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20 pages, 3046 KiB  
Article
Fractions and Compounds Obtained from Transformed Plant Cell Cultures of Lopezia racemosa Show Anti-Inflammatory and Cytotoxic Activities
by Lizbeth Coronel-Pastor, María Luisa Villarreal, Alejandro Zamilpa, Maribel Herrera-Ruiz, Manases González-Cortazar, Laura Alvarez, Irene Perea-Arango, Norma Elizabeth Moreno-Anzúrez, Mario Rodríguez Monroy and José de Jesús Arellano-García
Plants 2025, 14(16), 2585; https://doi.org/10.3390/plants14162585 - 20 Aug 2025
Abstract
Lopezia racemosa Cav., commonly known as “cancer herb” in indigenous communities, has long been used for its medicinal properties. The biotechnological production of its bioactive compounds through genetic transformation represents a valuable approach for obtaining pharmacologically relevant substances. The initial focus of this [...] Read more.
Lopezia racemosa Cav., commonly known as “cancer herb” in indigenous communities, has long been used for its medicinal properties. The biotechnological production of its bioactive compounds through genetic transformation represents a valuable approach for obtaining pharmacologically relevant substances. The initial focus of this study was to identify compounds previously reported in the species; however, phytochemical analysis by HPLC and NMR led to the isolation and identification of two pentacyclic triterpene esters not previously described in L. racemosa: 3-O-[(E)-feruloyl]-maslinic acid (1) and 3-O-[(E)-feruloyl]-corosolic acid (2), identified as constituents of fraction 33. The LRTC3.1 callus line was obtained from hairy roots generated by infecting L. racemosa leaf explants with Agrobacterium rhizogenes strain ATCC15834/pTDT. The crude extract, specific fractions, and the mixture of these compounds demonstrated significant anti-inflammatory and cytotoxic activities. Anti-inflammatory activity was evaluated using the carrageenan-induced mouse paw edema model, where the crude extract achieved 51.02% inhibition of inflammation compared to meloxicam (30.86%). Cytotoxicity was assessed against three human cancer cell lines: breast carcinoma (MCF7), cervical carcinoma (SiHa), and colon carcinoma (HCT-15). Fractions FD (28–29) and 33 exhibited potent cytotoxic effects, with IC50 values of 0.508 and 1.345 µg/mL against SiHa cells, and 0.053 and 2.693 µg/mL against MCF-7 cells, respectively. These findings suggest that transformed L. racemosa cultures represent a promising source of bioactive compounds for potential therapeutic development. Full article
(This article belongs to the Section Phytochemistry)
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31 pages, 2785 KiB  
Review
Mechanisms and Therapeutic Advances of PXR in Metabolic Diseases and Cancer
by Yuanbo Bi, Sifan Liu, Lei Wang, Daiyin Peng, Weidong Chen, Yue Zhang and Yanyan Wang
Int. J. Mol. Sci. 2025, 26(16), 8029; https://doi.org/10.3390/ijms26168029 (registering DOI) - 20 Aug 2025
Abstract
The pregnane X receptor (PXR), a ligand-activated nuclear receptor, plays a central role in regulating the metabolism of both endogenous substances and xenobiotics. In recent years, increasing evidence has highlighted its involvement in chronic diseases, particularly metabolic disorders and cancer. PXR modulates drug-metabolizing [...] Read more.
The pregnane X receptor (PXR), a ligand-activated nuclear receptor, plays a central role in regulating the metabolism of both endogenous substances and xenobiotics. In recent years, increasing evidence has highlighted its involvement in chronic diseases, particularly metabolic disorders and cancer. PXR modulates drug-metabolizing enzymes, transporters, inflammatory factors, lipid metabolism, and immune-related pathways, contributing to the maintenance of hepatic–intestinal barrier homeostasis, energy metabolism, and inflammatory responses. Specifically, in type 2 diabetes mellitus (T2DM), PXR influences disease progression by regulating glucose metabolism and insulin sensitivity. In obesity, it affects adipogenesis and inflammatory processes. In atherosclerosis (AS), PXR exerts protective effects through cholesterol metabolism and anti-inflammatory actions. In metabolic dysfunction-associated steatotic liver disease (MASLD), it is closely associated with lipid synthesis, oxidative stress, and gut microbiota balance. Moreover, PXR plays dual roles in various cancers, including hepatocellular carcinoma, colorectal cancer, and breast cancer. Currently, PXR-targeted strategies, such as small molecule agonists and antagonists, represent promising therapeutic avenues for treating metabolic diseases and cancer. This review comprehensively summarizes the structural features, signaling pathways, and gene regulatory functions of PXR, as well as its role in metabolic diseases and cancer, providing insights into its therapeutic potential and future drug development challenges. Full article
(This article belongs to the Section Molecular Endocrinology and Metabolism)
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20 pages, 744 KiB  
Review
HER2/neu as a Signaling and Therapeutic Marker in Uterine Serous Carcinoma
by Victoria M. Ettorre, Luca Palmieri, Valentino Clemente and Alessandro D. Santin
Cells 2025, 14(16), 1282; https://doi.org/10.3390/cells14161282 - 19 Aug 2025
Abstract
Research into aggressive gynecologic cancers such as uterine serous carcinoma (USC) has recently evolved from chemotherapy to the development of drugs targeting specific biomarkers differentially expressed/active in tumor cells. One such target is HER2/neu, which plays an important role in the coordination of [...] Read more.
Research into aggressive gynecologic cancers such as uterine serous carcinoma (USC) has recently evolved from chemotherapy to the development of drugs targeting specific biomarkers differentially expressed/active in tumor cells. One such target is HER2/neu, which plays an important role in the coordination of cell growth and differentiation. Importantly, when overexpressed and/or amplified in tumor cells, the downstream tyrosine kinase of HER2/neu becomes constitutively activated, causing dysregulated gene transcription. In breast cancer patients, HER2/neu has been successfully utilized for many years as a target for multiple monoclonal antibodies and more recently antibody–drug conjugates (ADCs). Use in gynecologic malignancies has been slower, however, due to recently identified unique characteristics of HER2/neu protein expression and gene amplification in biologically aggressive tumors such as USC including its major heterogeneity and lack of apical staining when compared to breast cancer. Accordingly, the use of optimal testing algorithms for HER2/neu status in patients with USC may have important implications for the development of novel, effective, and targeted treatment modalities against this lethal variant of endometrial cancer. In this review, we discuss HER2/neu gene expression in USC, evaluate the efficacy of HER2/neu-directed therapies in both preclinical and clinical settings, and discuss possible mechanisms of resistance to HER2/neu targeting agents. Full article
(This article belongs to the Special Issue Signaling Pathways in Endometrial Cancer Cells)
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18 pages, 511 KiB  
Review
Roles and Prospective Applications of Ferroptosis Suppressor Protein 1 (FSP1) in Malignant Tumor Treatment
by Zhesi Jin, Qian Zhang, Yinlong Pan, Hao Chen, Ke Zhou, Huazhong Cai and Pan Huang
Curr. Oncol. 2025, 32(8), 456; https://doi.org/10.3390/curroncol32080456 - 14 Aug 2025
Viewed by 151
Abstract
Ferroptosis suppressor protein 1 (FSP1) has emerged as a critical regulator of ferroptosis, an iron-dependent form of programmed cell death with significant therapeutic potential in cancer treatment. Despite rapidly expanding research, current knowledge on FSP1 remains fragmented across various tumor types and experimental [...] Read more.
Ferroptosis suppressor protein 1 (FSP1) has emerged as a critical regulator of ferroptosis, an iron-dependent form of programmed cell death with significant therapeutic potential in cancer treatment. Despite rapidly expanding research, current knowledge on FSP1 remains fragmented across various tumor types and experimental contexts. The aim of this review is to systematically integrate the latest evidence regarding the molecular structure, biological functions, and regulatory mechanisms controlling FSP1 expression, emphasizing its involvement in tumor progression and resistance to therapy. Readers can expect comprehensive coverage of FSP1’s structural characteristics, enzymatic roles, transcriptional and post-transcriptional regulation, and its pathological significance in hepatocellular carcinoma, colorectal cancer, pancreatic cancer, gastric cancer, breast cancer, lung cancer, and leukemia. We further evaluate emerging therapeutic strategies targeting FSP1 aimed at overcoming resistance and improving clinical outcomes. Relevant studies were systematically identified by searching PubMed, Web of Science, and Embase databases, focusing particularly on the recent and impactful literature to guide future research directions. Full article
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16 pages, 1932 KiB  
Article
2.5D Deep Learning and Machine Learning for Discriminative DLBCL and IDC with Radiomics on PET/CT
by Fei Liu, Wen Chen, Jianping Zhang, Jianling Zou, Bingxin Gu, Hongxing Yang, Silong Hu, Xiaosheng Liu and Shaoli Song
Bioengineering 2025, 12(8), 873; https://doi.org/10.3390/bioengineering12080873 - 12 Aug 2025
Viewed by 418
Abstract
We aimed to establish non-invasive diagnostic models comparable to pathology testing and explore reliable digital imaging biomarkers to classify diffuse large B-cell lymphoma (DLBCL) and invasive ductal carcinoma (IDC). Our study enrolled 386 breast nodules from 279 patients with DLBCL and IDC, which [...] Read more.
We aimed to establish non-invasive diagnostic models comparable to pathology testing and explore reliable digital imaging biomarkers to classify diffuse large B-cell lymphoma (DLBCL) and invasive ductal carcinoma (IDC). Our study enrolled 386 breast nodules from 279 patients with DLBCL and IDC, which were pathologically confirmed and underwent 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography/computed tomography (PET/CT) examination. Patients from two centers were separated into internal and external cohorts. Notably, we introduced 2.5D deep learning and machine learning to extract features, develop models, and discover biomarkers. Performances were assessed using the area under curve (AUC) and confusion matrix. Additionally, the Shapley additive explanation (SHAP) and local interpretable model-agnostic explanations (LIME) techniques were employed to interpret the model. On the internal cohort, the optimal model PT_TDC_SVM achieved an accuracy of 0.980 (95% confidence interval (CI): 0.957–0.991) and an AUC of 0.992 (95% CI: 0.946–0.998), surpassing the other models. On the external cohort, the accuracy was 0.975 (95% CI: 0.913–0.993) and the AUC was 0.996 (95% CI: 0.972–0.999). The optimal imaging biomarker PET_LBP-2D_gldm_DependenceEntropy demonstrated an average accuracy of 0.923/0.937 on internal/external testing. Our study presented an innovative automated model for DLBCL and IDC, identifying reliable digital imaging biomarkers with significant potential. Full article
(This article belongs to the Section Biosignal Processing)
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36 pages, 543 KiB  
Review
Homologous Recombination Deficiency in Ovarian and Breast Cancers: Biomarkers, Diagnosis, and Treatment
by Bhaumik Shah, Muhammad Hussain and Anjali Seth
Curr. Issues Mol. Biol. 2025, 47(8), 638; https://doi.org/10.3390/cimb47080638 - 8 Aug 2025
Viewed by 1125
Abstract
Homologous recombination deficiency (HRD) is a pivotal biomarker in precision oncology, driving therapeutic strategies for ovarian and breast cancers through impaired DNA double-strand break repair. This narrative review synthesizes recent advances (2021–2025) in HRD’s biological basis, prevalence, detection methods, and clinical implications, focusing [...] Read more.
Homologous recombination deficiency (HRD) is a pivotal biomarker in precision oncology, driving therapeutic strategies for ovarian and breast cancers through impaired DNA double-strand break repair. This narrative review synthesizes recent advances (2021–2025) in HRD’s biological basis, prevalence, detection methods, and clinical implications, focusing on high-grade serous ovarian carcinoma (HGSOC; ~50% HRD prevalence) and triple-negative breast cancer (TNBC; 50–70% prevalence). HRD arises from genetic (BRCA1/2, RAD51C/D, PALB2) and epigenetic alterations (e.g., BRCA1 methylation), leading to genomic instability detectable via scars (LOH, TAI, LST) and mutational signatures (e.g., COSMIC SBS3). Advanced detection integrates genomic assays (Myriad myChoice CDx, Caris HRD, FoundationOne CDx), functional assays (RAD51 foci), and epigenetic profiling, with tools like HRProfiler and GIScar achieving >90% sensitivity. HRD predicts robust responses to PARP inhibitors (PARPi) and platinum therapies, extending progression-free survival by 12–36 months in HGSOC. However, resistance mechanisms (BRCA reversion, SETD1A/EME1, SOX5) and assay variability (60–70% non-BRCA concordance) pose challenges. We propose a conceptual framework in Section 10, integrating multi-omics, methylation analysis, and biallelic reporting to enhance detection and therapeutic stratification. Regional variations (e.g., Asian cohorts) and disparities in access underscore the need for standardized, cost-effective diagnostics. Future priorities include validating novel biomarkers (SBS39, miR-622) and combination therapies (PARPi with ATR inhibitors) to overcome resistance and broaden HRD’s applicability across cancers. Full article
(This article belongs to the Special Issue DNA Damage and Repair in Health and Diseases)
25 pages, 1677 KiB  
Review
The Multifaceted Role of Growth Differentiation Factor 15 (GDF15): A Narrative Review from Cancer Cachexia to Target Therapy
by Daria Maria Filippini, Donatella Romaniello, Francesca Carosi, Laura Fabbri, Andrea Carlini, Raffaele Giusti, Massimo Di Maio, Salvatore Alfieri, Mattia Lauriola, Maria Abbondanza Pantaleo, Lorena Arribas, Marc Oliva, Paolo Bossi and Laura Deborah Locati
Biomedicines 2025, 13(8), 1931; https://doi.org/10.3390/biomedicines13081931 - 8 Aug 2025
Viewed by 564
Abstract
Background: Growth Differentiation Factor 15 (GDF15) has emerged as a key biomarker and therapeutic target in oncology, with roles extending beyond cancer cachexia. Elevated GDF15 levels correlate with poor prognosis across several solid tumors, including colorectal, gastric, pancreatic, breast, lung, prostate, and head [...] Read more.
Background: Growth Differentiation Factor 15 (GDF15) has emerged as a key biomarker and therapeutic target in oncology, with roles extending beyond cancer cachexia. Elevated GDF15 levels correlate with poor prognosis across several solid tumors, including colorectal, gastric, pancreatic, breast, lung, prostate, and head and neck cancers. GDF15 modulates tumor progression through PI3K/AKT, MAPK/ERK, and SMAD2/3 signaling, thereby promoting epithelial-to-mesenchymal transition, metastasis, immune evasion, and chemoresistance via Nrf2 stabilization and oxidative stress regulation. Methods: We performed a narrative review of the literature focusing on the role of GDF15 in solid tumors, with a particular emphasis on head and neck cancers. Results: In head and neck squamous cell carcinoma (HNSCC), GDF15 overexpression is linked to aggressive phenotypes, radioresistance, poor response to induction chemotherapy, and failure of immune checkpoint inhibitors (ICIs). Similar associations are observed in colorectal, pancreatic, and prostate cancer, where GDF15 contributes to metastasis and therapy resistance. Targeting the GDF15-GFRAL axis appears therapeutically promising: the monoclonal antibody ponsegromab improved cachexia-related outcomes in the PROACC-1 trial, while visugromab combined with nivolumab enhanced immune response in ICI-refractory tumors. Conclusions: Further investigation is warranted to delineate the role of GDF15 across malignancies, refine patient selection, and evaluate combinatorial approaches with existing treatments. Full article
(This article belongs to the Special Issue Head and Neck Tumors, 4th Edition)
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16 pages, 2369 KiB  
Article
HMGB1 Deficiency Occurs in a Broad Range of Human Cancers and Is Often Associated with Unfavorable Tumor Phenotype
by Viktoria Chirico, Hena Sharifi, Maria Christina Tsourlakis, Seyma Büyücek, Clara Marie von Bargen, Katharina Möller, Florian Lutz, David Dum, Martina Kluth, Claudia Hube-Magg, Georgia Makrypidi-Fraune, Piero Caneve, Maximilian Lennartz, Morton Freytag, Sebastian Dwertmann Rico, Simon Kind, Viktor Reiswich, Eike Burandt, Till S. Clauditz, Patrick Lebok, Christoph Fraune, Till Krech, Sarah Minner, Andreas H. Marx, Waldemar Wilczak, Ronald Simon, Guido Sauter, Stefan Steurer and Kristina Jansenadd Show full author list remove Hide full author list
Diagnostics 2025, 15(15), 1974; https://doi.org/10.3390/diagnostics15151974 - 6 Aug 2025
Viewed by 329
Abstract
Background/Objectives: Aberrant expression of high-mobility group protein B1 (HMGB1) has been linked to cancer development and progression. Methods: To better comprehend the role of HMGB1 expression in cancer, a tissue microarray containing 14,966 samples from 134 different tumor entities and 608 [...] Read more.
Background/Objectives: Aberrant expression of high-mobility group protein B1 (HMGB1) has been linked to cancer development and progression. Methods: To better comprehend the role of HMGB1 expression in cancer, a tissue microarray containing 14,966 samples from 134 different tumor entities and 608 samples of 76 different normal tissue types was analyzed by immunohistochemistry. Results: Strong HMGB1 staining occurred in almost all normal cell types and in most cancers. Of 11,808 evaluable cancers, only 7.8% showed complete absence of HMGB1 staining (HMGB1 deficiency) while 9.9% showed 1+, 25.0% showed 2+, and 57.2% showed 3+ HMGB1 positivity. Absence of HMGB1 staining mostly occurred in pheochromocytoma (90.0%), seminoma (72.4%), gastrointestinal stromal tumor (28.6%), adrenal cortical carcinoma (25.0%), and Hodgkin’s lymphoma (25.0%). Low HMGB1 staining was linked to poor histologic grade (p < 0.0001), advanced pT stage (p < 0.0001), high UICC stage (p < 0.0001), and distant metastasis (p = 0.0413) in clear cell renal cell carcinoma, invasive tumor growth in urothelial carcinoma (pTa vs. pT2–4, p < 0.0001), mismatch repair deficiency (p = 0.0167) in colorectal cancers, and advanced pT stage in invasive breast carcinoma of no special type (p = 0.0038). Strong HMGB1 staining was linked to nodal metastases in high-grade serous ovarian carcinomas (p = 0.0213) and colorectal adenocarcinomas (p = 0.0137), as well as to poor histological grade in squamous cell carcinomas (p = 0.0010). Conclusions: HMGB1 deficiency and reduced HMGB1 expression occur in a broad range of different tumor entities. Low rather than strong HMGB1 staining is often linked to an aggressive tumor phenotype. Whether HMGB1 deficiency renders cells susceptible to specific drugs remains to be determined. Full article
(This article belongs to the Section Pathology and Molecular Diagnostics)
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7 pages, 1809 KiB  
Case Report
Seronegative Paraneoplastic Opsoclonus–Myoclonus–Ataxia Syndrome Secondary to Low Volume Endocrine-Sensitive Malignancy of Likely Breast Origin
by Geraint Berger, Caitlin Jackson-Tarlton, Daniel Rayson, Alexander Silver, Mark Walsh and Ashley Drohan
Curr. Oncol. 2025, 32(8), 440; https://doi.org/10.3390/curroncol32080440 - 6 Aug 2025
Viewed by 221
Abstract
A 51-year-old female presented to the emergency department with vertigo, visual disturbances, involuntary rapid repetitive eye movements, incoordination, and imbalance. Physical examination revealed opsoclonus, myoclonus, and bilateral limb and gait ataxia. Initial workup was negative for intracranial abnormalities, and no abnormalities were noted [...] Read more.
A 51-year-old female presented to the emergency department with vertigo, visual disturbances, involuntary rapid repetitive eye movements, incoordination, and imbalance. Physical examination revealed opsoclonus, myoclonus, and bilateral limb and gait ataxia. Initial workup was negative for intracranial abnormalities, and no abnormalities were noted on blood work or cerebrospinal fluid analysis. Tumor markers were within normal limits. As part of her diagnostic workup, a positron emission tomography (PET) scan was performed, which showed a highly FDG-avid solitary 7 mm left axillary lymph node. Ultrasound-guided percutaneous biopsy revealed metastatic poorly differentiated carcinoma. Histopathological examination could not conclusively distinguish between adenocarcinoma and squamous cell carcinoma. She was diagnosed with seronegative opsoclonus-myoclonus ataxia syndrome of paraneoplastic origin from an occult primary malignancy and started on pulsatile corticosteroids and intravenous immunoglobulin (IVIG), with only moderate symptomatic improvement. Given the anatomic location and immunohistochemical staining pattern of the lymph node, the malignancy was considered as being of primary breast origin. A left axillary lymph node dissection was performed, with 1/12 nodes testing positive for poorly differentiated carcinoma. The patient experienced significant improvement in her neurological symptoms 2–3 days following resection of the solitary malignant lymph node, largely regaining her functional independence. She went on to receive adjuvant radiotherapy to the breast and axilla, as well as adjuvant hormonal therapy. Full article
(This article belongs to the Section Surgical Oncology)
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17 pages, 2353 KiB  
Article
Repurposing a Lipid-Lowering Agent to Inhibit TNBC Growth Through Cell Cycle Arrest
by Yi-Chiang Hsu, Kuan-Ting Lee, Sung-Nan Pei, Kun-Ming Rau and Tai-Hsin Tsai
Curr. Issues Mol. Biol. 2025, 47(8), 622; https://doi.org/10.3390/cimb47080622 - 5 Aug 2025
Viewed by 297
Abstract
Triple-negative breast cancer (TNBC) is a highly aggressive and therapeutically challenging subtype of breast cancer due to its lack of estrogen receptors, progesterone receptors, and HER2 (Human epidermal growth factor receptor 2) expression, which severely limits available treatment options. Recently, Simvastatin—a widely used [...] Read more.
Triple-negative breast cancer (TNBC) is a highly aggressive and therapeutically challenging subtype of breast cancer due to its lack of estrogen receptors, progesterone receptors, and HER2 (Human epidermal growth factor receptor 2) expression, which severely limits available treatment options. Recently, Simvastatin—a widely used HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitor for hyperlipidemia—has garnered interest for its potential anticancer effects. This study investigates the therapeutic potential of Simvastatin in triple-negative breast cancer (TNBC). The results demonstrate that Simvastatin significantly inhibits the proliferation of TNBC cells, particularly MDA-MB-231, in a dose- and time-dependent manner. Mechanistically, Simvastatin primarily induces G1 phase cell cycle arrest to exert its antiproliferative effects, with no significant evidence of apoptosis or necrosis. These findings support the potential repositioning of Simvastatin as a therapeutic agent to suppress TNBC cell growth. Further analysis shows that Simvastatin downregulates cyclin-dependent kinase 4 (CDK4), a key regulator of the G1/S cell cycle transition and a known marker of poor prognosis in breast cancer. These findings highlight a novel, apoptosis-independent mechanism of Simvastatin’s anticancer action in TNBC. Importantly, given that many breast cancer patients also suffer from hyperlipidemia, Simvastatin offers dual therapeutic benefits—managing both lipid metabolism and tumor cell proliferation. Thus, Simvastatin holds promise as an adjunctive therapy in the treatment of TNBC and warrants further clinical investigation. Full article
(This article belongs to the Section Molecular Medicine)
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14 pages, 2501 KiB  
Article
Therapeutic Patterns and Surgical Decision-Making in Breast Cancer: A Retrospective Regional Cohort Study in Romania
by Ramona Andreea Cioroianu, Michael Schenker, Virginia-Maria Rădulescu, Tradian Ciprian Berisha, George Ovidiu Cioroianu, Mihaela Popescu, Cristina Mihaela Ciofiac, Ana Maria Petrescu and Stelian Ștefăniță Mogoantă
Clin. Pract. 2025, 15(8), 145; https://doi.org/10.3390/clinpract15080145 - 5 Aug 2025
Viewed by 199
Abstract
Background: Breast cancer is the most prevalent malignancy among women globally. In Romania, it is the most frequent form of cancer affecting women, with approximately 12,000 new cases diagnosed annually, and the second most common cause of cancer-related mortality, second only to [...] Read more.
Background: Breast cancer is the most prevalent malignancy among women globally. In Romania, it is the most frequent form of cancer affecting women, with approximately 12,000 new cases diagnosed annually, and the second most common cause of cancer-related mortality, second only to lung cancer. Methods: This study looked at 79 breast cancer patients from Oltenia, concentrating on epidemiology, histology, diagnostic features, and treatments. Patients were chosen based on inclusion criteria such as histopathologically verified diagnosis, availability of clinical and treatment data, and follow-up information. The analyzed biological material consisted of tissue samples taken from the breast parenchyma and axillary lymph nodes. Even though not the primary subject of this paper, all patients underwent immunohistochemical (IHC) evaluation both preoperatively and postoperatively. Results: We found invasive ductal carcinoma to be the predominant type, while ductal carcinoma in situ (DCIS) and mixed types were rare. We performed cross-tabulations of metastasis versus nodal status and age versus therapy type; none reached significance (all p > 0.05), suggesting observed differences were likely due to chance. A chi-square test comparing surgical interventions (breast-conserving vs. mastectomy) in patients who did or did not receive chemotherapy showed, χ2 = 3.17, p = 0.367, indicating that chemotherapy did not significantly influence surgical choice. Importantly, adjuvant chemotherapy and radiotherapy were used at similar rates across age groups, whereas neoadjuvant hormonal (endocrine) therapy was more common in older patients (but without statistical significance). Conclusions: Finally, we discussed the consequences of individualized care and early detection. Romania’s shockingly low screening rate, which contributes to delayed diagnosis, emphasizes the importance of improved population medical examination and tailored treatment options. Also, the country has one of the lowest rates of mammography uptake in Europe and no systematic population screening program. Full article
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20 pages, 2286 KiB  
Article
PD-1, PD-L1, and PD-L2 Expression as Predictive Markers in Rare Feline Mammary Tumors
by Maria Franco, Fernanda Seixas, Maria dos Anjos Pires, Anabela Alves, Andreia Santos, Carla Marrinhas, Hugo Vilhena, Joana Santos, Pedro Faísca, Patrícia Dias-Pereira, Adelina Gama, Jorge Correia and Fernando Ferreira
Vet. Sci. 2025, 12(8), 731; https://doi.org/10.3390/vetsci12080731 - 3 Aug 2025
Viewed by 438
Abstract
Feline mammary carcinoma (FMC) exhibits aggressive behavior, with limited treatment options. Given the relevance of the PD-1/PD-L1/PD-L2 axis in human breast cancer immunotherapy, this study assessed PD-1 and its ligands in rare FMC histotypes (n = 48) using immunohistochemistry on tumor cells (TCs), [...] Read more.
Feline mammary carcinoma (FMC) exhibits aggressive behavior, with limited treatment options. Given the relevance of the PD-1/PD-L1/PD-L2 axis in human breast cancer immunotherapy, this study assessed PD-1 and its ligands in rare FMC histotypes (n = 48) using immunohistochemistry on tumor cells (TCs), intratumoral lymphocytes (iTILs), and stromal tumor-infiltrating lymphocytes (sTILs). PD-1 was expressed in 13% of TCs, 85% of iTILs, and 94% of sTILs, while PD-L1 was observed in 46% of TCs, 96% of iTILs, and 100% of sTILs. PD-L2 was expressed in 79% of TCs and 100% of both iTILs and sTILs, with PD-L1/PD-L2 co-expression in 42% of TCs. Higher PD-1 IHC scores in TCs were associated with a less aggressive biological behavior; PD-L1 in iTILs was linked to skin ulceration, whereas PD-L2 in TCs was associated with its absence. Our findings highlight the relevance of the PD-1/PD-L1/PD-L2 immune checkpoint in rare FMC subtypes and support further investigation into checkpoint-blockade therapies. Full article
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17 pages, 2108 KiB  
Article
Unraveling the Role of Metabolic Endotoxemia in Accelerating Breast Tumor Progression
by Daniela Nahmias Blank, Ofra Maimon, Esther Hermano, Emmy Drai, Ofer Chen, Aron Popovtzer, Tamar Peretz, Amichay Meirovitz and Michael Elkin
Biomedicines 2025, 13(8), 1868; https://doi.org/10.3390/biomedicines13081868 - 31 Jul 2025
Viewed by 391
Abstract
Background: Obese women have a significantly higher risk of bearing breast tumors that are resistant to therapies and are associated with poorer prognoses/treatment outcomes. Breast cancer-promoting action of obesity is often attributed to elevated levels of insulin, glucose, inflammatory mediators, and misbalanced estrogen [...] Read more.
Background: Obese women have a significantly higher risk of bearing breast tumors that are resistant to therapies and are associated with poorer prognoses/treatment outcomes. Breast cancer-promoting action of obesity is often attributed to elevated levels of insulin, glucose, inflammatory mediators, and misbalanced estrogen production in adipose tissue under obese conditions. Metabolic endotoxemia, characterized by chronic presence of extremely low levels of bacterial endotoxin (lipopolysaccharide [LPS]) in the circulation, is a less explored obesity-associated factor. Results: Here, utilizing in vitro and in vivo models of breast carcinoma (BC), we report that subclinical levels of LPS typical for metabolic endotoxemia enhance the malignant phenotype of breast cancer cells and accelerate breast tumor progression. Conclusions: Our study, while focusing primarily on the direct effects of metabolic endotoxemia on breast tumor progression, also suggests that metabolic endotoxemia can contribute to obesity–breast cancer link. Thus, our findings add novel mechanistic insights into how obesity-associated metabolic changes, particularly metabolic endotoxemia, modulate the biological and clinical behavior of breast carcinoma. In turn, understanding of the mechanistic aspects underlying the association between obesity and breast cancer could help inform better strategies to reduce BC risk in an increasingly obese population and to suppress the breast cancer-promoting consequences of excess adiposity. Full article
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10 pages, 1468 KiB  
Article
Noninvasive Mapping of Extracellular Potassium in Breast Tumors via Multi-Wavelength Photoacoustic Imaging
by Jeff Folz, Ahmad Eido, Maria E. Gonzalez, Roberta Caruso, Xueding Wang, Celina G. Kleer and Janggun Jo
Sensors 2025, 25(15), 4724; https://doi.org/10.3390/s25154724 - 31 Jul 2025
Viewed by 335
Abstract
Elevated extracellular potassium (K+) in the tumor microenvironment (TME) of breast and other cancers is increasingly recognized as a critical factor influencing tumor progression and immune suppression. Current methods for noninvasive mapping of the potassium distribution in tumors are limited. Here, [...] Read more.
Elevated extracellular potassium (K+) in the tumor microenvironment (TME) of breast and other cancers is increasingly recognized as a critical factor influencing tumor progression and immune suppression. Current methods for noninvasive mapping of the potassium distribution in tumors are limited. Here, we employed photoacoustic chemical imaging (PACI) with a solvatochromic dye-based, potassium-sensitive nanoprobe (SDKNP) to quantitatively visualize extracellular potassium levels in an orthotopic metaplastic breast cancer mouse model, Ccn6-KO. Tumors of three distinct sizes (5 mm, 10 mm, and 20 mm) were imaged using multi-wavelength photoacoustic imaging at five laser wavelengths (560, 576, 584, 605, and 625 nm). Potassium concentration maps derived from spectral unmixing of the photoacoustic images at the five laser wavelengths revealed significantly increased potassium levels in larger tumors, confirmed independently by inductively coupled plasma mass spectrometry (ICP-MS). The PACI results matched ICP-MS measurements, validating PACI as a robust, noninvasive imaging modality for potassium mapping in tumors in vivo. This work establishes PACI as a promising tool for studying the chemical properties of the TME and provides a foundation for future studies evaluating the immunotherapy response through ionic biomarker imaging. Full article
(This article belongs to the Special Issue Advances in Photoacoustic Resonators and Sensors)
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21 pages, 2038 KiB  
Article
Germline BARD1 Mutation in High-Risk Chinese Breast and Ovarian Cancer Patients
by Ava Kwong, Cecilia Y. S. Ho, Chun Hang Au and Edmond S. K. Ma
Cancers 2025, 17(15), 2524; https://doi.org/10.3390/cancers17152524 - 30 Jul 2025
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Abstract
Background: The prevalence of BARD1 mutations in breast and ovarian cancers varies across different ethnic groups. Evaluating the cancer risk and clinical significance of BARD1 mutations in the local Chinese patients with breast cancer, ovarian cancer, or both is clinically important for designing [...] Read more.
Background: The prevalence of BARD1 mutations in breast and ovarian cancers varies across different ethnic groups. Evaluating the cancer risk and clinical significance of BARD1 mutations in the local Chinese patients with breast cancer, ovarian cancer, or both is clinically important for designing an appropriate surveillance scheme. Methods: This study used a 30 gene panel to identify BARD1 germline mutations in 2658 breast and ovarian cancer patients. Results: Among this cohort, the BARD1 mutation prevalence was 0.45% for breast cancer and 0.29% for ovarian cancer. In our 12 mutation carriers, we identified eight types of mutation variants, including three novel mutations. BARD1 mutation carriers were more likely to have a family history of liver, prostate, and cervical cancers (p-values = 0.004, 0.018, and 0.037, respectively) than patients who tested negative for mutations. Among the BARD1 mutants, the majority of the breast tumors were invasive ductal carcinoma (NOS type) (10/11, 90.9%) of high-grade disease (9/9, 100%) and half of them were triple-negative breast cancer (5/10, 50%). Conclusions: Although the prevalence of BARD1 mutations is low and the penetrance is incomplete, we recommend including BARD1 in the test panel for breast cancer patients. Our data suggest that more comprehensive surveillance management may be considered in mutation carriers due to the familial aggregation of a relatively wide spectrum of cancers. Full article
(This article belongs to the Section Cancer Causes, Screening and Diagnosis)
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