Clinical breast cancer最新文献

Introduction: Advancements in health technologies have enabled the performance of minimally invasive procedures using ionizing radiation for radioscopy and fluoroscopy by various physicians including orthopedic surgeons, radiologists, urologists, cardiologists, vascular surgeons, and plastic surgeons. Simultaneously, there appears to be an increasing frequency of breast cancer among these professionals. In addition to other risk factors to which they are exposed, ionizing radiation plays a role in carcinogenesis. This study is a systematic review and meta-analysis conducted to summarize the available literature on breast cancer risk among female physicians occupationally exposed to ionizing radiation.

Methods: A systematic search was conducted in the PubMed, Embase, and LILACS databases, as well as reference lists based on PRISMA checklist (PROSPERO CRD42024553635). The methodological quality of the included studies was assessed using the Newcastle-Ottawa Scale (NOS). Statistical analyses were performed at Review Manager.

Results: Six observational studies were included, evaluating 34,744 participants: 8103 exposed to ionizing radiation and 26,641 controls, with a minimum 10-year follow-up. According to the NOS, 5 studies were classified as high quality and one as moderate. The meta-analysis revealed an increased breast cancer risk among female physicians exposed to ionizing radiation, with an odds ratio (OR) 1.84 (95% CI 1.11-3.06). A sensitivity analysis excluding the study classified as moderate quality showed a breast cancer risk in the exposed group with an OR 1.42 (95% CI 1.06-1.89).

Conclusions: Based on the results of this meta-analysis, female physicians occupationally exposed to ionizing radiation have an increased risk of breast cancer compared to those who are not exposed.

Objective: To explore the trajectory patterns and influencing factors of chemotherapy-induced peripheral neuropathy (CIPN) in breast cancer patients using latent class growth analysis (LCGA).

Methods: This study was conducted from September 2022 to September 2023 at a tertiary hospital in Tangshan, China. A total of 350 hospitalized breast cancer patients undergoing chemotherapy were recruited. Data were collected through questionnaires, including general demographic information, disease-related characteristics, lifestyle factors, and psychological status. CIPN was assessed at 5 time points: baseline (T0) and the 21st day after the completion of the 1st (T1), 2nd (T2), 3rd (T3), and 4th (T4) chemotherapy cycles. Latent class growth models (LCGMs) were used to identify distinct trajectory patterns. Univariate analysis and multinomial logistic regression models were applied to examine the influencing factors.

Results: Three distinct CIPN trajectory groups were identified: the low-risk stable group (42.3%, n = 148), the moderate-risk progressive group (41.4%, n = 145), and the high-risk rapidly progressing group (16.3%, n = 57). Compared with the low-risk stable group, the predictive factors for the moderate-risk progressive group included body mass index (BMI), hypertension, and depression. For the high-risk rapidly progressing group, predictive factors included BMI, physical activity, social support, hypertension, vitamin D levels, nutritional status, and depression.

Conclusion: This study elucidates the heterogeneous trajectory patterns of chemotherapy-induced peripheral neuropathy (CIPN) in breast cancer patients and identifies key influencing factors. Recognizing these characteristics in clinical practice may facilitate the early identification of high-risk patients and enable timely interventions to mitigate CIPN severity.

Background: Triple-negative breast cancer (TNBC) carries a substantial risk of recurrence and metastasis, posing significant threats to patients' health and quality of life. Centrosomal protein 55 (CEP55) has been demonstrated to exhibit elevated expression levels in TNBC. However, its molecular regulatory mechanism in TNBC remains unclear.

Methods: Bioinformatics databases, qRT-PCR, and Western blot were employed to analyze CEP55 expression in TNBC tissues and cells. EdU assays, flow cytometry, and Transwell assays were utilized to monitor cell proliferation, apoptosis, and invasion. Subsequently, macrophage polarization was detected by flow cytometry. Fe²⁺, malondialdehyde (MDA), glutathione (GSH), and reactive oxygen species (ROS) levels were determined using corresponding kits. Immunoprecipitation (IP) was used to detect the ubiquitination level of CEP55, and co-IP was applied to confirm the interaction between CEP55 and Charged Multivesicular Body Protein 6 (CHMP6). Finally, a xenograft tumor model was established, and immunohistochemistry (IHC) was conducted to evaluate the expression of specific proteins.

Results: CEP55 levels were increased in TNBC tissues and cells. Silencing CEP55 repressed TNBC cell proliferation, invasion, and macrophage M2 polarization, and facilitated cell apoptosis and ferroptosis. Additionally, ubiquitin-specific protease 8 (USP8) maintained CEP55 stability through deubiquitination, and CEP55 overexpression reversed the cellular effects caused by USP8 knockdown. Moreover, CEP55 bound to CHMP6 to promote its expression, thereby facilitating the malignant progression of TNBC cells. CEP55 overexpression abolished the inhibitory influence of USP8 silencing on tumor growth in vivo.

Conclusion: USP8 stabilized CEP55 expression through deubiquitination, and CEP55 further promoted CHMP6 expression to inhibit ferroptosis progression, thereby facilitating macrophage M2 polarization and malignant biological behaviors of TNBC cells.

Breast cancer (BC) remains a significant health problem globally, with complex underlying processes that are not fully understood. This study investigates the intricate relationship between endothelial nitric oxide synthase (eNOS) and reactive oxygen species (ROS) in the progressions of BC. Here we examine the essential roles of superoxide (O2·¯), hydrogen peroxide (H₂O₂), and hydroxyl free radicals (OH·) in promoting tumor development, angiogenesis, and metastasis. In addition, this review also analyzes the significant role of eNOS in BC, which highlighting its activation by estrogen and the impact of eNOS gene polymorphisms on cancer risk. Furthermore, we elucidate the mechanisms of eNOS uncoupling, primarily focusing on the deficiency of tetrahydrobiopterin (BH4), the depletion of L-Arginine (L-Arg), and the buildup of asymmetric dimethylarginine (ADMA). This extensive study provides novel insights into the molecular mechanisms connecting oxidative stress and NO signaling in BC. It identifies prospective targets for innovative treatment strategies. Hence, the outcomes of the study may highlight the importance of comprehending the complex balance between eNOS activity and ROS production in the progression of BC. This provides the foundation for further studies and targeted therapies in BC treatment.

Background: Spondin-2 (SPON2) expression is associated with various types of cancer, but its role in breast cancer (BC) remains ambiguous, especially in hormone receptor-positive (HR+)/human epidermal growth factor receptor 2-negative (HER2-) BC.

Methods: The expression of SPON2 in HR+/HER2- BC tissues and adjacent tissues was detected using immunohistochemical staining and western blotting. Cell proliferation and migration were assessed via CCK-8 assay, EdU assay, and transwell assay. Animal studies were performed to assess the effect of SPON2 knockdown on tumor growth.

Results: Herein, increased expression of SPON2 was found in HR+/HER2- BC, and silencing SPON2 suppressed cell proliferation, clonogenicity, and migration, whereas SPON2 overexpression had the opposite effects. Notably, SPON2 knockdown significantly suppressed tumor growth in a xenograft tumor assay. Mechanistically, a reduction in SPON2 expression inhibited β-catenin activation, whereas its overexpression promoted β-catenin-mediated proliferation and migration.

Conclusion: These data indicate that SPON2 plays oncogenic roles in HR+/HER2- BC via activating the β-catenin pathway, and may represent a potential therapeutic target for patients diagnosed with HR+/HER2- BC.