Breast cancer remains the leading cause of cancer-related death among women worldwide. An increasing number of studies highlight the contribution of environmental and lifestyle factors, including cosmetic use, in its development.

To assess the association between cosmetic and dietary habits and breast cancer risk among women in Benin.

A case-control study was conducted involving 100 women diagnosed with breast cancer and matched 200 controls in the departments of visceral surgery, internal medicine, dermatology-venereology, and rheumatology at CNHU-HKM, and the gynecology-obstetrics department of CHU-MEL. Data were collected using a standardized questionnaire addressing family history, dietary patterns, and cosmetic product usage.

In multivariate analysis, several cosmetic practices including the use of alkaline soaps (OR_a = 7.26; p = 0.001), scented body lotions (OR_a = 25.90; p < 0.001), perfumes (OR_a = 30.43; p < 0.01), deodorants (OR_a = 5.76; p = 0.009), shampoos/conditioners (OR_a = 31.92; p < 0.001), and lipsticks (OR_a = 69.12; p = 0.018) were significantly associated with increased breast cancer risk. First-degree family history of breast cancer was associated with more than a threefold increase in risk. Contrary to existing literature, the consumption of soy, beans, and sesame also appeared to be linked to a higher risk of breast cancer in this population.

Our results show a possible association between environmental factors-particularly the use of cosmetic products-and breast cancer. These results underscore a compelling need for a national cosmetovigilance system in Benin and public health initiatives promoting healthier lifestyles, especially among genetically predisposed women.

Numerous psychosocial interventions have been developed to improve physical and psychological health-related outcomes among breast cancer survivors (BCS). Given the longstanding racial and ethnic disparities in breast cancer, culturally adapted psychosocial interventions aim to meet the unique needs of racial and ethnic minority BCS. This systematic review evaluates the efficacy of culturally adapted psychosocial interventions in improving psychological distress and quality of life for racial and ethnic minority BCS.

Search criteria included the following: studies reported psychosocial interventions with a control group, were conducted in the U.S., were culturally adapted for a racial or ethnic minority group, and included at least one of our target outcomes (distress, depression, anxiety, stress, mood disturbance, quality of life, coping, adjustment). Systematic searches were conducted using PubMed/MEDLINE, Scopus, CINAHL, and PsycINFO databases. The Effective Public Health Practice Project Quality Assessment Tool was used to evaluate risk of bias.

Twenty-three studies met inclusion criteria. Interventions were adapted for Asian/Asian American, Latina, and African American/Black female patients, the vast majority of whom were diagnosed with non-metastatic breast cancer. Most studies used methodology classified as "weak" and did not report significant improvements in target outcomes compared to the control group.

Future culturally adapted psychosocial interventions should include more diverse patient populations (e.g., race and ethnicity, gender identity) and more rigorous study designs. Review findings have important implications for future research and practice, as survivorship needs for BCS increase and notable disparities for racial and ethnic minority patients persist.

PROSPERO CRD42022384472.

Therapy-related myeloid neoplasms (t-MN) are an aggressive and heterogeneous group of myeloid disorders with no established guidelines for frontline treatment. This retrospective study of 53 consecutive t-MN patients at our institution evaluated the influence of clinical features, treatment approaches, and prognostic indicators on clinical outcomes of t-MN. The 1-year, 3-year, and 5-year overall survival (OS) rates were 61.0%, 50.0%, and 36.0%, respectively. Multivariate analysis revealed that age ≥ 60 (p = 0.009), TP53 (p = 0.040) and RAS mutations (p = 0.018) were associated with inferior OS. After induction therapy, patients who received a venetoclax-based regimen (venetoclax group) had an overall response rate (ORR) of 96.2%, compared with 63.6% in the chemotherapy group (p = 0.007). The venetoclax group tended to have better OS and DFS than the chemotherapy group (p = 0.052 and p = 0.078). Importantly, ORR rates and OS were higher in some subgroups of the venetoclax group, especially in patients over 60 years old and patients with intermediate/adverse risk. This study demonstrates the feasibility of venetoclax-based combination regimens for the treatment of t-MN and may influence decision-making for frontline therapy.

IHP is a rare inflammatory disorder characterized by dural thickening. Its nonspecific presentation often leads to diagnostic challenges and potential misdiagnosis as a neoplasm. Literature review and illustrative case example. PubMed search using terms related to IHP yielded 272 candidate citations, 50 of which met study criteria and were included. A 40-year-old woman presented with headache, dizziness, and blurred vision. Surgical intervention via right craniotomy was recommended due to diagnostic uncertainty, symptomatic mass effect, and the potential for a malignant diagnosis. A near-total resection of the mass and its dural base was performed given the involvement of the transverse-sigmoid sinuses; histopathology revealed dense fibrous tissue with chronic inflammatory cell infiltration. Immunohistochemistry was positive for CD3 and CD20, and negative for EMA, SSTR2, IgG, and IgG4, confirming the diagnosis of IHP. Review of the literature identified 117 patients presenting at a median age of 51 years with slight female predominance. Headache was the most common symptom (94%), followed by cranial nerve deficits (49%). MRI was used in all cases, with the tentorium being the most frequent site of involvement (48%). Treatment typically involved biopsy (47%), resection (11%), long-term steroids (56%), or steroid taper (44%). Radiographic recurrence was observed in 35%. Based on the experience from our case and supportive summative evidence from the literature, we developed a clinical decision-making schema to assist clinicians in recognizing and managing IHP. IHP remains a diagnostic challenge due to its rarity, nonspecific presentation, and potentially confounding radiographic features.

Mesenchymal stem cell (MSC)-derived exosomes revealed therapeutic ability, particularly in cancer treatment, by transferring bioactive molecules like miRNAs. Hypoxia, a common tumor condition, influences both tumor progression and MSC behavior. This review explores how hypoxic conditions affect MSC-derived exosomes and their impact on cancer-related pathways and genes.

The current systematic review study was conducted by searching four different databases, including PubMed, Scopus, Embase, and Web of Science, using keywords such as mesenchymal stem cells, exosomes, hypoxia, cancer, and related terms. All original pre-clinical studies that focused on the role and effect of hypoxia in MSC-derived extracellular vesicles in different cancers were included. Data were collected qualitatively.

Overall, 264 articles were identified from searching in databases, and eight of them met the eligibility criteria and were included in the current study. Among the articles, four focused on lung cancer, two on breast cancer, one on hepatocellular carcinoma, and one on Multiple Myeloma. The results indicated that MSC-derived exosomes have an enhanced effect on cell viability, migration, proliferation, and invasion of cancerous cells both in vitro and in vivo settings, and also cause a reduction in apoptosis in these cells. Besides, hypo MSC-exosomes can change the expression of some miRNAs in cancer cells, which affect different signaling pathways.

In general, the current study suggests that hypoxia-preconditioning of MSC-derived exosomes can influence specific genes, miRNAs, and signaling pathways in cancer cells, leading to increased proliferation, migration, and invasion, as well as decreased apoptosis. Besides, the biological effects of hypoxia-modulated exosomes seem to be significantly context-dependent. Although they may exacerbate malignancy in cancer microenvironments, analogous pathways can also facilitate tissue repair and regeneration in non-cancerous situations.

We performed a systematic review and meta-analysis to investigate the efficacy of peptide receptor radionuclide therapy (PRRT) by using radiolabeled somatostatin analogues in high grade gastro-entero-pancreatic neoplasms (GEP-NEN).

All clinical studies published up to March 2025, including patients with grade 3 (G3) GEP-NEN treated with [¹⁷⁷Lu] Lu-DOTA-TATE and/or [⁹⁰Y] Y-SSA, were identified based on systematic searches in the PubMed and Embase databases. Eligible studies had to report at least one of the following outcomes: 1) response to therapy evaluated according to RECIST (version 1.1 as complete response, partial response, stable disease, progressive disease; 2) median progression free survival (PFS) with 95% confidence intervals (CI); 3) median overall survival (OS) with 95% CI. Objective response rate (ORR) and disease control rate (DCR) were considered as primary outcomes.

The final analysis included 7 studies accounting for a total of 317 patients with G3 disease (ranging from 18 to 112). Six studies evaluated response to therapy according to RECIST in 288 patients, and in 4 of them patients were also stratified according to ki67 values. The pooled ORR and DCR were 34% (95% CI: 22-46) and 64% (95% CI: 52-76), respectively. The funnel plot indicated no publication bias among these studies. Five studies reported in 239 patients median PFS with 95% CI, with a pooled estimate of 13.88 (95% CI: 10.33-18.64) months. Three studies fully reported in 174 patients median OS with 95% CI, with a pooled estimate of 29.95 (95% CI: 19.80-45.30) months.

In patients with G3 GEP-NEN, PRRT may provide substantial disease control and response rates, and it seems able to delay the progression of the disease.

Neuroendocrine neoplasms (NENs) are a heterogeneous group of neoplasms encompassing both well differentiate neuroendocrine tumors (NETs), and poorly differentiated neuroendocrine carcinomas (NECs). This classification is supported by distinct histological, clinical, and molecular profiles. NETs are typically slow-growing and hormone-producing, with organoid architecture and frequent associations with hereditary syndromes such as multiple endocrine neoplasia type 1 (MEN1) and von Hippel-Lindau (VHL) disease. In contrast, NECs are highly malignant, rapidly proliferating tumors characterized by mutations in adenocarcinoma-driver genes and in addition to TP53 mutations and RB1 inactivation, without hereditary links to endocrine tumor syndomes. Recent WHO classifications introduced site-specific grading systems, including NET G3 in the digestive, urogenital, gynecological and head and neck organs. There is growing evidence of progression from NET G1 to G3 with occasionally NEC-like features via acquired TP53 mutations. Advances in transcription factor profiling related to hormonal expression, molecular alterations resulted in further subtyping especially in pancreatic, pulmonary, and pituitary NETs. These tools support more precise treatment strategies. Genomic studies focusing on pancreatic NETs highlighted mutations in MEN1, DAXX, ATRX, and targets in mTOR pathway. NECs display higher tumor mutation burdens and harbor various actionable alterations. Approximately 5-10% of NETs are associated with hereditary syndromes, though recent findings suggest germline pathogenic variants, which were present in additional 5% of apparently sporadic NETs and NECs, requiring further study. An integrated histological, molecular, and clinical approach is essential to improve the classification, prognostication, and management of NENs, while recognizing the distinct biology of individual subtypes.

Familial non-medullary, follicular cell-derived thyroid neoplasms represent a genetically diverse and under-recognized group of tumors arising from follicular epithelial cells. These familial thyroid tumors are subclassified into syndromes where thyroid tumors represent the major disease manifestation and syndromes with a predominance of non-thyroid neoplasms. Among the latter group, germline mutations in the DICER1 and PTEN genes are increasingly implicated in syndromic forms of follicular-derived thyroid disease. DICER1 syndrome and PTEN-hamartoma tumor syndrome, encompassing Cowden syndrome and related entities, confer a high organ-specific predisposition to benign and malignant thyroid lesions. Both syndromes demonstrate distinctive clinicopathologic patterns, including early-onset thyroid follicular nodular disease, multifocal follicular adenomas, and increased risk for thyroid malignancies. Recognizing clinical, anatomical, and histomorphological clues when evaluating thyroid specimens (particularly bilateral nodules, multinodularity, histologically distinct neoplasms, multiple adenomatous nodules, macrofollicular pattern, oncocytic features, unusual adenoma subtypes, young male gender, or early presentation) can prompt genetic evaluation. Here, we review the molecular pathogenesis, clinical features, histologic spectrum, and diagnostic strategies associated with familial follicular cell-derived thyroid tumors caused by DICER1 and PTEN germline alterations. Increased awareness of these entities by pathologists and clinicians is critical to ensure timely diagnosis, risk-appropriate surveillance, and cascade testing in affected families.

HCC is characterized by extensive ECM remodeling, primarily mediated by stromal cells. While cancer-associated fibroblasts are known contributors to tumor fibrosis, their transcriptional diversity and role in immune modulation within the HCC tumor microenvironment remain poorly resolved. Integrative analysis of six public HCC scRNA-seq datasets was employed to identify ECM-active stromal cells. High-ECM cells were re-clustered and fibroblast subtypes were defined through differential expression, pathway enrichment, lineage scoring and cell-cell interaction modeling. Spatial transcriptomic mapping and tissue-level profiling were performed to validate and prioritize ECM-related genes for experimental analysis. COL1A1 and COL3A1 were selected for siRNA-mediated knockdown in HepG2 and HepB3 cells followed by RT-qPCR, Western blot, proliferation, colony formation and wound healing assays. ECM activity analysis identified fibroblasts as the most ECM-enriched stromal population. Reclustering of ECM-high stromal cells identified eight distinct subtypes and targeted fibroblast clustering revealed five functionally diverse states. GO and spatial transcriptomic analysis confirmed subtype-specific functions and localization. In silico tissue profiling further prioritized COL1A1 and COL3A1 as pan-mesenchymal ECM genes enriched in fibrogenic fibroblast subsets. CellChat analysis revealed myofibroblasts and inflammatory CAFs as dominant signal senders. Knockdown reduced COL1A1 and COL3A1 expression at both mRNA and protein levels, and enhanced HCC cell proliferation, migration and colony formation. This study identifies transcriptionally and functionally distinct fibroblast subtypes in HCC and highlights COL1A1 and COL3A1 as key matrix-regulatory genes expressed in fibrogenic stromal subsets.

Although defects in the mismatch repair (MMR) system have been occasionally reported in aggressive/metastatic pituitary neuroendocrine tumors (PitNETs), the potential role of MMR dysregulation in pituitary tumorigenesis is largely unknown. This study aimed to evaluate the expression of the four key MMR components in a large series of PitNETs. MMR gene expression was studied by RT-qPCR in 127 tumors (54 PIT1, 51 SF1, 22 TPIT), and semi-quantitative immunohistochemistry (score 0-12) in selected cases (n=46). MSH2/6 and MLH1 promoters methylation was studied in 96 tumors. Except for MLH1, tumor lineage of origin was the most significant factor influencing MMR transcripts (P=0.005, <0.001 and 0.039 for MSH2/6 and PMS2, respectively), the highest levels being observed in SF1 tumors. Within subgroups, MMR transcripts were significantly lower in large/invasive PIT1 and in functioning TPIT tumors. MSH2 promoter methylation was occasionally associated with reduced MSH2 expression. Global loss of MSH6 (score 0), defining MMR deficiency, was observed in a single silent lactotroph PitNET, unrelated to the Lynch's syndrome. Near global loss involving MSH6, MSH2 or PMS2 (score 1) was observed in 5 tumors (1 lactotroph, 1 SF1, 3 TPIT). MMR mutations were excluded in 4/5 cases but 2 had LOH at MSH2/MSH6 loci. Heterogeneous immunostaining for any MMR (score 2-4) was also observed in 15 cases. In conclusion, MMR deficiency was rarely observed (2.2%) but reduced MMR expression could be found, especially in functioning corticotroph and invasive lactotroph tumors. The molecular mechanisms and prognostic significance of such findings would deserve further investigation.