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Ovarian cancer, a leading cause of cancer deaths, poses challenges due to insidious development and vague signs and symptoms. Risk factors include age, reproductive history, genetic mutations, and environmental factors. Treatment involves surgery, chemotherapy, and targeted therapy, with nursing interventions focusing on symptom management and supportive care. [ABSTRACT FROM AUTHOR]

Aims: A higher risk of cancer among patients with heart failure (HF) has been suggested in recent community‐based studies. This study aimed to investigate the impact of HF during hospitalization with acute coronary syndrome (ACS) on the long‐term cancer risk. Methods and results: The study included 572 patients admitted with ACS to three Italian hospitals, discharged cancer‐free, and prospectively followed for 24 years or until death. All but three patients completed the follow‐up, which represented 6440 person‐years (mean age: 66 ± 12 years; 70% males). Baseline HF was diagnosed in 192 (34%) patients. A total of 129 (23%) patients developed cancer (103 without HF and 26 with HF), and 107 (19%) patients died due to it (81 without HF and 26 with HF). The incidence rates for cancer onset and cancer death were not different according to HF status. Cox regression analysis revealed no association between HF or left ventricular ejection fraction (LVEF) and cancer risk. In addition, no difference in cancer risk was observed among patients with HF with preserved ejection fraction, HF with mildly reduced ejection fraction, and HF with reduced ejection fraction. In competing risk regression analysis, the risk of cancer onset associated with HF was sub‐hazard ratio (SHR) 0.47 [95% confidence interval (CI): 0.30–0.72; P = 0.001] and SHR 1.02 (95% CI: 1.01–1.04; P = 0.002) with LVEF. Results were the same in the adjusted model. Yet the fully adjusted model showed an attenuated association between cancer death and HF (SHR: 0.63; 95% CI: 0.37–1.05; P = 0.08) and LVEF (SHR: 1.02; 95% CI: 0.99–1.06; P = 0.08). Consistent results were obtained after using propensity score matching analysis that created 192 pairs. A negative interaction between age and HF and a positive interaction between age and LVEF for cancer risk have also been found. Conclusions: An inverse association between baseline HF and long‐term cancer risk has been observed among the ABC Study on heart disease patients who were followed for 24 years after ACS. [ABSTRACT FROM AUTHOR]

Background: Active surveillance (AS), where treatment is deferred until cancer progression is detected by a biopsy, is acknowledged as a way to reduce overtreatment in prostate cancer. However, a consensus on the frequency of taking biopsies while in AS is lacking. In former studies to optimize biopsy schedules, the delay in progression detection was taken as an evaluation indicator and believed to be associated with the long‐term outcome, prostate cancer mortality. Nevertheless, this relation was never investigated in empirical data. Here, we use simulated data from a microsimulation model to fill this knowledge gap. Methods: In this study, the established MIcrosimulation SCreening Analysis model was extended with functionality to simulate the AS procedures. The biopsy sensitivity in the model was calibrated on the Canary Prostate Cancer Active Surveillance Study (PASS) data, and four (tri‐yearly, bi‐yearly, PASS, and yearly) AS programs were simulated. The relation between detection delay and prostate cancer mortality was investigated by Cox models. Results: The biopsy sensitivity of progression detection was found to be 50%. The Cox models show a positive relation between a longer detection delay and a higher risk of prostate cancer death. A 2‐year delay resulted in a prostate cancer death risk of 2.46%–2.69% 5 years after progression detection and a 10‐year risk of 5.75%–5.91%. A 4‐year delay led to an approximately 8% greater 5‐year risk and an approximately 25% greater 10‐year risk. Conclusion: The detection delay is confirmed as a surrogate for prostate cancer mortality. A cut‐off for a "safe" detection delay could not be identified. [ABSTRACT FROM AUTHOR]

Although some studies have found that short-term PM 2.5 exposure is associated with lung cancer deaths, its impact on other cancer sites is unclear. To answer this research question, this time-stratified case-crossover study used individual cancer death data between January 1, 2000, and December 31, 2019, extracted from the Brazilian mortality information system to quantify the associations between short-term PM 2.5 exposure and cancer mortality from 25 common cancer sites. Daily PM 2.5 concentration was aggregated at the municipality level as the key exposure. The study included a total of 34,516,120 individual death records, with the national daily mean PM 2.5 exposure 15.3 (SD 4.3) μg/m3. For every 10-μg/m3 increase in three-day average PM 2.5 exposure, the odds ratio (OR) for all-cancer mortality was 1.04 (95% CI 1.03–1.04). Apart from all-cancer deaths, PM 2.5 exposure may impact cancers of oesophagus (1.04, 1.00–1.08), stomach (1.05, 1.02–1.08), colon-rectum (1.04, 1.01–1.06), lung (1.04, 1.02–1.06), breast (1.03, 1.00–1.06), prostate (1.07, 1.04–1.10), and leukaemia (1.05, 1.01–1.09). During the study period, acute PM 2.5 exposure contributed to an estimated 1,917,994 cancer deaths, ranging from 0 to 6,054 cases in each municipality. Though there has been a consistent downward trend in PM 2.5 -related all-cancer mortality risks from 2000 to 2019, the impact remains significant, indicating the continued importance of cancer patients avoiding PM 2.5 exposure. This nationwide study revealed a notable association between acute PM 2.5 exposure and heightened overall and site-specific cancer mortality for the first time to our best knowledge. The findings suggest the importance of considering strategies to minimize such exposure in cancer care guidelines. The 20-year analysis of nationwide death records in Brazil revealed that heightened short-term exposure to PM 2.5 is associated with increased cancer mortality at various sites, although this association has gradually decreased over time. Despite the declining impact, the research highlights the persistent adverse effects of PM 2.5 on cancer mortality, emphasizing the importance of continued research and preventive measures to address the ongoing public health challenges posed by air pollution. [Display omitted] • First investigation for acute PM2.5 exposure and site-specific cancer mortality. • Significant adverse effects were observed at various cancer sites. • Potential adaptation exists in the PM2.5-cancer association. • Cancer guidelines may include acute PM2.5 exposure avoidance. [ABSTRACT FROM AUTHOR]

Using patient-specific data, the present study aimed to identify organ and effective dose to estimate the lifetime attributable risks (LARs) of cancer incidence and mortality associated with routine CT procedures. A cross-sectional investigation was conducted on 515 patients who underwent CT scan. The effective dose was computed using two methods: first, the ImPACT software and relevant conversion factors. Second, the effective dose was determined using the scanner-derived DLP and AAPM TG 23's conversion factor. Using the biological effects of ionizing radiation (BEIR VII) report, LAR of cancer incidence and mortality were computed. The greatest mean organ doses for abdomen-pelvis, routine chest, chest HRCT, brain, and sinus examinations were 20.64 ± 3.27 mGy (kidneys), 21.55 ± 5.47 mGy (thymus and esophagus), 10.51 ± 1.31 mGy (thymus and esophagus), 22.72 ± 3.01 mGy (lens), and 18.56 ± 1.25 mGy (lens) respectively. Using ImPACT dosimetry software, the mean effective dose for routine chest, abdomen-pelvis, HRCT chest, brain, and sinus examinations was 8.46 mSv, 10.13 mSv, 4.19 mSv, 1 mSv, and 0.68 mSv, respectively. Using the DLP to effective dose conversion factor, the mean effective dose was lower. The mean cancer incidence risks per 100,000 people were 63.33, 54.98, 27.82, 6.31, and 5.22 for abdomen-pelvis, routine chest, HRCT, brain, and sinus examinations, respectively. The mean LAR of cancer mortality for all cancer was 38.22, 33.17, 16.72, 3.87, 2.93 for abdomen-pelvis, routine chest, HRCT, brain, and sinus examinations, respectively, per 100,000 people. Thus, CT scan exams are connected with a non-negligible risk of cancer, and patient radiation dose must be optimized to limit radiation risk. • The effective dose of routine CT examinations was calculated by two methods. • Abdomen-pelvis scans had the highest mean DLP, scan length, and effective dose. • The current study's CTDIvol and DLP were below recognized diagnostic reference levels. • The abdomen-pelvis had the highest mean LAR of all cancers, all solid, and leukemia, respectively, at 63.33, 56.56, and 6.77. [ABSTRACT FROM AUTHOR]