study group were given dissolved polyethylene glycol electrolyte powder and a cleansing enema the day before surgery. Patients in the control group were neither given polyethylene glycol electrolyte powder nor cleansing enemas before surgery. The postoperative recovery of the two groups were compared. Results: Postoperative bed rest time, bowel function recovery time and the time of first flatus and defecation after surgery were significantly shorter in patients with bowel preparation than in those without bowel preparation, and the differences were statistically significant. (P=0.038, P<0.001, P<0.001, P<0.001; respectively). Conclusions: Preoperative bowel preparation can promote the recovery of patients with esophageal cancer, especially the recovery of bowel function, which can reduce the pain caused by abdominal distension and improve the quality of life of patients.

Methyltransferase-like 14 silencing relieves the development of atherosclerosis via m6A modification of p65 mRNA.

To explore the METTL14-dependent m6A modification mechanism involved in the development of atherosclerosis. Oxidized low-density lipoprotein (ox-LDL) and the HUVEC cell line were used to establish an atherosclerosis cell model in vitro, and APOE-/- mice fed a high-fat diet were used as the animal model. Cell viability and apoptosis were assessed using MTT assays and flow cytometry. The status of m6A in HUVECs was examined using MeRIP-qPCR. Oil Red O staining was used to evaluate the lesions or plaques on aortas separated from the target mice. METTL14 and METTL3 were upregulated in HUVECs after ox-LDL treatment. After transfection with si-METTL14, the bcl-2 expression level and the viability of ox-LDL-incubated cells increased, whereas the apoptosis rate and the expressions of Bax and cleaved caspase-3 decreased. However, the effect of METTL14 knockdown was reversed by p65 overexpression. After METTL14 knockdown, there was a decrease in the total m6A content in HUVECs, m6A modification, and p65 expression. The plaques and lesion areas on the high-fat diet APOE-/- mouse aortas were smaller after METTL14 silencing. METTL14 reduced cell viability and promoted apoptosis of HUVECs, which were both induced by ox-LDL via m6A modification of p65. Knocking down METTL14 could inhibit the development of atherosclerosis in high-fat diet-treated APOE-/- mice.

Study on Stability of Mechanical Properties for Porous Fe-Cr-Al Alloys after Long-Term Aging.

Nowadays, both the ferrite phase and B2-structured intermetallic in the Fe-Cr-Al alloy system are developed as porous materials, which have been further applied as high-temperature filter materials in industry. This work presents a comparative study of the mechanical properties of porous Fe20Cr5Al, Fe10Cr10Al and Fe10Cr20Al aged at 480 °C for 500 h. The changes in tensile strength, elongation and hardness were determined, and the microstructure changes as well as slight oxidation states of the aged samples were investigated. The results show that the precipitated Cr-rich phase in porous Fe20Cr5Al can increase the hardness and decrease the ductility, while intergranular oxidation can degrade the mechanical performance of the three porous Fe-Cr-Al materials. It is noted that porous Fe10Cr20Al exhibits relatively superior mechanical stability during long-term aging. Meanwhile, by introducing boron, the mechanical performance of the aged porous Fe-Cr-Al alloys can be stabilized since the possible internal oxidation of the exposed grain boundaries is inhibited.

The role of exosomal miR-181b in the crosstalk between NSCLC cells and tumor-associated macrophages.

BACKGROUND: It has been reported that tumor-associated macrophages (TAMs) participate in modulating the progression of cancer in the tumor microenvironment. However, the crosstalk between TAMs and non-small cell lung cancer (NSCLC) is still unclear. OBJECTIVE: We investigated whether NSCLC-derived exosomes could affect TAMs, which feedback modulated progression of NSCLC. METHODS: MiR-181b expression was measured by RT-PCR. Human THP-1 monocyte was differentiated into macrophages with phorbol myristate acetate, which were further identified by transmission electron microscopy and western blot. Macrophage M1 and M2 polarizations were detected by flow cytometry, RT-PCR and western blot. Proliferation, migration, and invasion of NSCLC cells treated with conditioned mediums were detected by EdU and Transwell assays. RESULTS: We demonstrated that miR-181b was up-regulated in exosomes derived from NSCLC patients' serum and NSCLC cells. MiR-181b could be transferred to macrophages via exosomes in the co-culture system of macrophages and NSCLC cells, which promoted macrophage M2 polarization. Further examinations revealed that exosomes derived from NSCLC cells could enhanced macrophage M2 polarizations by regulating miR-181b/JAK2/STAT3 axis, and silencing miR-181b in NSCLC cells and JAK2 inhibitor used in macrophages could reverse the effects. Importantly, the conditioned medium of macrophages treated with NSCLC cell-derived exosomes could promote NSCLC cell proliferation, migration, and invasion. Silencing miR-181b in NSCLC cells and JAK2 inhibitor used in macrophages could block the effects. CONCLUSIONS: All of these results indicated that exosomal miR-181b participated in the crosstalk between NSCLC cells and TAMs, providing potential therapeutic targets for NSCLC.

Minimally invasive esophagectomy via Sweet approach in combination with cervical mediastinoscopy is a valuable approach for surgical treatment of esophageal cancer. / 治疗食管癌的一种有价值的方法­­Sweetå ¥è·¯è”åˆçºµéš”é•œé£Ÿç®¡åˆ‡é™¤æœ¯.

OBJECTIVES: To compare the short-, mid-, and long-term outcomes in patients with esophageal cancer between minimally invasive esophagectomy via Sweet approach in combination with cervical mediastinoscopy (MIE-SM) and minimally invasive esophagectomy via McKeown approach (MIE-MC), and to evaluate the value of MIE-SM in the surgical treatment of esophageal cancer. METHODS: A prospective, nonrandomized study was adopted. A total of 65 esophageal cancer patients after MIE-SM and MIE-MC from June 2014 to May 2016 were included. Among them, 33 patients underwent MIE-SM and 32 patients underwent MIE-MC. Short-term outcomes (including the duration of surgery, intraoperative blood loss volume, ICU stay time, postoperative complications, postoperative hospital stay, reoperation, open surgery, number of dissected lymph nodes, and 30-day mortality), mid-term outcomes, [including Quality of Life Core Questionnaire (QLQ-C30) and the esophageal site-specific module (QLQ-OES18)], long-term outcomes [including overall survival and disease-free survival] were compared between the 2 groups. RESULTS: Radical resection (R0) were achieved in all patients. There were no significant differences in the duration of surgery, intraoperative blood loss volume, ICU stay time, postoperative complications, and postoperative hospital stay between the 2 groups (all P>0.05). More lymph nodes were dissected in the MIE-SM group (24.1±7.3) than those in the MIE-MC group (17.8±5.0, P<0.001). The emotional function, global health status scale scores in QLQ-C30 scale in the MIE-SM group were significantly higher than those in the MIE-MC group (P=0.025, P<0.001, respectively), and the pain score in the MIE-SM group was significantly lower than that in the MIE-MC group (P=0.013). QLQ-OES18 results showed that the pain score in the MIE-SM group was significantly lower than that in the MIE-MC group (P=0.021). Survival analysis showed that the overall survival and disease-free survival were similar between the 2 groups. CONCLUSIONS: MIE-SM appears to be a safe surgical approach, which may get better quality of life, suffer less pain, and can achieve the same therapeutic effect as MIE-MC. Therefore, MIE-SM should be considered as a valuable approach for the treatment of middle and lower esophageal cancer.

Parthenolide Inhibits Angiogenesis in Esophageal Squamous Cell Carcinoma Through Suppression of VEGF.

BACKGROUND: Parthenolide (PT), the effective active ingredient of the medicinal plant, feverfew (Tanacetum parthenium), has been used as an anti-inflammatory drug due to its involvement in the inhibition of the NF-кB pathway. Moreover, recent studies have demonstrated the anti-tumor effect of PT in several cancers. However, the effect of PT on esophageal carcinoma remains unclear to date. In this study, we examined the inhibitory effects of PT and its underlying mechanism of action in human esophageal squamous cell carcinoma (ESCC) cells - Eca109 and KYSE-510. METHODS: The proliferation ability of Eca109 and KYSE-510 treated with PT was detected using the Cell Counting Kit-8 and colony forming assay. The Transwell assay and the wound healing assay were used to analyze the cell invasion and migration ability, respectively. The tube formation assay was used to investigate the effect of PT on tube formation of endothelial cells. The expression level of NF-кB, AP-1 and VEGF was analyzed by Western blot. RESULTS: We demonstrated that PT attenuates the proliferation and migration ability of ESCC cells in vitro and also inhibits tumor growth in the mouse xenograft model. In addition, PT exhibited anti-angiogenesis activity by weakening the proliferation, invasion and tube formation of endothelial cells in vitro and reduced microvessel density in the xenograft tumors. Further studies revealed that PT reduced the expression level of NF-кB, AP-1 and VEGF in ESCC cells. CONCLUSION: Collectively, the results of our study demonstrated that PT exerts anti-tumor and anti-angiogenesis effects possibly by inhibiting the NF-кB/AP-1/VEGF signaling pathway on esophageal carcinoma and might serve as a promising therapeutic agent for ESCC.

Author Correction: Genome-wide analyses of long non-coding RNA expression profiles and functional network analysis in esophageal squamous cell carcinoma.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

SNHG7: A novel vital oncogenic lncRNA in human cancers.

Long noncoding RNAs (lncRNAs) are a group of RNAs that lack protein-coding ability, with lengths greater than 200 nucleotides. Increasing evidence has indicated that they mediate multiple physiological and pathological processes by regulating gene expression at the epigenetic, transcriptional, post-transcriptional, and translational levels. The deregulation of lncRNAs was demonstrated to have tumor suppressive or oncogenic effects, and thus, these molecules play vital regulatory roles in tumor initiation and progression. Small nucleolar RNA hostgene 7 (SNHG7) is a lncRNA located on chromosome 9q34.3. Different studies have explored the potential role of SNHG7 in the development and progression of multiple human malignancies such as bladder, breast, colorectal, esophageal, gastric, and prostate cancer, as well as osteosarcoma, among others, and high expression predicts poor prognosis and poor survival for such patients. Moreover, this molecule can promote proliferation and metastasis, while inhibiting apoptosis in cancer cells. The present review highlights the latest insights into the expression, functional roles, and molecular mechanisms of SNHG7 in different human malignancies.

Long noncoding RNA lnc-ABCA12-3 promotes cell migration, invasion, and proliferation by regulating fibronectin 1 in esophageal squamous cell carcinoma.

Long noncoding RNAs (lncRNAs) have been shown to play important roles in human cancers, including esophageal squamous cell carcinoma (ESCC). We previously demonstrated that a novel lncRNA, lnc-ABCA12-3, was overexpressed in ESCC tissues. However, the exact function of lnc-ABCA12-3 is unknown. In the current study, we aimed to evaluate the expression of lnc-ABCA12-3 in ESCC and to explore the potential mechanism of lnc-ABCA12-3 in cell migration, invasion, and proliferation. We showed that lnc-ABCA12-3 was upregulated in ESCC tumor tissues and cell lines. The increased expression of lnc-ABCA12-3 was positively associated with advanced tumor-node-metastasis stages and poor prognosis. The knockdown of lnc-ABCA12-3 inhibited the cell migration, invasion, and proliferation abilities of KYSE-510 and Eca-109 cells. We also found that fibronectin 1 (FN1) was upregulated in ESCC tumor tissues. The expression of FN1 messenger RNA was positively correlated with the expression of lnc-ABCA12-3 in ESCC tumor tissues. After lnc-ABCA12-3 knockdown, the expression of FN1 was downregulated. In addition, the overexpression of FN1 restored the abilities of cell migration, invasion and proliferation in Eca-109 cells. Further studies indicated that lnc-ABCA12-3 acted as a competing endogenous RNA for miR-200b-3p to regulate FN1 expression. In conclusion, these results suggest that lnc-ABCA12-3 is a novel oncogene in tumorigenesis and that its high expression is related to a poor prognosis for patients with ESCC. lnc-ABCA12-3 promotes cell migration, invasion, and proliferation via the regulation of FN1 in ESCC. Our data suggest that lnc-ABCA12-3 might serve as a potential prognostic biomarker and therapeutic target for ESCC.

Involvement of noncoding RNAs in epigenetic modifications of esophageal cancer.

Esophageal cancer (EC) is a serious digestive malignancy and is a leading cause of cancer-related mortality. Apart from genetic mutations, many epigenetic alterations including DNA methylation and histone modifications associated with chromatin remodeling have been identified in the regulation of gene expression in EC. Recently, noncoding RNAs, and mainly lncRNAs and miRNAs, have been revealed to be involved in the epigenetic regulation of EC. In this review, we focus on describing new insights on epigenetic processes associated with noncoding RNAs, which have been characterized to be responsible for the development and progression of EC.

Author Correction: Engineering Auger recombination in colloidal quantum dots via dielectric screening.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Genome-wide analyses of long non-coding RNA expression profiles and functional network analysis in esophageal squamous cell carcinoma.

Esophageal cancer (EC) is a serious malignancy and that is the fifth leading cause of cancer-related death worldwide. Esophageal squamous cell carcinoma (ESCC) is the main subtype of EC in China. In recent years, long non-coding RNAs (lncRNAs) have demonstrated to be novel tumor-associated regulatory factors. However, the functions and mechanisms of lncRNAs in ESCC have not been fully understood. In this study, we attempted to construct Genome-wide expression profiles of lncRNAs and their potential functions in ESCC. By using microarray, we found a total of 2,366 lncRNAs (1,032 upregulated and 1,334 downregulated) and 3,052 mRNAs (1,477 upregulated and 1,575 downregulated) were differentially expressed between the paired five ESCC tumor tissues and adjacent normal esophageal tissues (fold change, FC ≥2.0 or ≤0.5, p ≤ 0.05). Eight lncRNAs were detected by qRT-PCR to verify the results of the microarray, and the clinicopathological parameters were analyzed in 53 patients with ESCC. GO analysis and KEGG pathway analysis showed that the main biological functions of these abnormal lncRNAs were related to immune response, extracellular vesicular exosome, and protein binding. At the same time, the cis and trans models were used to analyze the potential synergistic regulatory relationship between lncRNAs and their potential target genes. Related genes were the processes that affect cell growth, differentiation, and migration. Then we mapped the lncRNAs-mRNAs co-expression pattern by calculating the PCCs of each lncRNA and mRNA expression value. Furthermore, we investigated the function and potential mechanism of a novel highly expressed lncRNA, lnc-KIAA1244-2, and found that its expression is associated with tumor size, N classification and clinical stage. Knockdown of lnc-KIAA1244-2 inhibited the cell proliferation and inhibited the TNFAIP3 expression in Eca-109 cells. Taken together, the expression patterns of lncRNAs and mRNAs in ESCC tumor tissues are different from those in normal adjacent tissues, and some abnormal expressed lncRNAs may play important roles in the development and progression of ESCC. Lnc-KIAA1244-2 could promote the cell proliferation of ESCC cells and might be a potent therapeutic target for ESCC.

Circular RNAs in Cancer: emerging functions in hallmarks, stemness, resistance and roles as potential biomarkers.

Circular RNAs (circRNAs) are a class of RNA molecules with closed loops and high stability. CircRNAs are abundantly expressed in eukaryotic organisms and exhibit both location- and step-specificity. In recent years, circRNAs are attracting considerable research attention attributed to their possible contributions to gene regulation through a variety of actions, including sponging microRNAs, interacting with RNA-binding proteins, regulating transcription and splicing, and protein translation. Growing evidence has revealed that circRNAs play critical roles in the development and progression of diseases, especially in cancers. Without doubt, expanding our understanding of circRNAs will enrich knowledge of cancer and provide new opportunities for cancer therapy. In this review, we provide an overview of the characteristics, functions and functional mechanisms of circRNAs. In particular, we summarize current knowledge regarding the functions of circRNAs in the hallmarks, stemness, resistance of cancer, as well as the possibility of circRNAs as biomarkers in cancer.

Engineering Auger recombination in colloidal quantum dots via dielectric screening.

Auger recombination is the main non-radiative decay pathway for multi-carrier states of colloidal quantum dots, which affects performance of most of their optical and optoelectronic applications. Outstanding single-exciton properties of CdSe/CdS core/shell quantum dots enable us to simultaneously study the two basic types of Auger recombination channels-negative trion and positive trion channels. Though Auger rates of positive trion are regarded to be much faster than that of negative trion for II-VI quantum dots in literature, our experiments find the two rates can be inverted for certain core/shell geometries. This is confirmed by theoretical calculations as a result of geometry-dependent dielectric screening. By varying the core/shell geometry, both types of Auger rates can be independently tuned for ~ 1 order of magnitude. Experimental and theoretical findings shed new light on designing quantum dots with necessary Auger recombination characteristics for high-power light-emitting-diodes, lasers, single-molecular tracking, super-resolution microscope, and advanced quantum light sources.

Role of lncRNA and EZH2 Interaction/Regulatory Network in Lung Cancer.

Lung cancer is the leading cause of cancer-related deaths worldwide. Long non-coding RNAs (lncRNAs) are non-protein-coding transcripts and longer than 200 nucleotides. LncRNAs have been demonstrated to modulate gene expression at transcriptional, post-transcriptional, as well as epigenetic levels in lung cancer. Interestingly, compelling studies have revealed that lncRNAs participated in the EZH2 oncogenic regulatory network. EZH2 plays an important role in the initiation, progression and metastasis of cancer. On one hand, lncRNAs can directly bind to EZH2, recruit EZH2 to the promoter region of genes and repress their expression. On the other hand, lncRNAs can also serve as EZH2 effectors or regulators. In this review, we summarized the types of lncRNA-EZH2 interaction and regulatory network identified till date and discussed their influence on lung cancer. Better understanding regarding the interaction and regulatory network will provide new insights on lncRNA- or EZH2-based therapeutic development in lung cancer.

Long non-coding RNAs in esophageal cancer: molecular mechanisms, functions, and potential applications.

Esophageal cancer (EC) is the sixth leading cause of cancer-related death worldwide. The lack of early diagnostic biomarkers and effective prognostic indicators for metastasis and recurrence has resulted in the poor prognosis of EC. In addition, the underlying molecular mechanisms of EC development have yet to be elucidated. Accumulating evidence has demonstrated that lncRNAs play a vital role in the pathological progression of EC. LncRNAs may regulate gene expression through the recruitment of histone-modifying complexes to the chromatin and through interactions with RNAs or proteins. Recent evidence has demonstrated that the dysregulation of lncRNAs plays important roles in the proliferation, metastasis, invasion, angiogenesis, apoptosis, chemoradiotherapy resistance, and stemness of EC, which suggests potential clinical implications. In this review, we highlight the emerging roles and regulatory mechanisms of lncRNAs in the context of EC and discuss their potential clinical applications as diagnostic and prognostic biomarkers.

Left minimally invasive esophagectomy in a patient with synchronous esophageal and lung cancers: Case report.

RATIONALE: Minimally invasive esophagectomy (MIE) have been increasingly used and are regarded as suitable alternatives to open esophagectomy. However, few previous reports described minimally invasive esophagectomy using a left-sided approach. PATIENT CONCERNS AND DIAGNOSES: A 71-year-old man was admitted to our hospital because of progressive dysphagia. Synchronous double primary thoracic esophageal and left lung cancers were considered before the operation. INTERVENTIONS AND OUTCOMES: A lobectomy and MIE, via a left video-assisted thoracoscopic approach, was performed. Preparation of a gastric conduit and an intra-abdominal lymphadenectomy were completed by laparoscopy and a cervical anastomosis was made. In addition, a cervical mediastinoscopy was performed to dissect the lymph nodes along the bilateral recurrent laryngeal nerves. No postoperative complications were observed. The patient achieved a favorable short-term outcome. LESSONS: This is the first report of a patient with synchronous esophageal and left lung cancers treated with minimally invasive resection via left thoracoscopy, laparoscopy, and cervical mediastinoscopy. Our results showed that the left MIE approach in combination with cervical mediastinoscopy is potentially most appropriate for some esophageal cancer patients, when the right MIE approach is not applicable in certain conditions.