Introduction: Breast carcinoma is a heterogeneous disease, characterised by diverse clinical behaviour. The aim of this study was to assess how cleaved caspase-3 and Ki-67 index, evaluated on diagnostic biopsy, are related to response to neoadjuvant chemotherapy in the context of molecular subtype, post-treatment tumour, N category, and grade.
Material And Methods: A retrospective analysis was carried out among 110 breast cancer patients. Ki-67 levels and caspase-3 expression on diagnostic biopsy were explored regarding their relation to tumour grade and molecular subtype, ypT, ypN categories, and T and N categories according to Sataloff tumour response evaluation.
Results: A statistically significant relationship was found between Ki-67 levels and tumour grade K-W = 24.2932, < 0.0001; molecular subtype K-W = 28.5439, < 0.00000967538; size and invasion of the primary tumour after neoadjuvant chemotherapy K-W = 11.7944, < 0.0377169; caspase-3 expression after neoadjuvant therapy, evaluated according to the Sataloff classification χ = 5.97, df = 1, = 0.0145.
Discussion: No significant difference was found between Ki-67 expression in patients with pathological complete response, compared to those with partial and no response, a statistically significant difference in cases with different molecular subtype, histology grade, and tumour stage after neoadjuvant therapy. Cleaved caspase-3-positive breast cancer cases are often better responders to neoadjuvant therapy, but with no significant correlation to molecular subtype, high-grade categories, or tumour stage.
Conclusions: The caspase-3 and Ki-67 index on diagnostic biopsy are related to post-neoadjuvant treatment prognostic factors (ypT stage, grade), proving them useful for prediction of treatment response to neoadjuvant therapy and further patient management.
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http://dx.doi.org/10.5114/pm.2024.136962 | DOI Listing |
Gastric Cancer
January 2025
Department of Biochemistry and Molecular Biology, Key Laboratory of Breast Cancer Prevention and Therapy, Ministry of Education, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China.
Background: Gastroesophageal junction adenocarcinoma (GEJAC) exhibits distinct molecular characteristics due to its unique anatomical location. We sought to investigate effective and reliable molecular classification of GEJAC to guide personalized treatment.
Methods: We analyzed the whole genomic, transcriptomic, T-cell receptor repertoires, and immunohistochemical data in 92 GEJAC patients and delineated the landscape of genetic and immune alterations.
J Epidemiol Glob Health
January 2025
Department of Internal Medicine, National Taiwan University Hospital and College of Medicine, National Taiwan University, No.7, Chung Shan S. Rd., Zhongzheng District, Taipei City, 100225, Taiwan.
Background: Lipids are known to be involved in carcinogenesis, but the associations between lipid profiles and different lung cancer histological classifications remain unknown.
Methods: Individuals who participated in national adult health surveillance from 2012 to 2018 were included. For patients who developed lung cancer during follow-up, a 1:2 control group of nonlung cancer participants was selected after matching.
Background: Although invasiveness is one of the major determinants of the poor glioblastoma (GBM) outcome, the mechanisms of GBM invasion are only partially understood. Among the intrinsic and environmental processes promoting cell-to-cell interaction processes, eventually driving GBM invasion, we focused on the pro-invasive role played by Extracellular Vesicles (EVs), a heterogeneous group of cell-released membranous structures containing various bioactive cargoes, which can be transferred from donor to recipient cells.
Methods: EVs isolated from patient-derived GBM cell lines and surgical aspirates were assessed for their pro-migratory competence by spheroid migration assays, calcium imaging, and PYK-2/FAK phosphorylation.
mBio
January 2025
Department of Medical and Molecular Genetics and Center for Computational Biology and Bioinformatics, Indiana University School of Medicine, Indianapolis, Indiana, USA.
causes the genital ulcer disease chancroid and cutaneous ulcers in children. To study its pathogenesis, we developed a human challenge model in which we infect the skin on the upper arm of human volunteers with to the pustular stage of disease. The model has been used to define lesional architecture, describe the immune infiltrate into the infected sites using flow cytometry, and explore the molecular basis of the immune response using bulk RNA-seq.
View Article and Find Full Text PDFDis Model Mech
January 2025
Divisions of Developmental Biology, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA.
Gsx2 is a homeodomain transcription factor critical for development of the ventral telencephalon and hindbrain of the mouse. Loss of Gsx2 function results in severe basal ganglia dysgenesis as well as defects in the nucleus tractus solitarius (nTS) of the hindbrain together with respiratory failure at birth. De Mori et al.
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