Journal of Cancer Research and Clinical Oncology最新文献

Background: Social inequalities in cancer constitute a major public health challenge. A lower socioeconomic position (SEP) is consistently associated with higher exposure to cancer risk factors, lower participation in screening, more advanced stage at diagnosis, poorer survival, and adverse survivorship outcomes. In Germany, these inequalities remain insufficiently addressed in research and health policy.

Methods: This paper synthesises evidence and expert perspectives derived from a national workshop organised by the Cancer Epidemiology Working Group of the German Society for Epidemiology (DGEpi) in collaboration with the German Cancer Research Center. More than 30 experts in cancer epidemiology and social inequality research, together with international contributors, reviewed-based on existing conceptual frameworks-the German data landscape, and empirical evidence across the cancer continuum. Structural, methodological, and ethical barriers were identified, and implications for research, policy, and practice were discussed. An international comparison with Denmark was used to contextualise findings.

Results: Available evidence demonstrates pronounced socioeconomic inequalities across nearly all stages of the cancer continuum in Germany, including prevention, screening, incidence, diagnosis, survival, and survivorship. However, major research gaps persist. Key barriers include limited availability of individual-level SEP data, reliance on area-based deprivation indices, restricted data linkage, fragmented healthcare structures, and limited integration of equity considerations into national cancer strategies. International experience shows that comprehensive registries, data linkage, and targeted interventions can reduce inequalities.

Conclusions: Reducing social inequalities in cancer in Germany requires coordinated and evidence-based action. Priorities include improving SEP data availability and linkage, embedding equity objectives into the National Cancer Plan, implementing targeted interventions for vulnerable groups, and strengthening intersectoral collaboration. Ethical and patient perspectives strongly support responsible use of health data to address avoidable inequalities.

Premenopausal women carrying a BRCA1 or BRCA2 mutation are frequently advised to undergo risk-reducing bilateral salpingo-oophorectomy (BSO) to lower their significantly increased lifetime risk of ovarian cancer. However, this procedure induces abrupt estrogen deprivation, resulting in premature menopause with well-documented consequences including vasomotor symptoms (e.g., hot flashes, night sweats), urogenital atrophy, and long-term risks such as osteoporosis, cardiovascular disease, and cognitive decline (Nelson in Lancet 371(9614):760-770, 2008; Shuster et al. in Maturitas 65(2):161-166, 2010). To alleviate symptoms and prevent sequelae, hormone replacement therapy (HRT) remains the most effective intervention. However, the issue becomes complex when the patient has a personal history of triple-negative breast cancer (TNBC). Although TNBC lacks hormone receptor expression, systemic HRT has traditionally been contraindicated in breast cancer survivors, as early studies indicated an increased risk of recurrence with hormone therapy, even in receptor-negative subtypes (Kenemans et al. Lancet Oncol 10(2):135-146, 2009a). This leads to a critical question: Is HRT appropriate in BRCA mutation carriers with a history of TNBC following BSO, and if so, under what clinical conditions? What do current international guidelines, evidence, and expert recommendations suggest?

Drug resistance is a pivotal factor leading to the failure of cancer therapy, within which heme oxygenase-1 (HMOX1) plays a complex and paradoxical dual role. On one hand, HMOX1 protects cancer cells from oxidative damage induced by chemotherapeutic drugs through its antioxidant properties. Concurrently, its catalytic downstream product, carbon monoxide (CO), inhibits cancer cell apoptosis, thereby mediating acquired drug resistance. On the other hand, HMOX1 is a key source of intracellular free iron. When its activity is excessively induced, it leads to the accumulation of excessive free iron, triggering the buildup of lipid peroxides and ferroptosis, which presents a novel opportunity to overcome drug resistance. This demonstrates that the function of HMOX1 can switch depending on its degree of activation. Therefore, a thorough analysis of its regulatory network and the mechanisms of its functional switch within different microenvironments is crucial for developing novel therapeutic strategies that target HMOX1 to overcome drug resistance. This review systematically summarizes the multiple mechanisms of HMOX1 in drug resistance, with a focus on HMOX1 inducers and inhibitors, as well as synergistic sensitization strategies in combination with other therapies. It aims to provide a comprehensive theoretical foundation and a forward-looking perspective for translating HMOX1-targeted therapy from basic research to clinical practice.

Purpose: In recent decades, small renal masses (SRMs) have become common incidental findings in cross-sectional studies; however, a widely implemented approach for the characterization of SRMs is still lacking. Thus, in this study, we aimed to explore the diagnostic performance of existing algorithms and to propose - as a conceptual framework rather than a clinically verified tool - a new simple radiological scale for estimating the probability of malignancy in SRMs.

Methods: Patients with indeterminate solid SRMs (N = 50), discovered using magnetic resonance imaging (MRI) between 2012 and 2023 were included. In 38 cases, the final diagnosis was based on histopathology, while in 12 cases it relied on regression or lack of progression during follow-up. Modified versions of the clear cell likelihood score (ccLS) were calculated, and its diagnostic performance was assessed. Moreover, we analyzed the newly created score, which consisted of selected MRI and clinical features. All of our modified scales used a Likert score for the likelihood of clear cell renal cell carcinoma (ccRCC).

Results: Based on the results of our statistical analyses, we modified the ccLS by adding T1 SI ratio < 0.73, arterial to delayed ratio (ADER) > 0.99, and smoking as independent predictors of ccRCC. We created a new scale, the CAT score, which combined hyperintensity in the Corticomedullary phase, ADER > 0.99, and TI SI ratio < 0.73 (with 1 point being assigned to each of the above-mentioned MRI parameters). In our results, the best diagnostic accuracy was observed for a CAT score ≥ 2, with a sensitivity of 73.9% (51.6-89.8%), a specificity of 77.8% (57.7-91.4%), and an accuracy of 76.0% (61.8-86.9%). Univariate logistic regression analyses demonstrated that all scales created by our group were significant predictors of ccRCC. Importantly, they showed a better predictive ability than the standard ccLS score.

Conclusions: The CAT score appears to improve the prediction of ccRCC compared with both standard and modified versions of the ccLS and may serve as a potential aid in the routine assessment of indeterminate SRMs. Nonetheless, this study should be regarded as a preliminary, proof-of-concept analysis rather than a definitive model-development study. The main limitation of our study is its small, single-center cohort, which limits the statistical power and robustness of model development. Moreover, a substantial proportion of benign diagnoses based only on radiological follow-up rather than histopathology. Therefore, before clinical implementation, the CAT score requires prospective validation in larger, independent, multicenter cohorts.

Mitophagy, a key mechanism of selective autophagy, maintains cellular homeostasis by removing dysfunctional mitochondria, and its dysregulation is closely associated with tumor initiation and progression. As breast cancer remains one of the most prevalent malignancies among women worldwide, its heterogeneity and therapeutic resistance have prompted growing interest in identifying novel molecular targets. Emerging evidence indicates that mitophagy plays a dual role in breast cancer development, metastasis, and treatment resistance by regulating energy metabolism, oxidative stress, and cell-fate decisions. This review systematically summarizes the molecular mechanisms of mitophagy and its dynamic regulatory networks in breast cancer. Further, it discusses emerging mitophagy-targeted therapeutic strategies, aiming to provide a theoretical foundation for the precision treatment of breast cancer.