Breast cancer-induced activated fibroblasts support tumor progression. However, the role of normal fibroblasts in tumor progression remains controversial. In this study, we used modified patient-derived organoid cultures and demonstrate that constitutively secreted cytokines from normal breast fibroblasts initiate a paracrine signaling mechanism with estrogen receptor-positive (ER) breast cancer cells, which results in the creation of an interleukin (IL)-1β-enriched microenvironment. We found that this paracrine signaling mechanism is shared between normal and activated fibroblasts. Interestingly, we observed that in reconstructed tumor microenvironment containing autologous ER breast cancer cells, activated fibroblasts, and immune cells, tamoxifen is more effective in reducing tumor cell proliferation when this paracrine signaling is blocked. Our findings then suggest that ER tumor cells could create a growth-promoting environment without activating stromal fibroblasts and that in breast-conserving surgeries, normal fibroblasts could be a significant modulator of tumor recurrence by enhancing the proliferation of residual breast cancer cells in the tumor-adjacent breast tissue.
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http://dx.doi.org/10.1016/j.isci.2019.07.034 | 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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