This review shows how mammary stem cells (MaSCs) influence breast development, breastfeeding, and breast cancer risk. MaSCs, which can differentiate into various cell types, are vital for breast tissue health, but also disease development in breast tissue. Research shows that breastfeeding affects MaSCs, offering protection against breast cancer through various mechanisms. Hormonal changes such as increased prolactin concentration, oxytocin secretion, lower progesterone levels, and reduced exposure to estrogen during lactation promote apoptosis in potential cancer cells, boost immune surveillance, and modulate inflammation. Key findings reveal that pregnancy at an earlier age and extended breastfeeding reduce MaSC numbers, lowering cancer risk. Additionally, breastfeeding induces various epigenetic changes, such as DNA methylation and histone modification, which provide long-term protection against the development of cancer. Components of breast milk, like alpha-lactalbumin and lactoferrin, contribute by promoting cancer cell apoptosis and inhibiting tumor growth. The dual benefits of breastfeeding are reduced breast cancer risk for mothers and immunological advantages for infants. Multicenter epidemiology research has focused particular attention on longer breastfeeding duration associated with a reduced risk of triple-negative breast cancer. This review offers comprehensive evidence that breastfeeding protects against breast cancer through various biological, hormonal, and molecular mechanisms, showing the importance of promoting breastfeeding as a natural cancer prevention method. This article reviews the role of mammary stem cells in breast development, lactation, and breast cancer.
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http://dx.doi.org/10.12659/MSM.945451 | DOI Listing |
Health Serv Insights
December 2024
Department of Surgery, Faculty of Medicine, Universiti Malaya, Kuala Lumpur, Malaysia.
One of the main challenges in breast cancer management is health system literacy to provide optimal and timely diagnosis and treatments within complex and multidisciplinary health system environments. Digitalised patient navigation programs have been developed and found to be helpful in high- and low-resource settings, but gaps remain in finding cost-effective navigation in the public sector in Malaysia, where resources are scarce and unstable. Hence, we set out to develop a virtual patient navigation application for breast cancer patients to enhance knowledge about cancer diagnosis and treatments and provide a tracking mechanism to ensure quality care.
View Article and Find Full Text PDFFront Oncol
December 2024
Analysis of Circulating Tumor Cells, Laboratory of Analytical Chemistry, Department of Chemistry, University of Athens, Athens, Greece.
Introduction: Detection of mutations in primary tumors and liquid biopsy samples is of increasing importance for treatment decisions and therapy resistance in many types of cancer. The aim of the present study was to directly compare the efficacy of a relatively inexpensive ultrasensitive real-time PCR with the well-established and highly sensitive technology of ddPCR for the detection of the three most common hotspot mutations of , in exons 9 and 20, that are all of clinical importance in various types of cancer.
Patients And Methods: We analyzed 42 gDNAs from primary tumors (FFPEs), 29 plasma-cfDNA samples, and 29 paired CTC-derived gDNAs, all from patients with ER+ metastatic breast cancer, and plasma from 10 healthy donors.
Ann Surg Open
December 2024
Duke Cancer Institute, Duke University, Durham, NC.
Nanoscale Adv
December 2024
Department of "Scienze e Tecnologie Biologiche, Chimiche e Farmaceutiche" (STEBICEF), University of Palermo Via Archirafi 32 90123 Palermo Italy nicolo.mauroatunipa.it.
Carbon dot (CD)-based theranostics offers a promising approach for breast cancer (BC) treatment, integrating ultra-localized chemo-photothermal effects to address chemoresistance and enhance therapeutic control. Herein, the development of a targeted theranostic nanosystem for the chemo-phototherapy of breast cancer is described. Fluorescent and biocompatible CDs were passivated with 1,2-bis(3-aminopropylamino)ethane (bAPAE) and decorated with the targeting agent folic acid (FA) through conjugation with a PEG spacer.
View Article and Find Full Text PDFActivation of PLCβ enzymes by G and G proteins is a common mechanism to trigger cytosolic Ca increase. We and others reported that G inhibitor FR900358 (FR) can inhibit both and G - and, surprisingly, G -mediated intracellular Ca mobilization. Thus, the G -G -PLCβ-Ca signaling axis depends entirely on the presence of active G , which reasonably explained FR-inhibited G -induced Ca release.
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