Risk-reducing mastectomy significantly decreases the incidence of breast cancer in women with a genetic predisposition. However, its effects on psychosocial and sexual well-being remain insufficiently explored, particularly among women without a previous diagnosis of breast cancer.

To evaluate the psychosocial and sexual well-being of women undergoing risk-reducing mastectomy with immediate breast reconstruction.

This observational, cross-sectional study involved the retrospective collection of clinical data and was conducted at a specialized center. Women aged >18 years, with no history of breast cancer, who underwent bilateral risk-reducing mastectomy with immediate implant-based reconstruction between 2018 and 2023 were included. Psychosocial and sexual well-being domains were assessed using the BREAST-Q™, with standardized scores ranging from 0 to 100. Descriptive analyses, Spearman's correlation, and nonparametric tests were performed, adopting a significance level of P < 0.05.

Twenty-eight patients were included. The mean age was 41.8 ± 9.6 years at the time of surgery and 45.5 ± 9.4 years at the time of assessment. Mean scores were 68.5 ± 20.4 for psychosocial well-being and 55.4 ± 17.8 for sexual well-being. A strong correlation was observed between the two domains (ρ = 0.81; p < 0.001). Early postoperative complications and the need for reoperations were associated with lower scores in both domains. Higher educational attainment was associated with better sexual well-being scores. No significant associations were found for the remaining variables.

Risk-reducing mastectomy with immediate reconstruction is associated with variable psychosocial and sexual outcomes, primarily influenced by postoperative complications and reoperations. These findings highlight the importance of incorporating quality-of-life assessment into the counseling and follow-up of these patients.

Metastatic castration‑resistant prostate cancer (mCRPC) remains an incurable disease characterized by relentless progression and universal resistance to standard therapies. The limited efficacy of immunotherapies in this malignancy reflects an immunosuppressive tumor microenvironment orchestrated by regulatory T cells, myeloid‑derived suppressor cells, tumor‑associated macrophages and cancer‑associated fibroblasts, along with androgen receptor signaling, metabolic reprogramming and spatially organized immune exclusion zones. The present review synthesized emerging evidence from single‑cell and spatial transcriptomics to propose a spatiotemporal coevolution paradigm, wherein resistance emerges not through linear genetic selection alone but through dynamic, reciprocal interactions among tumor cells, stromal components and immune populations across both temporal and spatial dimensions. The framework integrates clonal evolution dynamics, preexisting castration‑tolerant progenitors, fibroblast‑dominated barriers and metabolic crosstalk that collectively enforce immune evasion. Key therapeutic vulnerabilities, including YAP1‑TGF‑β1 axis disruption, PKMYT1 inhibition, metabolic targeting and biomarker‑guided patient stratification, are critically evaluated within this ecological context. Ultimately, the present review aimed to establish spatiotemporal co‑evolution as a unifying framework that transforms mCRPC from a uniformly fatal disease into a chronically manageable condition through precisely timed, spatially informed and mechanistically rational interventions.

Adenomatoid tumor (AT) is a rare benign mesothelial neoplasm that typically arises in the genital tract. Adrenal involvement is exceptionally uncommon, with fewer than 50 cases reported in the literature. Because of its nonspecific clinical and radiological features, preoperative diagnosis is challenging and malignancy is often suspected. We report the case of a 48-year-old man in whom a left adrenal mass was incidentally discovered during evaluation for renal colic. Hormonal assessment demonstrated a non-functioning adrenal lesion. Computed tomography and magnetic resonance imaging revealed a large, well-circumscribed 12-cm heterogeneous mass with predominant cystic degeneration, thick septations, and intralesional calcifications, raising suspicion of a malignant adrenal neoplasm. The patient underwent open left adrenalectomy. Gross examination showed a well-defined yellowish tumor with extensive cystic changes and calcifications. Histologically, the lesion consisted of anastomosing cystic spaces lined by bland flattened to cuboidal cells, associated with lymphoid aggregates, fibrosis, calcifications, and focal ossification. Immunohistochemistry demonstrated strong positivity for CK7, calretinin, WT1, and D2-40, confirming mesothelial differentiation, while CD31 and CD34 were negative. These findings established the diagnosis of adrenal AT. The postoperative course was uneventful, and no recurrence has been observed during follow-up. Adrenal AT is a rare benign lesion that may mimic malignant adrenal neoplasms, particularly when large and cystic. Histopathological and immunohistochemical examination remains essential for definitive diagnosis. Complete surgical excision is curative and associated with an excellent prognosis.

Papillary thyroid carcinoma (PTC) is an uncommon neoplasm in pediatric and transitional age groups, characterized by a biologically more aggressive local behavior than in adults. Although its coexistence with Hashimoto's thyroiditis (HT) is widely documented, the impact of this chronic inflammation on massive lymphatic dissemination remains a subject of debate. We present the case of a 17-year-old male who presented with cervical lymphadenopathy and computed tomography imaging suggestive of primary superior mediastinal involvement (prevascular and pretracheal). Initial fine-needle aspiration biopsy (FNAB) of the right cervical lymph node revealed atypical follicular cells with nuclear grooves, consistent with metastatic PTC. The patient underwent total thyroidectomy combined with modified bilateral radical neck dissection and central compartment neck dissection. Definitive histopathological examination confirmed a multifocal PTC (classic type and follicular variant) measuring 1.1 cm in its largest diameter, with lymphatic invasion on a background of HT (pathological staging pT1b pN1b pMx). Compartmental lymph node analysis revealed a massive metastatic burden, with 13 of 39 lymph nodes exhibiting bilateral involvement, highlighted by a 4.0 cm macrometastasis in the right middle jugular chain. Following surgery, adjuvant radioactive iodine (I-131) ablation therapy was administered after thyroid hormone withdrawal, and subsequent post-ablation follow-up laboratory testing confirmed severe endogenous hypothyroidism with a markedly elevated thyroid-stimulating hormone (TSH) level. This clinical case highlights the striking clinicopathological discrepancy that can exist between the small size of a primary thyroid tumor and the potential for disproportionate lymphovascular dissemination in the adolescent population. When encountering bulky mediastinal and cervical masses that mimic lymphomas, PTC must be considered a critical differential diagnosis, justifying comprehensive preoperative mapping and an aggressive compartmental surgical approach.

Multiple primary malignant neoplasms (MPMNs) diagnosed synchronously are rare, with an incidence of less than 1%. The occurrence of triple synchronous malignancies is exceedingly uncommon, and to our knowledge, no prior reports describe the concurrent presentation of a myeloproliferative neoplasm, plasma cell dyscrasia and breast cancer. Such cases pose considerable diagnostic and therapeutic challenges, particularly in settings with limited access to advanced molecular testing and oncologic therapies.

A 67-year-old woman presented with a pathological femoral fracture, marked leucocytosis and thrombocytosis. Histological examination of the fracture site revealed a kappa-restricted plasmacytoma meeting diagnostic criteria for multiple myeloma (R-ISS Stage 3). Bone marrow biopsy demonstrated hypercellularity with atypical clustered megakaryocytes, consistent with prefibrotic primary myelofibrosis, and molecular analysis confirmed a JAK2 V617F mutation. During evaluation, a right breast mass was confirmed on core biopsy as an invasive carcinoma with focal mucinous differentiation (ER/PR-positive, HER2-negative and Ki-67 25%), consistent with a luminal B-like profile. The patient commenced therapy with melphalan and prednisone for myeloma and anastrozole for breast carcinoma, with multidisciplinary input guiding treatment sequencing.

This case represents an exceptionally rare triad of synchronous malignancies spanning myeloid, plasma-cell and epithelial lineages. While myeloproliferative neoplasms are associated with an elevated risk of secondary neoplasia, the simultaneous occurrence of three independent malignancies raises the possibility of shared pathogenic mechanisms such as clonal haematopoiesis or an underlying germline predisposition. The presentation highlights the diagnostic complexity of distinguishing independent primaries from metastatic disease and illustrates the importance of maintaining diagnostic vigilance. Limited access to next-generation sequencing and novel therapies further complicates management in resource-constrained healthcare environments.

Triple synchronous primary malignancies are exceedingly rare and diagnostically challenging. This case emphasises the necessity of a systematic, multidisciplinary approach to evaluation and management, even in low-resource settings, to ensure accurate diagnosis and optimal coordination of care across multiple oncologic pathologies.

A woman in her late 60s presented with obstructive jaundice. She had mucinous adenocarcinoma of the colon six months ago and underwent surgery followed by adjuvant chemotherapy. A computed tomography scan revealed a prominent ampulla with duodenal wall thickening, dilated intrahepatic biliary radicles, bile ducts, and the main pancreatic duct. Duodenoscopy revealed a bulky, friable, and ulcerated ampulla of Vater (AOV) with partial luminal narrowing. The biopsy and immunohistochemistry (IHC) confirmed adenocarcinoma of colonic origin metastasizing to the AOV. She underwent an endoscopic retrograde cholangiogram and biliary drainage, and best supportive care before dying of her illness. Metastatic involvement of AOV is extremely rare. This case reiterates the need to consider AOV metastasis in the differential diagnosis of obstructive jaundice, especially in patients with a history of malignancy. It also underscores the role of IHC to differentiate AOV primary malignancy from metastasis.

Multitarget stool DNA (mt-sDNA) testing is an established noninvasive colorectal cancer (CRC) screening option for average-risk adults, but real-world completion of the screening cascade through colonoscopy remains incompletely characterized.

This study aimed to evaluate mt-sDNA adherence, test positivity, and follow-up colonoscopy completion in a regional healthcare system and identify factors associated with screening cascade completion.

This retrospective cohort study analyzed mt-sDNA test kits ordered for average‑risk, screening‑eligible individuals in the Spartanburg Regional Healthcare System (South Carolina, USA) from January 2016 to June 2023. Analyses were conducted at the test-kit level; patients could contribute more than one eligible test during the study period. Eligible tests were from patients aged 45 to 85 years with ≥6 months of prior continuous insurance coverage and no high-risk CRC conditions. Outcomes were adherence (kit return within 365 days), test positivity among adherent test kits, and follow‑up colonoscopy within 365 days among eligible positive cases. Multivariable logistic regression and Cox proportional hazards regression models evaluated factors associated with adherence and time to colonoscopy.

Of 8439 included test kits, 5733 (67.9%) were returned within 1 year. Among returned test kits, 1018 (17.8%) yielded a positive mt-sDNA result. Of 853 positive tests eligible for follow-up assessment, 596 (69.9%) were for patients who completed follow-up colonoscopy. Adherence to mt-sDNA testing was associated with non-Medicaid insurance, higher income, digital outreach, prior test return, and lower comorbidity burden. Time to colonoscopy was shorter for patients in the middle vs lowest income group.

Medicaid insurance was the strongest insurance-related predictor of nonadherence, with rates approximately 20 percentage points below those with commercial or Medicare-type coverage. Digital outreach and prior test return history were among the independent predictors of adherence. Income was the primary independent predictor of time to follow-up colonoscopy, potentially reflecting financial barriers to diagnostic follow-up.

In this real-world cohort study, approximately two-thirds of tests were returned and 70% of eligible positive tests completed follow-up colonoscopy within 1 year. These findings identify potentially modifiable socioeconomic and outreach-related factors associated with screening cascade completion and support targeted interventions for lower-income and Medicaid-insured populations.

Osteosarcoma(OS) exhibits poor and heterogeneous responses to immune checkpoint inhibitors(ICIs), largely due to its highly tumor immunosuppressive microenvironment(TIME). This review explores how nutritional biomarkers regulate the OS tumor microenvironment(TME) and serve as predictors of ICIs efficacy. Key biomarkers, including prognostic nutritional index(PNI), vitamin D and IDO modulate tumor-infiltrating lymphocytes (TILs), CD8⁺ T-cell function, macrophage polarization, and cytokine-metabolite crosstalk through mechanisms such as nutrient depletion, lactate acidification, and inflammatory signaling. These biomarkers not only reflect host nutritional and inflammatory status but also actively shape an TIME that contributes to ICIs resistance. Targeted nutritional interventions and combinations with IDO show potential to reprogram the TME and enhance antitumor immunity. This review highlights the value of nutritional biomarkers for patient stratification, prognostic assessment, and the development of personalized nutrition-immunotherapy strategies, providing a foundation for overcoming treatment resistance in OS.

Chemotherapy and immune checkpoint inhibitors (ICIs) are distinct anticancer treatments. We studied their impact on plasma protein profiles in cancer patients, potentially providing insight into treatment-specific prothrombotic mechanisms.

To compare baseline and longitudinal changes in protein profiles of patients with non-small cell lung cancer or head and neck cancer receiving ICI or chemotherapy.

We analyzed a matched cohort of 30 treatment-naïve patients from the Vienna Cancer and Thrombosis and Bleeding (CAT-BLED) study (10 non-small cell lung cancer and 5 head and neck cancer pairs). Plasma was collected before treatment, after 3 weeks, and at 3 months. We used quantitative protein mass spectrometry to measure 159 protein levels. Longitudinal changes were evaluated using linear mixed models with multiple testing correction.

Baseline protein profiles clustered by treatment assignment. Patients starting ICIs showed higher immune-related protein levels (eg, CD5 antigen-like, immunoglobulin mu chain C) and lower coagulation protein levels (factor[F]X, prothrombin) than those initiating chemotherapy. Two proteins changed during ICI, while 34 proteins (21%)changed during chemotherapy, with none and 12 (7%) remaining after multiple testing correction, respectively. At 3 months, chemotherapy was associated with increased levels of activated factor XIII (FXIIIa) (mean difference: 0.30; 95% confidence interval [CI], 0.06-0.54) and B (0.18; 95% CI, 0.03-0.34), fibulin-1 (0.25; 95% CI, 0.10-0.43), metalloproteinase inhibitor 2 (0.16; 95% CI, 0.02-0.31), and sex hormone-binding globulin (0.71; 95% CI, 0.23-1.14) and decreased serotransferrin (-0.10; 95% CI, -0.18 to -0.01) and cartilage acid protein 1 (-0.21; 95% CI, -0.33 to -0.09).

In this pilot, chemotherapy and ICI were associated with treatment-specific changes in protein profiles, suggesting distinct pathophysiological processes driving thrombosis and adverse outcomes during treatment.

Lung cancer remains the leading cause of cancer-related mortality worldwide, with metastasis, therapeutic resistance, and an immunosuppressive TME representing major barriers to successful treatment. Among the chemokine signaling networks implicated in these processes, the CCL2-CCR2 axis has emerged as an important regulator of tumor progression. By orchestrating the recruitment of monocytes, tumor-associated macrophages, myeloid-derived suppressor cells, and other stromal components, this pathway can establish an immune-permissive niche that supports angiogenesis, epithelial-mesenchymal transition, extracellular-matrix remodeling, metastatic dissemination, and resistance to chemotherapy, targeted therapies, and immunotherapy. Mechanistically, CCL2-CCR2 signaling interacts with key oncogenic pathways, including PI3K/Akt/mTOR, STAT3, NF-κB, Toll-like receptor signaling, and non-coding RNA-mediated networks, thereby amplifying pro-tumor inflammatory circuits within the lung TME. Although accumulating evidence indicates that the axis can exert context-dependent tumor-suppressive effects under specific biological conditions, such as promoting M1 macrophage recruitment or enhancing antitumor immunity in selected settings, its overall contribution in lung cancer appears predominantly tumor-promoting. This review comprehensively summarizes the molecular mechanisms governing CCL2-CCR2 signaling in primary lung cancer and in lung metastases. We further discuss emerging therapeutic strategies directed at this axis, including CCR2 antagonists, CCL2-neutralizing agents, engineered immune-cell approaches, and rational combinations with immune-checkpoint inhibitors and targeted therapies. Collectively, the current evidence provides a strong biological rationale and preliminary translational support for further investigation of the CCL2-CCR2 axis as a potential therapeutic target and exploratory biomarker in advanced lung cancer. However, clinical validation remains limited, and additional well-designed studies are required to determine whether modulation of this pathway can meaningfully improve patient outcomes.