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Correction surgery for dropped head syndrome (DHS) is a challenging procedure that requires extensive realignment of the cervical spine and is associated with a high rate of complications. Postoperative occurrence of dysphagia related to the change of the cervical alignment is well known as a complication of occipito-cervical fusion, and it is thought to be caused by narrowing of the pharyngeal airway space (PAS) due to the change of the alignment. We experienced a case of severe dysphagia requiring tracheotomy and gastrostomy after correction surgery for DHS. Revision surgery which downgraded the cervical lordosis immediately solved this problem. We report this case and discuss the possible risk factors causing this complication.

The year 2021 marked the 10th anniversary of the publication of Cells [...]

Sensitivity to mitomycin C, a chemotherapeutic agent, was shown to correlate with DNA damage foci formation in the S phase. [...]the activation of CHEK1 induced resistance to mitomycin C. CHEK1-mediated damage response could prevent replication stress, and ATR-CHEK1 signaling could thus compensate for the reduced function of homologous recombination and errors in double-strand break repair. The overexpression of progerin resulted in an induction of endothelial cell dysfunction characterized by increased inflammation, oxidative stress along with persistent DNA damage, an elevated expression of cell cycle arrest proteins, and cellular senescence. Prevention of DNA replication stress by CHK1 leads to chemoresistance despite a DNA repair defect in homologous recombination in breast cancer.

Background Postoperative dysphagia has been reported to occur as the result of narrowing of the pharyngeal airway space (PAS) due to a change in the alignment of the cervical spine. This study aimed to investigate potential risk factors for postoperative PAS obstruction following corrective surgery for dropped head syndrome (DHS) by analyzing clinical and radiographic parameters. Methods This retrospective design included 42 patients (7 men, 35 women; mean age, 71.5 years) who underwent corrective surgery for DHS. The following measurements were obtained: narrowest PAS (nPAS), cervical vertebra 2 (C2)–7 angle, occipito (O)–C1 angle, C1–2 angle, and swallowing line (S-line). The correlations between the postoperative nPAS and clinical and radiographic factors were assessed. Logistic regression analysis was used to analyze the specific factors for the occurrence of postoperative dysphagia. ROC analysis was also used to determine the cut-off values. P - values < 0.05 were considered statistically significant. Results The mean preoperative nPAS was 15.0 ± 4.1 mm, which significantly decreased to 11.4 ± 3.6 mm postoperatively. The mean preoperative O-C1 angle was 7.8 ± 7.1°, which decreased to −7.2 ± 6.6° postoperatively. The mean pre- and postoperative C1–2 angles were 38.9 ± 5.8° and 34.8 ± 5.8°, respectively. Among this cohort, the mean nPAS of patients with S-line(-) was significantly smaller (8.5 ± 2.5 mm) than that of those with S-line(+) (11.7 ± 3.6 mm). Postoperative nPAS was correlated with O–C1 angle ( r  = 0.55, P  < 0.015). Forward stepwise multivariate logistic regression showed that C0-1 angle (odds ratio (OR: 5.774) was the most impactable factor for the occurrence of postoperative dysphagia. ROC analysis revealed that the cut-off value for the occurrence of postoperative dysphagia was nPAS of 10.78 mm. Conclusion The reduction of the O–C1 angle as a reciprocal change after the surgical correction of mid/lower cervical spine kyphosis for DHS may be a key factor in the occurrence of postoperative dysphagia due to airway obstruction.

Although pancreatic cancer often invades peripancreatic adipose tissue, little information is known about cancer‐adipocyte interaction. We first investigated the ability of adipocytes to de‐differentiate to cancer‐associated adipocytes (CAAs) by co‐culturing with pancreatic cancer cells. We then examined the effects of CAA‐conditioned medium (CAA‐CM) on the malignant characteristics of cancer cells, the mechanism underlying those effects, and their clinical relevance in pancreatic cancer. When 3T3‐L1 adipocytes were co‐cultured with pancreatic cancer cells (PANC‐1) using the Transwell system, adipocytes lost their lipid droplets and changed morphologically to fibroblast‐like cells (CAA). Adipocyte‐specific marker mRNA levels significantly decreased but those of fibroblast‐specific markers appeared, characteristic findings of CAA, as revealed by real‐time PCR. When PANC‐1 cells were cultured with CAA‐CM, significantly higher migration/invasion capability, chemoresistance, and epithelial‐mesenchymal transition (EMT) properties were observed compared with control cells. To investigate the mechanism underlying these effects, we performed microarray analysis of PANC‐1 cells cultured with CAA‐CM and found a 78.5‐fold higher expression of SAA1 compared with control cells. When the SAA1 gene in PANC‐1 cells was knocked down with SAA1 siRNA, migration/invasion capability, chemoresistance, and EMT properties were significantly attenuated compared with control cells. Immunohistochemical analysis on human pancreatic cancer tissues revealed positive SAA1 expression in 46/61 (75.4%). Overall survival in the SAA1‐positive group was significantly shorter than in the SAA1‐negative group (P = .013). In conclusion, we demonstrated that pancreatic cancer cells induced de‐differentiation in adipocytes toward CAA, and that CAA promoted malignant characteristics of pancreatic cancer via SAA1 expression, suggesting that SAA1 is a novel therapeutic target in pancreatic cancer. Cancer‐associated adipocyte (CAA) promotes migration/invasion of pancreatic cancer cells. CAA also induced pancreatic cancer cells drug resistance, epithelial‐mesenchymal transition.

Emerging preclinical evidence suggests the involvement of sex hormones and their receptor signals in the development and progression of bladder cancer. Meanwhile, previous studies have demonstrated conflicting results on the relationship between the status of sex hormone receptors in urothelial tumors and histopathological characteristics of the tumors or patient outcomes. We therefore conducted this meta-analysis to assess the clinicopathological impact of the expression of androgen receptor (AR) and estrogen receptors (ERs) in bladder cancer. A comprehensive literature search in databases (i.e. PubMed, Web of Science, Cochrane) was performed for all immunohistochemical studies stained for AR, ERα, and/or ERβ in surgically resected bladder cancer specimens and analyzed for patient outcomes. We selected eligible studies in accordance with the PRISMA guidelines and analyzed data using R software. A total of 2,049 patients from 13 retrospective studies were included in this meta-analysis. The difference in ERα expression between non-tumors and tumors was significant [odds ratio (OR) = 0.412; P<0.001], while those of AR (OR = 3.256; P = 0.336) or ERβ (OR = 0.580; P = 0.674) were not statistically significant. AR positivity in tumors was strongly correlated with gender (male vs. female: OR = 0.658; P = 0.027) or tumor grade (low-grade vs. high-grade: OR = 0.575; P<0.001). ERβ positive rates were significantly higher in high-grade (OR = 2.169; P<0.001) and muscle-invasive (OR = 3.104; P<0.001) tumors than in low-grade and non-muscle-invasive tumors, respectively. Survival analysis in patients with non-muscle-invasive bladder cancer revealed associations between AR expression and better recurrence-free survival [hazard ration (HR) = 0.593; P = 0.006) as well as between ERβ expression and worse recurrence-free (HR = 1.573; P = 0.013) or progression-free (HR = 4.148; P = 0.089) survivals. These data suggest down-regulation of ERα expression in bladder tumors, compared with non-neoplastic urothelial tissues. AR or ERβ expression was down- or up-regulated, respectively, in high-grade and/or muscle-invasive bladder cancers. Moreover, immunohistochemistry of AR/ERβ in surgical specimens may serve as prognosticators in patients with non-muscle-invasive bladder tumor.

PurposePrevious reports on the outcome of conservative treatment for dropped head syndrome (DHS) are scarce. The purpose of this study was to elucidate the efficacy of conservative treatment for DHS and to identify possible predictive factors relating to the outcome.MethodsAmong 76 DHS patients, conservative treatment (2–3 months collar application, active neck range of motion exercise, and occasional prescription of analgesics) succeeded in 17 patients (22.4%, group S, 4 male, 13 female, mean age 75.9 years). The treatment failed in the remaining 59 patients (group F). Clinical and radiological parameters were compared between the groups. Radiological findings of group S were compared between before treatment and at follow-up.ResultsDuration of disease was 6.6 ± 9.3 months in group S and 20.0 ± 27.6 months in group F. C2-7 angle (degree), the incidence of anterior slippage of the vertebra (%), reducibility (%), and upper thoracic kyphosis angle (degree) in group S/F were − 19.2 ± 17.5/− 34.6 ± 26.6, 23.5/62.7, 100/52, and 6.7 ± 8.6/17.9 ± 13.7, respectively. C2-7 angles were − 19.2 ± 17.5 degrees at pre-treatment and 10.2 ± 20.7 degrees at follow-up. These differences were statistically significant.ConclusionsThe present study indicated that conservative treatment was successful in 22% of DHS patients, with improvement in their cervical kyphotic alignment. Shorter duration of disease, relatively smaller cervical kyphosis without anterior slippage of the vertebra, reducibility, and abundant compensation at the upper thoracic region were good indications for the success of conservative treatment.

Although right‐sided colorectal cancer (CRC) shows a worse prognosis than left‐sided CRC, the underlying mechanism remains unclear. We established patient‐derived organoids (PDOs) from left‐ and right‐sided CRCs and directly compared cell proliferation and invasion capability between them. We then analyzed the expression of numerous genes in signal transduction pathways to clarify the mechanism of the differential prognosis. Cell proliferation activity and invasion capability in right‐sided cancer PDOs were significantly higher than in left‐sided cancer PDOs and normal PDOs, as revealed by Cell Titer Glo and transwell assays, respectively. We then used quantitative RT‐PCR to compare 184 genes in 30 pathways among right‐sided and left‐sided cancer and normal PDOs and found that the TIMP1 mRNA level was highest in right‐sided PDOs. TIMP1 protein levels were upregulated in right‐sided PDOs compared with normal PDOs but was downregulated in left‐sided PDOs. TIMP1 knockdown with shRNA significantly decreased cell proliferation activity and invasion capability in right‐sided PDOs but not in left‐sided PDOs. Moreover, TIMP1 knockdown significantly decreased pFAK and pAkt expression levels in right‐sided PDOs but not in left‐sided PDOs. A database analysis of The Cancer Genome Atlas revealed that TIMP1 expression in right‐sided CRCs was significantly higher than in left‐sided CRCs. Kaplan–Meier survival analysis showed significantly shorter overall survival in high‐TIMP1 patients versus low‐TIMP1 patients with right‐sided CRCs but not left‐sided CRCs. Our data suggest that TIMP1 is overexpressed in right‐sided CRCs and promotes cell proliferation and invasion capability through the TIMP1/FAK/Akt pathway, leading to a poor prognosis. The TIMP1/FAK/Akt pathway can be a target for therapeutic agents in right‐sided CRCs. Our study suggests that TIMP1 is overexpressed in the right‐sided colorectal cancer, and promotes cell proliferation and invasion capability through TIMP1/FAK/Akt pathway, leading to poor prognosis.

Emerging preclinical findings have indicated that steroid hormone receptor signaling plays an important role in bladder cancer outgrowth. In particular, androgen-mediated androgen receptor signals have been shown to correlate with the promotion of tumor development and progression, which may clearly explain some sex-specific differences in bladder cancer. This review summarizes and discusses the available data, suggesting the involvement of androgens and/or the androgen receptor pathways in urothelial carcinogenesis as well as tumor growth. While the precise mechanisms of the functions of the androgen receptor in urothelial cells remain far from being fully understood, current evidence may offer chemopreventive or therapeutic options, using androgen deprivation therapy, in patients with bladder cancer.

Emerging evidence has suggested that androgen receptor signaling plays an important role in ovarian cancer outgrowth. Specifically, androgen receptor activation appears to be associated with increased risks of developing ovarian cancer and inducing tumor progression. However, conflicting findings have also been reported. This review summarizes and discusses the available data indicating the involvement of androgens as well as androgen receptor and related signals in ovarian carcinogenesis and cancer growth. Although the underlying molecular mechanisms for androgen receptor functions in ovarian cancer remain far from being fully understood, current observations may offer effective chemopreventive and therapeutic approaches, via modulation of androgen receptor activity, against ovarian cancer. Indeed, several clinical trials have been conducted to determine the efficacy of androgen deprivation therapy in patients with ovarian cancer.