Background Primary acinar cell carcinoma (ACC) is a rare exocrine tumor of the pancreas with unclear clinical characteristics. Our goal was to determine the incidence and update the clinical characteristics and outcomes of ACC. Methods Through the Surveillance, Epidemiology, and End Results (SEER) database, we identified 252 patients with the latest diagnosis of ACC (2004–2016). The age-adjusted incidence (AAI) was calculated using the SEER*Stat Software version 8.3.6. The Kaplan–Meier method was used to draw survival curves and differences among them were compared by the log-rank test. Cox proportional hazards models were used to evaluate factors that had independent predictive effects on the overall survival. Results The AAI of pancreatic ACC was on the rise with the mean age at diagnosis of 63.79±14.79 years. Most patients (15.9%) had poorer differentiated tumors. The patients presented with distant stage were 54.4% compared with 53.1% between 1988 and 2003. The 1-, 2-, and 5-years survival rates for pancreatic ACC patients were 53.5%, 34.6%,17.5%, respectively (compared with 78.5%, 67.0%, and 42.8%, between 1988 and 2003). The multivariate COX analysis showed that the patient's age, surgery, chemotherapy, and summary stage, but not marital status were independent prognosis factors for ACC. Conclusions Pancreatic ACC is a highly malignant tumor with an increasing incidence in recent years. The rate of distant metastasis is increasing and the survival rate is worse than in the past, suggesting that it may require more aggressive treatment and follow-up. Surgery, radiotherapy, and chemotherapy are all effective treatments, but prospective studies are still needed to verify them.
A vast majority of colorectal cancer (CRC) patients with microsatellite stability (MSS) or proficient mismatch repair (pMMR) are refractory to immunotherapeutic strategies. The current research focusses on the combined treatment strategies for identification and optimization in order to improve the efficacy of immunotherapy among patients with microsatellite stability (MSS), who account for the majority of metastatic colorectal cancer (mCRC) cases. mCRC patients harboring MSS and the BRAFV600E mutation show a worse prognosis and barely benefit from immunotherapy. In this report, we discuss the case of a mCRC patient with MSS and BRAFV600E mutation, who exhibited significant response to the combined treatment with nivolumab and bevacizumab, and has been exhibiting a progression-free survival (PFS) of more than 17 months. Our findings indicate that combined anti-angiogenic therapy can improve the efficacy of immunotherapy, which results in the prolong survival of the patient. This is a case report on MSS and BRAFV600E colorectal cancer which presents with a response to immunotherapy and anti-angiogenic therapy.
Background Pancreatic signet ring cell carcinoma (PSRCC) is a rare tumour subtype with poorly understood epidemiological characteristics and prognosis. We attempted to comprehensively characterise the epidemiology and survival outcomes of PSRCC. Methods Patients diagnosed with PSRCC between 2000 and 2018 were identified using Surveillance, Epidemiology and End Results Stat 8.3.9.2 software. Age-adjusted incidence and survival were calculated. Survival curves were plotted using the Kaplan–Meier method, and the differences between survival curves were compared using the log-rank test. Cox proportional hazards models were used to evaluate factors that independently predict overall survival. The primary analysis was a complete case analysis; multiple imputations were employed in a sensitivity analysis. Results We identified 585 eligible patients with PSRCC. The overall annual incidence from 2000 to 2018 was 0.349 (95% CI, 0.321–0.379) per million population. The incidence increased significantly in patients over 55 years of age and peaked at about 80 years of age (2.12 per million). Males and Black patients had the highest incidence. The observed survival rates at 1, 2 and 5 years were 20.1, 8.3 and 3.4%, respectively. Survival analysis revealed that primary surgery and chemotherapy are effective treatments for patients with PSRCC (P < 0.05). According to multivariate Cox regression analysis, early stage and receiving surgery and chemotherapy were favourable factors (P < 0.05). Similar conclusions were drawn from the interpolated data. Conclusions PSRCC is a highly malignant tumour that predominates in elderly, male and Black patients. The prognosis is poor with a 5-year survival rate of 3.4%; however, multivariate analysis and adjusted models accounting for missing data revealed that early diagnosis, surgery and chemotherapy are effective in improving the prognosis.
BackgroundMetastatic pancreatic cancer (mPC) is a highly lethal malignancy with poorer survival. However, chemotherapy alone was unable to maintain long‐term survival. This study aimed to evaluate the individualized survival benefits of pancreatectomy plus chemotherapy (PCT) for mPC.MethodsA total of 4546 patients with mPC from 2004 to 2015 were retrieved from the Surveillance, Epidemiology, and End Results database. The survival curve was calculated using the Kaplan-Meier method and differences in survival curves were tested using log-rank tests. Cox proportional hazards regression analyses were performed to evaluate the prognostic value of involved variables. A new nomogram was constructed to predict overall survival based on independent prognosis factors. The performance of the nomogram was measured by concordance index, calibration plot, and area under the receiver operating characteristic curve.ResultsCompared to pancreatectomy or chemotherapy alone, PCT can significantly improve the prognosis of patients with mPC. In addition, patients with well/moderately differentiated tumors, age ≤66 years, tumor size ≤42 mm, or female patients were more likely to benefit from PCT. Multivariate analysis showed that age at diagnosis, sex, marital status, grade, tumor size, and treatment were independent prognostic factors. The established nomogram has a good ability to distinguish and calibrating.ConclusionPCT can prolong survival in some patients with mPC. Our nomogram can individualize predict OS of pancreatectomy combined with chemotherapy in patients with concurrent mPC.
IntroductionPrevious observational studies have reported that thyroid dysfunction is associated with hallux valgus (HV). However, the causal effect of thyroid dysfunction on hallux valgus is still unknown. To assess whether there is a causal relationship between thyroid dysfunction and hallux valgus, we performed a two-sample Mendelian randomization (MR) study.MethodsThe data of the two-sample Mendelian randomization study were obtained from public databases. In this study, hypothyroidism, hyperthyroidism, free thyroxine (FT4), and thyrotropin (TSH) were chosen as exposures. The single nucleotide polymorphisms (SNP) of hypothyroidism and hyperthyroidism were from the genome-wide association studies (GWAS) of the IEU database, including 337,159 subjects. Data for FT4 and TSH (72,167 subjects) were extracted from the ThyroidOmics Consortium. HV was used as the outcome. The SNPs associated with HV were selected from a GWAS of 202,617 individuals in the fignngen database. The inverse variance weighted (IVW) method was used as the primary analysis. Four complementary methods were applied, including MR-presso, MR-Egger, and weighted median. In addition, Cochran’s Q test, MR-presso, MR-Egger regression, and the leave-one-out test were used as sensitivity analysis, and the MR-pleiotropy test was performed to examine pleiotropy.ResultsAccording to the results of IVW, we found that there was a causal relationship between hypothyroidism and HV, and hypothyroidism increased the incidence of HV (OR = 2.838 (95% CI: 1.116–7.213); p = 0.028). There were no significant causal effects of hyperthyroidism, FT4, and TSH on HV (p > 0.05). Sensitivity analyses showed that the results were robust and reliable, and no horizontal pleiotropy was detected.ConclusionsOur findings provided genetic support that hypothyroidism might increase the risk of HV. It will predict the occurrence of HV in patients with hypothyroidism and provide suggestions for early prevention and intervention.
Observational studies have suggested a positive association between gastroesophageal reflux disease and lung cancer, but due to the existence of confounders, it remains undetermined whether gastroesophageal reflux disease (GERD) has a causal association with lung cancer. Therefore, Mendelian randomization (MR) analyses were applied to investigate the relationship between the two conditions. Two-sample Mendelian randomization analysis was utilized with summary genetic data from the European Bioinformatics Institute (602,604 individuals) and International Lung Cancer Consortium, which provides information on lung cancer and its histological subgroups. Furthermore, we used two-step Mendelian randomization and multivariable Mendelian randomization to estimate whether smoking initiation (311,629 cases and 321,173 controls) and alcohol intake frequency (n = 462,346) mediate any effect of gastroesophageal reflux disease on lung cancer risk. The Mendelian randomization analyses indicated that gastroesophageal reflux disease was associated with and significantly increased the risk of lung cancer (ORIVW = 1.35, 95% CI = 1.18–1.54; p = 1.36 × 10–5). Smoking initiation and alcohol intake frequency mediated 35% and 3% of the total effect of gastroesophageal reflux disease on lung cancer, respectively. The combined effect of these two factors accounted for 60% of the total effect. In conclusion, gastroesophageal reflux disease is associated with an increased risk of lung cancer, and interventions to reduce smoking and alcohol intake may reduce the incidence of lung cancer.
Cancer is a complex disease with several distinct characteristics, referred to as “cancer markers” one of which is metabolic reprogramming, which is a common feature that drives cancer progression. Over the last ten years, researchers have focused on the reprogramming of glucose metabolism in cancer. In cancer, the oxidative phosphorylation metabolic pathway is converted into the glycolytic pathway in order to meet the growth requirements of cancer cells, thereby creating a microenvironment that promotes cancer progression. The precise mechanism of glucose metabolism in cancer cells is still unknown, but it is thought to involve the aberrant levels of metabolic enzymes, the influence of the tumor microenvironment (TME), and the activation of tumor-promoting signaling pathways. It is suggested that glucose metabolism is strongly linked to cancer progression because it provides energy to cancer cells and interferes with antitumor drug pharmacodynamics. Therefore, it is critical to unravel the mechanism of glucose metabolism in tumors in order to gain a better understanding of tumorigenesis and to lay the groundwork for future research into the identification of novel diagnostic markers and therapeutic targets for cancer treatment. Traditional Chinese Medicine (TCM) has the characteristics of multiple targets, multiple components, and less toxic side effects and has unique advantages in tumor treatment. In recent years, researchers have found that a variety of Chinese medicine monomers and compound recipes play an antitumor role by interfering with the reprogramming of tumor metabolism. The underlying mechanisms of metabolism reprogramming of tumor cells and the role of TCM in regulating glucose metabolism are reviewed in this study, so as to provide a new idea for antitumor research in Chinese medicine.
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