Extracellular glycoproteins of the laminin family are essential components of basement membranes involved in a number of biological processes, including tissue differentiation, wound healing, and tumorigenesis. We present the first comprehensive study of promoter methylation status of the genes encoding laminin chains in normal tissues (peripheral blood leucocytes, buccal epithelial cells, autopsy breast tissue samples) and in breast carcinoma samples. Based on the results of this study, we divide laminin genes into three categories. Genes, constitutively methylated in breast tissues include LAMA3A, LAMB2, LAMB3, and LAMC2. Genes prone to abnormal methylation in breast carcinoma include LAMA1, LAMA2, LAMA3B, LAMA4, LAMB1, and LAMC3. Genes that are rarely if ever methylated in breast carcinoma include LAMA5 and LAMC1. The constitutively methylated group includes all of the genes that encode subunits of laminin-5 (the historical name of laminin 332), the promoters of which were previously considered unmethylated in normal tissues and prone to abnormal methylation in breast cancer.
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http://dx.doi.org/10.7868/S0026898415040163 | DOI Listing |
BMJ Oncol
September 2023
Department of Big Data in Health Science, School of Public Health and The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Objective: This study aimed to explore the global burden of early-onset cancer based on the Global Burden of Disease (GBD) 2019 study for 29 cancers worldwid.
Methods And Analysis: Incidence, deaths, disability-adjusted life years (DALYs) and risk factors for 29 early-onset cancer groups were obtained from GBD.
Results: Global incidence of early-onset cancer increased by 79.
Toxicol Rep
June 2025
National Research Center, Therapeutic Chemistry Department, Al Bohouth Street, Egypt.
Resistance of cancer cells, especially breast cancer, to therapeutic medicines represents a major clinical obstacle that impedes the stages of treatment. Carcinoma cells that acquire resistance to therapeutic drugs can reprogram their own metabolic processes as a way to overcome the effectiveness of treatment and continue their reproduction processes. Despite the recent developments in medical research in the field of drug resistance, which showed some explanations for this phenomenon, the real explanation, along with the ability to precisely predict the possibility of its occurrence in breast cancer cells, still necessitates a deep consideration of the dynamics of the tumor's response to treatment.
View Article and Find Full Text PDFFuture Sci OA
December 2025
Janssen Research & Development LLC, Raritan, NJ, USA.
Background: Including racial and ethnic minorities in clinical trials is essential for advancing health equity. Despite progress, trials often do not mirror patient population demographics.
Methods: The National Library of Medicine's Clinical Trials database was queried for phase III trials of lung, colorectal, breast, and prostate cancers.
J Transl Med
January 2025
Department of Medical and Surgical Sciences (DIMEC), University of Bologna, Bologna, Italy.
Background: HER2-targeted therapies have revolutionized the treatment of HER2-positive breast cancer patients, leading to significant improvements in tumor response rates and survival. However, resistance and incomplete response remain considerable challenges. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibition is a novel therapeutic strategy for the management of dyslipidemia by enhancing the clearance of low-density lipoprotein cholesterol receptors, however recent evidence also shows links between PCSK9 and cancer cells.
View Article and Find Full Text PDFJ Transl Med
January 2025
Department of Radiation Oncology, State Key Laboratory of Oncology in South China, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, People's Republic of China.
Background: Drug resistance constitutes one of the principal causes of poor prognosis in breast cancer patients. Although cancer cells can maintain viability independently of mitochondrial energy metabolism, they remain reliant on mitochondrial functions for the synthesis of new DNA strands. This dependency underscores a potential link between mitochondrial energy metabolism and drug resistance.
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