Ductal carcinoma in situ (DCIS) represents 18% to 25% of all diagnosed breast cancers, and is a noninvasive, nonobligate precursor lesion to invasive cancer. The diagnosis of DCIS represents a wide range of disease, including lesions with both low and high risk of progression to invasive cancer and recurrence. Over the past decade, research on the topic of DCIS has focused on the possibility of tailoring treatment for patients according to their risk for progression and recurrence, which is based on clinicopathologic, biomolecular and genetic factors. These efforts are ongoing, with recently completed and continuing clinical trials spanning the continuum of cancer care. We conducted a review to identify recent advances on the topic of diagnosis, risk stratification and management of DCIS. While novel imaging techniques have increased the rate of DCIS diagnosis, questions persist regarding the optimal management of lesions that would not be identified with conventional methods. Additionally, among trials investigating the potential for omission of surgery and use of active surveillance, 2 trials have completed accrual and 2 clinical trials are continuing to enroll patients. Identification of novel genetic patterns is expanding our potential for risk stratification and aiding our ability to de-escalate radiation and systemic therapies for DCIS. These advances provide hope for tailoring of DCIS treatment in the near future.
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http://dx.doi.org/10.1016/j.clbc.2023.12.010 | DOI Listing |
PLoS One
January 2025
Department of Chemistry, Ashoka University, Sonipat, Haryana, India.
Pancreatic Ductal Adenocarcinoma (PDAC) is a devastating disease with poor clinical outcomes, which is mainly because of delayed disease detection, resistance to chemotherapy, and lack of specific targeted therapies. The disease's development involves complex interactions among immunological, genetic, and environmental factors, yet its molecular mechanism remains elusive. A major challenge in understanding PDAC etiology lies in unraveling the genetic profiling that governs the PDAC network.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Pharmacology and Toxicology, University of Toronto, Toronto, ON, Canada.
Background: Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal forms of cancer, and despite low incidence rates, it remains the sixth leading cause of cancer related deaths worldwide. Immunotherapy, which aims to enhance the immune system's ability to recognize and eliminate cancer cells, has emerged as a promising approach in the battle against PDAC. PARP7, a mono-ADP-ribosyltransferase, is a negative regulator of the type I interferon (IFN-I) pathway and has been reported to reduce anti-tumour immunity.
View Article and Find Full Text PDFCureus
December 2024
Department of Breast, Plastic and Reconstructive Surgery, Royal Hallamshire Hospital, Sheffield, GBR.
Background The incidence of margin re-excision following breast conserving surgery (BCS) is a quality measure in the National Health Service. The threshold is less than 20% of all BCS procedures. Despite three decades of studies and a wealth of literature identifying multiple factors associated with increased risk for margin involvement, an accepted threshold rate affecting one in five procedures remains high.
View Article and Find Full Text PDFCancer Manag Res
January 2025
Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Background: Signaling pathways centered on the G-protein ADP-ribosylation factor 6 (Arf6) and its downstream effector ArfGAP with the SH3 Domain, Ankyrin Repeat and PH Domain 1 (AMAP1) drive cancer invasion, metastasis, and therapy resistance. The Arf6-AMAP1 pathway has been reported to promote receptor recycling leading to programmed cell death-ligand 1 (PD-L1) overexpression in pancreatic ductal carcinoma. Moreover, AMAP1 regulates of nuclear factor-kappa B (NF-κB), which is an important molecule in inflammation and immune activation, including tumor immune interaction through PD-L1 regulation.
View Article and Find Full Text PDFJ Exp Clin Cancer Res
January 2025
Department of Hepato-Biliary-Pancreatic Surgery, General Surgery, Huadong Hospital, Fudan University, Shanghai, 200040, PR China.
Purpose: Glucose starvation induces the accumulation of disulfides and F-actin collapse in cells with high expression of SLC7A11, a phenomenon termed disulfidptosis. This study aimed to confirm the existence of disulfidptosis in pancreatic ductal adenocarcinoma (PDAC) and elucidate the role of Cancer Susceptibility 8 (CASC8) in this process.
Methods: The existence of disulfidptosis in PDAC was assessed using flow cytometry and F-actin staining.
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