The pregnancy-lactation cycle (PLC) is a period in which the breast is transformed from a less-developed, nonfunctional organ into a mature, milk-producing gland that has evolved to meet the nutritional, developmental, and immune protection needs of the newborn. Cessation of lactation initiates a process whereby the breast reverts to a resting state until the next pregnancy. Changes during this period permanently alter the morphology and molecular characteristics of the breast (molecular histology) and produce important, yet poorly understood, effects on breast cancer risk. To provide a state-of-the-science summary of this topic, the National Cancer Institute invited a multidisciplinary group of experts to participate in a workshop in Rockville, Maryland, on March 2, 2012. Topics discussed included: 1) the epidemiology of the PLC in relation to breast cancer risk, 2) breast milk as a biospecimen for molecular epidemiological and translational research, and 3) use of animal models to gain mechanistic insights into the effects of the PLC on breast carcinogenesis. This report summarizes conclusions of the workshop, proposes avenues for future research on the PLC and its relationship with breast cancer risk, and identifies opportunities to translate this knowledge to improve breast cancer outcomes.
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http://dx.doi.org/10.1093/jnci/djs505 | DOI Listing |
Lymphat Res Biol
January 2025
Ankara Bilkent City Hospital, Physical Medicine and Rehabilitation Hospital, Health Science University, Ankara, Turkiye.
The aim of this study was to comparatively determine the frequency of breast cancer-related lymphedema (BCRL) by using prospective monitoring with perometer and circumferential measurements in a group of patients who underwent breast cancer surgery. We also aimed to evaluate the relationship between volume changes and functional status and quality of life (QoL) in patients with breast cancer-related subclinical lymphedema. Patients who had unilateral breast cancer surgery for breast were assessed with circumferential and perometer, respectively, for volumes at baseline, 3rd-month, 6th-month, 9th-month, and 12th-month by the same physiotherapist.
View Article and Find Full Text PDFJAMA Netw Open
January 2025
Northern Ireland Cancer Registry, Queen's University Belfast, Belfast, Northern Ireland, United Kingdom.
Nanoscale
January 2025
McMaster University, Department of Engineering Physics, Hamilton, ON M8S 4K1, Canada.
Photoresponsive drug delivery systems have great potential for improved cancer therapy. However, most of the currently available drug-delivery nanosystems are relatively large and require light excitation with low tissue penetration. Here, we designed a near infrared responsive drug delivery system by loading [Ru(terpyridine)(dipyridophenazine)(HO)] (Ru(tpy)DPPZ) in azobenzene-modified mesoporous silica coated NaGdF:Nd/Yb/Tm upconversion nanoparticles (azo-mSiO-UCNPs).
View Article and Find Full Text PDFJ Natl Cancer Inst
January 2025
Translational Radiobiology Group, Division of Cancer Sciences, University of Manchester, The Christie NHS Foundation Trust, Manchester, United Kingdom.
Purpose: Overlapping genes are involved with rheumatoid arthritis (RA) and DNA repair pathways. Therefore, we hypothesised that patients with a high polygenic risk score (PRS) for RA will have an increased risk of radiotherapy (RT) toxicity given the involvement of DNA repair.
Methods: Primary analysis was performed on 1494 prostate cancer, 483 lung cancer and 1820 breast cancer patients assessed for development of RT toxicity in the REQUITE study.
Appl Biochem Biotechnol
January 2025
Computational Biology Lab, Department of Genetic Engineering, School of Bioengineering, SRM Institute of Science and Technology, SRM Nagar, Kattankulathur, 603203, Tamil Nadu, India.
JAK1, a key regulator of multiple oncogenic pathways, is a sought-out target, and its expression in immune cells and tumour-infiltrating lymphocytes (TILs) is associated with a favorable prognosis in breast cancer. JAK1 activates IL-6 via ERBB2 receptor tyrosine kinase signalling and promotes metastatic cancer and STAT3 activation in breast cancer cells. Hence, targeting JAK1 in breast cancer is being explored as a potential therapeutic strategy.
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