scholarly journals Mortality Risk factors and SOX2 and mTOR expression in Patients with Esophageal Cancer

2022 ◽  
Vol 67 (4) ◽  
pp. 346-357
Author(s):  
Gao Yu ◽  
Yang Yuexin ◽  
Lv Yin ◽  
Zhang Yiyin ◽  
Kang Mei ◽  
...  

Causes of mortality in EC patients are not confined to cancer-specific mortality but include various protein expressions of SOX2 and mTOR in Esophageal Cancer patients and their correlation with the clinical stage. Data about the risk factors and involvement of cancer-specific protein are still lacking. This study aimed to define the risk factors and association of SOX2 and mTOR expression in mortality in patients with EC. We conducted a retrospective cohort study to assess the risk factors for cancer-specific mortality and cardiovascular mortality in patients with esophageal cancer (EC). The expression rates of SOX2, as well as MTO, were checked in patients. The multivariate analysis revealed a high-risk EC mortality with age ≥ 65 years, black race, grade, stage, and sequence of treatment; radiation after surgery; radiation before and after surgery; Surgery both before and after radiation. While the cardiovascular mortality increased with age ≥ 65 years, adenocarcinoma type, grade, stage, and sequence of treatment. The expression rates of SOX2, as well as mTOR, were 75.5 percent and 86.8 percent in Esophageal Cancer, while were 10.7 percent and 7.5 percent in osteochondroma, respectively, which was statistically significant (P<0.05). Risk factors for cancer-specific mortality and cardiovascular mortality in EC patients include older age at diagnosis, male sex, non-married status, grade III of the tumor, the regional or distant spread of the tumor, no cancer-directed therapy. The expression levels of SOX2, mTOR, and the total survival time were related to the different stages. It shows an upward trend for the expression levels of mTOR and SOX2 in Esophageal Cancer tissues. The expression levels of SOX2 and mTOR are related to the clinical stage, metastasis, and prognosis.

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Alaa Ahmed Elshanbary ◽  
Mohamed Sayed Zaazouee ◽  
Mohamed Abdelmonem ◽  
Yasmine Adel Mohammed ◽  
Walid Abdel-Aziz

2017 ◽  
Vol 35 (29) ◽  
pp. 3290-3297 ◽  
Author(s):  
Signe Benzon Larsen ◽  
Christian Dehlendorff ◽  
Charlotte Skriver ◽  
Susanne Oksbjerg Dalton ◽  
Christina Gade Jespersen ◽  
...  

Purpose Increasing evidence indicates that statin use may reduce mortality from prostate cancer. In this work, we examined whether postdiagnosis statin use was associated with reduced cancer-specific mortality or all-cause mortality among patients with prostate cancer in Denmark. Material and Methods From nationwide Danish registries, we identified all patients with incident prostate adenocarcinoma from 1998 to 2011 and retrieved data on tumor and patient characteristics, drug use, and primary treatment. We defined postdiagnosis use (two or more prescriptions) of statins as a time-varying covariate with 1-year lag. Cox proportional hazards regression models used to compute hazard ratios (HRs) for prostate cancer–specific mortality and all-cause mortality through 2013 associated with postdiagnosis statin use. In secondary and sensitivity analyses, we assessed statin use within exposure periods of 1 year or 5 years after prostate cancer diagnosis and evaluated the influence of prediagnosis statin use. Results Among 31,790 patients, 7,365 died of prostate cancer and 11,811 died from other causes during a median follow-up of 2.8 years (interquartile range, 1.3 to 5.1 years) from 1 year after diagnosis. Postdiagnosis statin use was associated with adjusted HRs of 0.83 (95% CI, 0.77 to 0.89) for prostate cancer mortality and 0.81 (95% CI, 0.76 to 0.85) for all-cause mortality. Similar results were observed in 1-year and 5-year sensitivity analyses. No substantial effect measure modification was found with estimated dose or type of statin, clinical stage, Gleason score, or with prediagnosis statin use; however, patients who were diagnosed early in the study period or who underwent radical prostatectomy or endocrine therapy exhibited slightly lower HRs for prostate cancer mortality with postdiagnosis statin use than did those in the overall analyses. Conclusion Postdiagnosis statin use was associated with reduced mortality from prostate cancer; however, it remains to be established whether this association is causal.


Cancers ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 252 ◽  
Author(s):  
Kentaro Inamura ◽  
Yasuyuki Shigematsu ◽  
Hironori Ninomiya ◽  
Yasuhiro Nakashima ◽  
Maki Kobayashi ◽  
...  

CSF1R-expressing tumor-associated macrophages (TAMs) induce a tumor-promoting microenvironment by regulating immunity. Evidence demonstrates that the expression and single nucleotide polymorphisms of CSF1R relate with survival and risk of lung cancer in never smokers. However, no previous studies have examined the association of CSF1R expression in TAMs with mortality or whether the prognostic association differs according to smoking status in lung adenocarcinoma. Quantitative phosphor-integrated dot staining was used to precisely assess CSF1R expression in TAMs. Using 195 consecutive cases of lung adenocarcinoma, we examined the association of CSF1R expression with mortality and whether the prognostic association differs according to smoking status. We observed high expression levels of CSF1R in TAMs in 65 of 195 (33%) cases of lung adenocarcinoma. High expression levels of CSF1R were associated with high lung cancer-specific mortality (log-rank p = 0.037; hazard ratio (HR) = 1.61, 95% confidence interval (CI) = 1.02−2.52, p = 0.043). This prognostic association differed according to smoking status (p for interaction = 0.049, between never-smoking and ever-smoking patients). The association between high expression levels of CSF1R and lung cancer-specific mortality was stronger in never-smoking patients (log-rank p = 0.0027; HR = 2.90, 95% CI = 1.41−6.11, p = 0.0041) than in ever-smoking patients (log-rank p = 0.73; HR = 1.11, 95% CI = 0.59−2.00, p = 0.73). The findings suggest that CSF1R-expressing TAMs may exert stronger tumor-promoting immunity in never-smoking patients with lung adenocarcinoma and serve as a therapeutic target in precision immunotherapies.


2021 ◽  
Author(s):  
Qikun Liu ◽  
Xiaojun Yu ◽  
Mengwei Li ◽  
Zhiwei Li ◽  
Yongqiao Jiang ◽  
...  

Abstract Background: To determine the risk factors for lymph node metastasis (LNM) of soft tissue sarcomas (STS) of the head, neck, and extremities, and the clinical outcome of negative lymph node dissection (NLND). Methods: We pooled patients of STS using the Surveillance, Epidemiology, and End Results (SEER) database from 1988 to 2015. Logistics regression analysis to identify risk factors for LNM, the Cox proportional hazards model and Fine-Grey’s model were used for survival analysis, Propensity score matching analysis (PSM) was further used to clarify the impact of NLND on patient prognosis.Results: A total of 3,276 patients were enrolled in our study, of whom 283 (8.6%) developed LNM. Rhabdomyosarcoma had the highest rate of LNM (25.3%), followed by clear cell sarcoma (16.8%) and epithelioid sarcoma (12.4%), while leiomyosarcoma had the lowest rate of LNM (1.3%). Sex, tumor size, grade, histology, and site were significantly associated with LNM. Age, tumor size, grade, stage, histology, and marital status were independent prognostic factors for the cancer-specific survival for patients without LNM. For specific histologic subtypes of STS, NLND significantly improves overall survival (HR: 0.718, 95%CI, 0.535-0.962; P=0.026) and cancer-specific survival (HR: 0.699, 95%CI, 0.506-0.967; P=0.031) and reduces cancer-specific mortality (Gray’s test, P=0.017). However, for patients with leiomyosarcoma, NLND did not improve overall survival (P=0.46) or reduce cancer-specific mortality (Gray’s test, P=0.772).Conclusions: We identified the rate of LNM and risk factors for LNM in STS of the head, neck and extremities. In addition, prophylactic NLND treatment is necessary and has a clinical benefit for patients with STS who are at high risk for LNM, but has no significant impact on the prognosis of patients with leiomyosarcoma.


BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Peipei Liu ◽  
Úna C. McMenamin ◽  
Andrew D. Spence ◽  
Brian T. Johnston ◽  
Helen G. Coleman ◽  
...  

Abstract Background Pre-clinical studies have shown that furosemide slows cancer cell growth by acting on the Na-K-2Cl transporter, particularly for gastric cancer cells. However, epidemiological studies have not investigated furosemide use and mortality in gastroesophageal cancer patients. Consequently, we conducted a population-based study to investigate whether furosemide use is associated with reduced cancer-specific mortality in esophageal/gastric cancer patients. Methods A cohort of patients newly diagnosed with esophageal or gastric cancer between 1998 and 2013 were identified from English cancer registries and linked to the Clinical Practice Research Datalink to provide prescription records and the Office of National Statistics to provide death data up to September 2015. Time-dependant Cox-regression models were used to calculate hazard ratios (HRs) comparing cancer-specific mortality in furosemide users with non-users. Analyses were repeated restricting to patients with common furosemide indications (heart failure, myocardial infarction, edema or hypertension) to reduce potential confounding. Results The cohort contained 2708 esophageal cancer patients and 2377 gastric cancer patients, amongst whom 1844 and 1467 cancer-specific deaths occurred, respectively. Furosemide use was not associated with reduced cancer-specific mortality overall (adjusted HR in esophageal cancer = 1.28, 95% CI 1.10, 1.50 and in gastric cancer = 1.27, 95% CI 1.08, 1.50) or when restricted to patients with furosemide indications before cancer diagnosis (adjusted HR in esophageal cancer = 1.07, 95% CI 0.88, 1.30 and in gastric cancer = 1.18, 95% CI 0.96, 1.46). Conclusions In this large population-based cohort study, furosemide was not associated with reduced cancer-specific mortality in patients with esophageal or gastric cancer.


1977 ◽  
Vol 5 (3) ◽  
pp. 137-140 ◽  
Author(s):  
Olof Lannerstad ◽  
Nils-Herman Sternby ◽  
Sven-Olof Isacsson ◽  
Gunnar Lindgren ◽  
Sven-Eric Lindell

All men born in even-numbered months in 1914 and domiciled in Malmö were invited in 1969 to participate in an investigation regarding risk factors for cardiovascular disease. Individuals with a blood pressure of 165/110 and over were treated and a sub-sample of heavy smokers were later invited to take part in a quit-smoking project. During the following five year period total and cause-specific mortality in the examined group was compared with corresponding data for men born in uneven months in 1914. Mortality in the examined cohort was lower than among controls and differed significantly from that in the control group with regard to cardiovascular mortality.


2015 ◽  
Vol 33 (3_suppl) ◽  
pp. 43-43 ◽  
Author(s):  
Sayako Yuda ◽  
Ken Kato ◽  
Yusuke Sasaki ◽  
Naoki Takahashi ◽  
Hirokazu Shoji ◽  
...  

43 Background: Although adding docetaxel to cisplatin plus 5-fluorouracil (i.e. the DCF regimen) for esophageal cancer treatment may improve outcomes, this regimen has increased toxicity. However, the risk factors for severe non-hematological toxicities remain unknown. Methods: We analyzed data on esophageal cancer patients given at least one cycle of DCF between July 2009 and April 2014 at the National Cancer Center Hospital, Japan. DCF consisted of docetaxel 70 mg/m2/day (day 1), cisplatin 70 mg/m2/day (day 1), and continuous infusion of 5-fluorouracil 750 mg/m2/day (days 1–5), repeated every 3 weeks. Data on adverse events developing within three cycles were collected from medical records. Risk factors for severe adverse events were analyzed. Results: One hundred patients were enrolled, with a median age of 63 (range, 37 to 76); 81 male and 19 female; 96 squamous cell carcinomas and 4 adenocarcinomas; clinical situation neoadjuvant/induction/palliative: 69/23/8/1; clinical stage I/II/III/IV: 1/12/64/23; and performance status (PS) 0/1/2: 44/55/1. Forty patients (40%) developed grade 3 or more non-hematological adverse events, including anorexia (12%), mucositis (6%), and esophagitis (2%); 45 developed grade 4 hematological adverse events. Seventeen experienced febrile neutropenia (FN). There was one case of treatment-related death from serious infection. In multivariate analysis, age≥63 was at significantly increased risk of FN (P=0.013). Conclusions: DCF chemotherapy was safe in most patients and its toxicity was controllable. However, elderly patients may suffer from intense toxicity during DCF therapy.


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