European Journal of Cancer Prevention最新文献

Pleural mesothelioma is a rare and aggressive cancer that affects the pleura. In recent years, there has been increasing interest and attention in detecting and diagnosing early-stage or precancerous forms of mesothelioma because of its severe prognosis and short life expectancy at the time of diagnosis. Mesothelioma in situ represents a clear opportunity to improve and innovate the diagnostic approach and the multimodality treatment of mesothelioma: the diagnosis of pleural mesothelioma at the 'in-situ phase' means early disease detection and thus paves the way to new possible curable strategies. Since 2021, when mesothelioma in situ was finally identified and described as a new histological entity, its diagnosis and management became a challenge and the subject of ongoing research; several aspects remain open and still outstanding as regards diagnostic techniques, time and probability of progression, need for and methods of follow up, aggressive and early surgery. This narrative review aims to provide a comprehensive overview of mesothelioma in situ covering its definition, risk factors, diagnostic criteria, and tricky aspects of early detection. It also highlights its clinical significance, new perspectives, and potential future indications in the context of pleural mesothelioma multidisciplinary management.

Oral cancer is a public health problem worldwide. Late diagnosis results in a low survival rate. However, this tumor can arise from oral precancerous lesions and identification of biomarkers in precursor lesions has the potential for early diagnosis, improving patient survival. In this context, proteins involved in the cell cycle control are potentially promising. This study aimed to evaluate the importance of immunohistochemical expression of BUBR1, MCM2, and GMNN as biomarkers of oral carcinogenesis considering different oral sites. Sixty-six samples of oral epithelial dysplasia (from 33 males and 33 females) and 63 samples of oral squamous cell carcinoma (from 44 males and 19 females) were subjected to immunohistochemistry to detect some human proteins. Ki67 expression was included as a marker of cell proliferation. Marker expression was quantified by manually counting at least 1000 cells, and the labeling index was used in all statistical analyses. GMNN, MCM2, BUBR1 (nuclear and cytoplasmic labeling), and Ki67 expression levels were higher in carcinomas than in dysplasia (P < 0.05). Cytoplasmic BUBR1 was a good marker of malignancy (AUC = 0.8525, P < 0.05), but Ki67 was not (AUC = 0.5943, P = 0.0713). GMNN, MCM2, BUBR1, and Ki67 had higher expression in carcinoma than in dysplasia, regardless of the site of the lesion. Cytoplasmic BUBR1 has the potential to be used as a marker of tumor progression.

Studies on the association between passive smoking and head and neck cancer (HNC) are controversial. This meta-analysis aimed to explore this association. A systematic search of the PubMed, Embase, Web of Science, and Cochrane Library databases was conducted up to July 2024 to identify relevant studies. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated using the DerSimonian-Laird random-effects model. Heterogeneity among studies was assessed, and the risk of bias was evaluated. A total of 1036 records were identified, of which 17 studies were included. Passive smoking was significantly associated with an increased risk of HNC overall (OR = 1.70, 95% CI: 1.27-2.28, P < 0.001). The association was particularly strong for oral cancer (OR = 1.85, 95% CI: 1.07-3.17, P = 0.026), oropharyngeal cancer (OR = 2.78, 95% CI: 1.29-5.98, P = 0.009), laryngeal cancer (OR = 1.60, 95% CI: 1.24-2.06, P < 0.001), and hypopharyngeal cancer (OR = 2.60, 95% CI: 1.45-4.66, P = 0.001). No significant association was observed for nasopharyngeal carcinoma (OR = 1.14, 95% CI: 0.78-1.66, P = 0.498). Geographically, the risk was elevated among both Asian and European populations. Passive smoking is associated with an increased risk of HNC, particularly for subtypes such as oral, oropharyngeal, laryngeal, and hypopharyngeal cancers. These findings underscore the importance of mitigating exposure to passive smoking as a public health measure.

Carriers with germline breast cancer 1/2 gene mutations (BRCAm) are likely to develop ovarian cancer (OC). Therefore, identifying these mutations may enable individualized therapy for OC and preventive measures to reduce OC risk in BRCAm carrier families. Thus, we investigated the prevalence of BRCAm in OC patients from Yunnan Province in Southwest China. In total, 674 unselected OC patients were enrolled and tested for BRCAm via next-generation sequencing. Data on clinicopathological characteristics and personal/family history of cancer were collected. The prevalence rates of pathogenic/likely pathogenic BRCAm were 26.6% overall, 20.8% among BRCA1m carriers, 5.5% among BRCA2m carriers, and 0.3% among carriers of both BRCA1m and BRCA2m. The most common pathogenic mutation in the BRCA1 gene was c.5114T>C (n = 9). The number of BRCAm carriers was significantly greater among patients with serous cancer, a personal tumor history, a family history of hereditary breast and ovarian cancer (HBOC)-related tumors, and bilateral tumors. The most common pathogenic mutation in this cohort was c.5114T>C (n = 9) in BRCA1. The prevalence and spectrum of BRCAm in OC patients from Yunnan Province are different from those in other groups. BRCA status testing is advised for all OC patients, particularly those with a family history of HBOC.

Lynch syndrome accounts for 3-5% of all colorectal and endometrial cancer cases, and suboptimal management of Lynch syndrome in the Middle East resulted in the underdiagnosis of mutation carriers. Probands from 24 unrelated Iranian families with a history of cancer(s) suggestive of Lynch syndrome underwent microsatellite instability analysis or immunohistochemistry, multigene panel testing, copy number variation detection, or multiplex ligation-dependent probe amplification. Pathogenic variants were identified in five patients (21%), including three in MSH2, one in MSH6, and one in PMS2. Microsatellite instability analysis showed the lengths of the CAT25 marker in tumor and normal samples were 149 and 148 bp, respectively. Among 21 family members with Lynch syndrome in the MSH2 gene, identified from the three families who previously underwent cascade screening, colorectal and endometrial cancers were the most frequent. While 66% of patients had insurance that included coverage for mutation carrier screening, only one insurance provider extended coverage for next-generation sequencing. Special attention to probands and telematic management of at-risk relatives to organize blood sample collection at their convenience enhanced cascade testing 20-fold per proband. In conclusion, the age of onset and segregation analysis indicated that PMS1 may not be a cancer susceptibility gene, and the tumor spectrum in MSH2 pathogenic carriers is similar to Western countries. Collecting blood samples at patients' convenience is a possible strategy to reduce the cost of identifying Lynch syndrome through cascade testing. The genetic analysis of patients for inherited cancers would optimize the current management of Lynch syndrome in Iran by omitting noncarriers from surveillance programs.

Previous studies have shown that general and central obesity are each linked to adverse outcomes in gastrointestinal cancers. However, their combined effect on gastrointestinal cancers surgery outcomes were less understood. This study aims to integrate both general and central obesity to examine the outcomes of gastric cancer surgery in different obesity patterns. We retrospectively analyzed 248 patients who underwent gastric cancer surgery between 2021 and 2023 in a single institute. The Inbody720 body composition analyzer measured body composition. We evaluated the relationship between obesity patterns - combining BMI with central obesity measures (waist circumference, waist-to-hip ratio, visceral fat area) - and postoperative complications and 30-day readmission. Central-only obesity were more likely to induce fistula (P = 0.025), while non-obesity was more likely to develop postoperative abdominal effusion (P = 0.049) and bleeding (P = 0.042). Central-only obesity was significantly associated with severe postoperative complications after adjustment for hypertension, diabetes, abdominal surgery history, preoperative albumin levels, age, sex, and surgical types. This remains significant even after adjusting for muscle mass. However, we did not find the same results for significant complications. Regarding 30-day readmission, there are no differences between different patterns of obesity. Central-only obesity is an independent risk factor for severe postoperative complications in gastric cancer, while a high BMI appears to be associated with a lower risk compared to non-obese patients, but not significant postoperative complications. The likelihood of readmission within 30 days post-surgery may not be related to the patient's pattern of obesity.

The purpose of this study is to explore the risk of coronary heart disease (CHD) in cancer patients who consume different flavonoids, and the impact of flavonoids on the prognosis of cancer patients with CHD. We extracted dietary flavonoids data on 1454 patients diagnosed with cancer from the National Health and Nutrition Examination Survey and Food and Nutrient Database for Dietary Studies. Logistic regression analysis was used to explore the relationship between the intake of flavonoids and the risk of CHD. Cox proportional hazard model was used to explore the impact of flavonoids intake on prognosis in 148 patients with cancer and CHD. Malvidin intake increased the risk of CHD by 1% [odds ratio (OR) = 1.01, 95% confidence interval (CI): 1.00-1.02, P < 0.05] in cancer patients, while epicatechin and isorhamnetin reduced the risk of CHD by 3% (OR = 0.97, 95% CI: 0.94-1.00, P < 0.05) and 15% (OR = 0.85, 95% CI: 0.72-1.00, P < 0.05), respectively. Adjusted by age, sex, and race, malvidin intake increased the risk of CHD in cancer patients by 1% (OR = 1.01, 95% CI: 1.00-1.02, P < 0.05), isorhamnetin decreased the risk by 15% (OR = 0.85, 95% CI: 0.72-1.00, P < 0.05), and epicatechin showed no effect on the risk of CHD ( P > 0.05). No flavonoids had impact on the prognosis of patients with cancer and CHD ( P > 0.05). For patients with cancer, consuming malvidin increases the risk of CHD, while isorhamnetin reduces the risk. Consuming flavonoids has no impact on the prognosis of patients with cancer and CHD.

The relationship between folate and the risk of cancer remains undetermined partially due to the dynamic changes in folate intakes at the population level caused by folic acid fortification implemented in the USA and other countries. To control for the interference from fortification, we assessed the relationship between folate and lung cancer death (LCD) risk among a national cohort established years before folic acid fortification. We followed up 14 528 adults aged 19 years or older who participated in the National Health and Nutrition Examination Survey (1988-1994) on average for 14 years. LCD's hazard ratios were estimated by the folate levels using Cox regressions. After 192 973 person-years (py) of follow-up, 233 LCDs were recorded. The LCD rates were 1.20/1000 py, 1.14/1000 py, and 1.38/1000 py for adults with low (1st quarter), moderate (2nd and 3rd quarter), and high (4th quarter) serum folate. In the first 10 years of follow-up, the adjusted hazard ratio was 2.87 (1.30-6.37) for adults with moderate, and 1.56 (0.58-4.23) for adults with high serum folate, compared to adults with low serum folate. For adults who survived longer than 10 years of follow-up, the hazard ratios were 0.45 (0.24-0.86) and 0.37 (0.16-0.87) respectively. No association was observed between LCD risk and red blood cell folate level. With minimized interference from folic acid fortification, we detected a time-dependent bidirectional association that supports the dual effects of folate on the carcinogenesis of lung cancer.

Triple-negative breast cancer (TNBC) is a complex and diverse group of malignancies. Invasive ductal carcinoma (IDC) is the predominant pathological subtype and is closely linked to the ominous potential for distant metastasis, a pivotal factor that significantly influences patient outcomes. In light of these considerations, the present study was conceived with the objective of developing a nomogram model. This model was designed to predict the prognosis observed in IDC with distant metastasis in TNBC. This was a retrospective study based on the SEER database. Data of 9739 IDC-TNBC patients diagnosed from 2010 to 2020 were included in our study. Independent risk factors were screened by univariate and multivariate Cox regression analyses successively, which were used to develop a nomogram model predicting for prognosis. Cox multivariable analysis showed statistical significance in bone metastasis, liver metastasis, surgery, and chemotherapy. Incorporating statistically significant variables, as well as clinically significant age, lung metastasis, and brain metastasis into the construction of the prediction model, the C-indexes of the training group and validation group were 0.702 (0.663-0.741) and 0.667 (0.600-0.734), respectively, while the calibration curves were all close to the ideal 45° reference line, and decision curve analysis curves show excellent net benefit in the predictive model. The prognostic prediction model developed in this study demonstrated enhanced predictive accuracy, enabling a more precise evaluation of mortality risks associated with IDC with distant metastasis in TNBC.

Despite significant advances in therapy, cancer remains the top cause of death in parts of the globe. For many types of cancer, the typical treatment is a combination of surgery, chemotherapy, and radiotherapy. However, this conventional treatment is not successful on its own. As a consequence, innovative approaches that improve treatment efficacy are urgently needed. The ketogenic diet is a high-fat, moderate protein, and low-carbohydrate diet that appears to sensitize most cancers to conventional therapies by exploiting cancer cells' altered metabolism, making it an effective adjuvant cancer treatment alternative. This diet could decrease glucose metabolism while enhancing lipid metabolism, interfering with the Warburg effect, and inhibiting tumor cell proliferation. The anticancer impact of ketogenic diet has been established in numerous animal trials and clinical investigations on a wide range of tumor types, including glioblastoma, pancreatic cancer, head and neck cancer, breast cancer, invasive rectal cancer, ovarian cancer, and endometrial cancer. In this review, we discussed the various types of ketogenic diets, the mechanism of action for ketogenic diet as a cancer therapy, and the data gathered from continuing preclinical and clinical studies, intending to establish a solid theoretical foundation for future research.