368 Stellate ganglion block induced by low level laser therapy to reduce adverse reactions of endocrine therapy in breast cancer patients

2010 ◽  
Vol 8 (3) ◽  
pp. 165
Author(s):  
H. Kaise ◽  
K. Yamada ◽  
A. Ogata ◽  
M. Oda ◽  
S. Komatsu ◽  
...  
2019 ◽  
Vol 10 (2) ◽  
pp. 125-130
Author(s):  
Soheir Shehata Rezk-Allah ◽  
Heba Mohamed Abd Elshafi ◽  
Reem Jan Farid ◽  
Mohamed Abd Elrahman Hassan ◽  
Samy A. Alsirafy

Introduction: Oral mucositis (OM) is an unavoidable condition of the oral cavity that accompanies chemotherapy for various malignant cases. Chemotherapy-induced oral Mucositis (COM) is a frequent complication due to mucotoxic drugs and is known to deteriorate the general health significantly, while negatively affecting the quality of life (QOL). Studies have reported that low-level laser therapy (LLLT) promotes the tissue healing. The objective of the present study was to explore the efficacy of gallium-arsenide (GaAs) laser in treating COM and its impact on inflammatory cytokine levels in patients receiving chemotherapy for various malignancies. Methods: A total of 80 patients with COM received LLLT 6 days/week. OM was graded according to the World Health Organization (WHO) grading scale. The outcome parameters were the serum levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) measured before, during and after administration of LLLT. Results: After LLLT, a significant decrease was found in the mean values of mucositis grade from 2.35 ± 0.695 to 1.13 ± 0.333 after (P < 0.001). A significant reduction in the level of TNF-α was found after LLLT among breast cancer patients (P = 0.0045), but not in head and neck cancer and lymphoma patients. A significant reduction was also found in IL-6 level after treatment among head and neck and breast cancer patients (P = 0.0307 and 0.019, respectively). Conclusion: The use of GaAs LLLT in treating COM in patients with various malignancies is well tolerated by patients, it results in improvement of mucositis, however; mechanism of action does not seem to be completely linked to the change of pro or anti-inflammatory cytokines.


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Sanne Løkkegaard ◽  
Daniel Elias ◽  
Carla L. Alves ◽  
Martin V. Bennetzen ◽  
Anne-Vibeke Lænkholm ◽  
...  

AbstractResistance to endocrine therapy in estrogen receptor-positive (ER+) breast cancer is a major clinical problem with poorly understood mechanisms. There is an unmet need for prognostic and predictive biomarkers to allow appropriate therapeutic targeting. We evaluated the mechanism by which minichromosome maintenance protein 3 (MCM3) influences endocrine resistance and its predictive/prognostic potential in ER+ breast cancer. We discovered that ER+ breast cancer cells survive tamoxifen and letrozole treatments through upregulation of minichromosome maintenance proteins (MCMs), including MCM3, which are key molecules in the cell cycle and DNA replication. Lowering MCM3 expression in endocrine-resistant cells restored drug sensitivity and altered phosphorylation of cell cycle regulators, including p53(Ser315,33), CHK1(Ser317), and cdc25b(Ser323), suggesting that the interaction of MCM3 with cell cycle proteins is an important mechanism of overcoming replicative stress and anti-proliferative effects of endocrine treatments. Interestingly, the MCM3 levels did not affect the efficacy of growth inhibitory by CDK4/6 inhibitors. Evaluation of MCM3 levels in primary tumors from four independent cohorts of breast cancer patients receiving adjuvant tamoxifen mono-therapy or no adjuvant treatment, including the Stockholm tamoxifen (STO-3) trial, showed MCM3 to be an independent prognostic marker adding information beyond Ki67. In addition, MCM3 was shown to be a predictive marker of response to endocrine treatment. Our study reveals a coordinated signaling network centered around MCM3 that limits response to endocrine therapy in ER+ breast cancer and identifies MCM3 as a clinically useful prognostic and predictive biomarker that allows personalized treatment of ER+ breast cancer patients.


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