BackgroundNutritional deficits, cachexia, and sarcopenia are extremely common in esophageal cancer. The aim of this article was to assess the effect of loss of skeletal muscle mass during neoadjuvant treatment on the prognosis of esophageal cancer patients.MethodsEsophageal cancer patients (N = 115) undergoing neoadjuvant therapy and surgery between 2010 and 2014 were identified from our surgery database and retrospectively analyzed. Computed tomography imaging of the total cross-sectional muscle tissue measured at the third lumbar level defined the skeletal muscle index, which defined sarcopenia (SMI < 52.4 cm2/m2 for men and < 38.5 cm2/m2 for women). Images were collected before and after neoadjuvant treatments.ResultsSarcopenia in preoperative imaging was prevalent in 92 patients (80%). Median overall survival was 900 days (interquartile range 334–1447) with no difference between sarcopenic (median = 900) and non-sarcopenic (median = 914) groups (p = 0.872). Complication rates did not differ (26.1% vs 32.6%, p = 0.725). A 2.98% decrease in skeletal muscle index during neoadjuvant treatment correlated with poor 2-year survival (log-rank p = 0.04).ConclusionLoss of skeletal muscle tissue during neoadjuvant treatment correlates with worse overall survival.Electronic supplementary materialThe online version of this article (10.1186/s12957-018-1327-4) contains supplementary material, which is available to authorized users.

Despite the VATS lobectomy and segmentectomy patients' being older, with more comorbid condition and poorer pulmonary function, the incidence of major complications was lower and hospitalization shorter than for open thoracotomy patients. For stage I NSCLC, VATS should be considered the primary surgical approach.

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We conclude that PCs are uncommon tumors. When resected, the long-term survival is in general favorable. In this consecutive, single-institution cohort of patients, presence of metastatic disease, tumor size, histological subtype and Ki-67 index were associated with shorter disease-specific survival. As TC and AC have different clinical behaviors, the correct tumor classification at the time of diagnosis is a necessity.

OBJECTIVETo describe the population-wide incidence of Zenker diverticulum over a 20-year period and characterize management strategies across specialties and treatment settings. DESIGN, SETTING, AND PARTICIPANTSThis retrospective national cohort study was conducted from January 1, 1996, through December 31, 2015, and reviewed patient records from the Care Register for Healthcare in Finland, from which patients with Zenker diverticulum were identified. The data were analyzed in October 2021. EXPOSURES Zenker diverticulum. MAIN OUTCOME AND MEASURE The incidence of Zenker diverticulum per 100 000 person-years. RESULTS A total of 2736 patients (median [IQR] age at diagnosis 72.0 [19-106] years; 1278 women [46.7%]) were identified, making the annual incidence of Zenker diverticulum in Finland 2.9/100 000 person-years. Men had higher incidence (3.7/100 000 person-years) compared with women (2.3/100 000 person-years), with an incidence rate ratio of 1.61 (95% CI, 1.48-1.76; P < .001). Within the study population, 1044 patients (38.2%) underwent surgical treatment and 227 (8.3%) underwent 2 or more surgeries. The choice of initial operative approach depended on the medical specialty (Cramer V = 0.41) and on specific catchment area (Cramer V = 0.41). Overall, endoscopic approaches for initial operations were most popular. CONCLUSIONS AND RELEVANCEThe cohort study results found that the incidence of Zenker diverticulum was 2.9/100 000 person-years. Most patients with Zenker diverticulum did not undergo definitive therapy. Some hospital districts and some medical specialties were more likely to opt for conservative treatment than others. The choice of operative approach depended more on physician-level factors rather than patient profiles.

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Activin A has previously been associated with cancer cachexia and in vitro resistance to platinum-based chemotherapy. We studied circulating activin A concentrations as well as activin B and their antagonists' follistatin/follistatin-like 3 in presurgical patients with nonesmall-cell lung cancer and malignant pleural mesothelioma. We found that circulating activing A levels were elevated in malignant pleural mesothelioma and associated with cancer cachexia and poor response to platinum-based chemotherapy. Circulating activing A separated nonesmall-cell lung cancer from benign lung lesion. Background: Previous preclinical studies have shown that activin A is overexpressed in malignant pleural mesothelioma (MPM), associates with cancer cachexia, and is observed in in vitro resistance to platinum-based chemotherapy. We evaluated circulating activin levels and their endogenous antagonists' follistatin/follistatin-like 3 in intrathoracic tumors. Materials and Methods: Patients suspected of thoracic malignancy were recruited prior to surgery. Serum samples were collected from 21 patients with MPM, 59 patients with nonesmall-cell lung cancer (NSCLC), and 22 patients with benign lung lesions. Circulating activin/follistatin levels were measured using enzymelinked immunosorbent assay and compared with clinicopathologic parameters. Results: Circulating activin A levels were elevated in patients with MPM when compared with patients with NSCLC or benign lung lesion samples (P < .0001). Also, follistatin and follistatin-like 3 levels were the highest in MPM, although with less difference compared with activin A. Receiver operating characteristic analysis for activin A for separating NSCLC from benign lung lesion showed an area under the curve of 0.856 (95% confidence interval, 0.77-0.94). Activin A levels were higher in patients with cachexia (P < .001). In patients with MPM, activin A levels correlated positively with computed tomographybased baseline tumor size (R ¼ 0.549; P ¼ .010) and the change in tumor size after chemotherapy (R ¼ 0.743; P ¼ .0006). Patients with partial response or stable disease had lower circulating activin A levels than the ones with progressive disease (P ¼ .028). Conclusion: Activin A serum level could be used as a biomarker in differentiating malignant and benign lung tumors. Circulating activin A levels were elevated in MPM and associates with cancer cachexia and reduced chemotherapy response.