Objective: To compare initial metastatic breast carcinoma (MBC) with recurrent MBC and assess their biologic phenotypes and clinical behaviors.
Methods: A comparison of clinical and biological characteristics and median overall survival times were assessed in the 251 patients with MBC at the Division of Medical Oncology, Ege University School of Medicine, and the Division of Radiation Oncology, Tepecik Government Hospital, Izmir, Turkey between 1995 and 2004. Hormone receptors, c-erbB-2, Ki-67, and p53 expressions were performed by immunohistochemistry.
Results: Out of 251 MBC patients, 206 patients had recurrent MBC, and 45 had initial MBC. Regarding survival, there was no difference between the recurrent MBC group and the initial MBC group. The initial MBC group had a higher proportion of T4 tumors (46% versus 27%), a lower proportion of T1-2 tumors (31% versus 55%; p=0.01), and a higher percentage of patients with high Ki-67 expression (64% versus 49%; p=0.05). Multivariate analysis showed that T stage was an independent prognostic factor (p=0.02).
Conclusion: Patients with initial MBC tended to present with larger tumors. This relationship can be explained by delayed diagnosis. The potential for reducing death rates from breast cancer is contingent on educational improvement and increased screening rates.
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Breast Cancer Res Treat
January 2025
Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Purpose: Individuals with metastatic breast cancer (MBC) may live with their disease for many years. We initiated the Johns Hopkins Hope at Hopkins Clinic to assess the needs and optimize the care of these patients.
Patients And Methods: Patients with MBC who agreed to participate in the Clinic in addition to usual care completed patient-reported outcome (PRO) surveys.
Future Oncol
January 2025
School of Nursing, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Background: The accessibility and outcomes of cyclin-dependent kinase 4 and 6 inhibitors (CDKi) in metastatic breast cancer (MBC) according to demographic factors are unknown.
Research Design And Methods: Retrospective review of patients with ER+ MBC prescribed first-line CDKi therapy from January 2015 through December 2022. Abstraction included time from CDKi prescription to drug initiation (TTI), time from CDKi initiation to progression (TTP), time from CDKi initiation to death or 6/30/2022, and variables (age, race, partner status, insurance type, BMI, number of comorbidities).
NPJ Breast Cancer
January 2025
Department of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Endocrine therapy with CDK4/6 inhibitors is standard for estrogen receptor-positive, HER2-negative metastatic breast cancer (ER+/HER2- MBC), yet clinical resistance develops. Previously, we demonstrated that low doses of palbociclib activate autophagy, reversing initial G1 cell cycle arrest, while high concentrations induce off-target senescence. The autophagy inhibitor hydroxychloroquine (HCQ) induced on-target senescence at lower palbociclib doses.
View Article and Find Full Text PDFEnviron Pollut
January 2025
Department of Civil and Environmental Engineering, Indian Institute of Technology Patna, Bihar, 801 106, India. Electronic address:
Perfluorooctanoic acid (PFOA) removal has gained significant attention due to its environmental stability and potential toxicity. This study aims to synthesize a chitosan-modified magnetic biochar (CS_MBC) for efficient PFOA removal from aqueous solutions. Various CS loading ratios (0.
View Article and Find Full Text PDFMol Biol Cell
January 2025
Department of Molecular, Cellular, and Developmental Biology; University of Michigan; Ann Arbor, Michigan, 48109; USA.
To preserve barrier function, cell-cell junctions must dynamically remodel during cell shape changes. We have previously described a rapid tight junction repair pathway characterized by local, transient activation of RhoA, termed "Rho flares", which repair leaks in tight junctions via promoting local actomyosin-mediated junction remodeling. In this pathway, junction elongation is a mechanical trigger that initiates RhoA activation through an influx of intracellular calcium and recruitment of p115RhoGEF.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!