Treatment of breast cancer with lymph nodes by volumetric arc therapy (VMAT): Pretreatment and in vivo dosimetry

2015 ◽  
Vol 31 ◽  
pp. e30
Author(s):  
D. Nguyen ◽  
G. Largeron ◽  
F. Josserand-Pietri ◽  
C. Sporea ◽  
M. Khodri
2016 ◽  
Vol 32 ◽  
pp. 27-28
Author(s):  
S. Giancaterino ◽  
A. De Nicola ◽  
N. Adorante ◽  
P. Bagalà ◽  
F. Perrotti ◽  
...  

2020 ◽  
Vol 61 (5) ◽  
pp. 747-754
Author(s):  
Yoshiko Doi ◽  
Minoru Nakao ◽  
Hideharu Miura ◽  
Shuichi Ozawa ◽  
Masahiro Kenjo ◽  
...  

ABSTRACT To improve the homogeneity and conformity of the irradiation dose for postoperative breast cancer including regional lymph nodes, we planned Hybrid volumetric-modulated arc therapy (VMAT), which combines conventional tangential field mainly for the chest area and VMAT mainly for the supraclavicular area and marginal zone. In this study, we compared the dosimetric impact between traditional 3D conformal radiotherapy (3DCRT) and Hybrid VMAT and observed toxicities following Hybrid VMAT. A total of 70 patients indicated between October 2016 and December 2017 were included. The prescribed dose was 50 Gy/25 fractions. For the dosimetric impact, 3DCRT and Hybrid VMAT plans were compared in each patient with respect to the dosimetric parameters. Toxicities were followed using the Common Terminology Criteria for Adverse Events version 4.0. The median follow-up duration was 319 days. For the dosimetric impact, the homogeneity index (HI) and conformity index (CI) of PTV were significantly improved in the Hybrid VMAT plan compared with that in the 3DCRT plan (HI, 0.15 ± 0.07 in Hybrid VMAT vs 0.41 ± 0.19 in 3DCRT, P < 0.001; CI, 1.61 ± 0.44 in Hybrid VMAT vs 2.10 ± 0.56 in 3DCRT, P < 0.001). The mean irradiated ipsilateral lung dose was not significantly different in both plans (12.0 ± 2.4 Gy in Hybrid VMAT vs 11.8 ± 2.8 Gy in 3DCRT, P < 0.533). Regarding toxicity, there were no patients who developed ≥grade 3 acute toxicity and ≥grade 2 pneumonitis during the follow-up. Hybrid VMAT for postoperative breast cancer including regional lymph nodes was a reasonable technique that improved the homogeneity and conformity of the irradiation dose to the planning target volume while keeping the irradiation dose to organs at risk to a minimum.


2019 ◽  
Vol 10 (12) ◽  
Author(s):  
Audrey Zamora ◽  
Melinda Alves ◽  
Charlotte Chollet ◽  
Nicole Therville ◽  
Tiffany Fougeray ◽  
...  

AbstractCytotoxic therapy for breast cancer inhibits the growth of primary tumors, but promotes metastasis to the sentinel lymph nodes through the lymphatic system. However, the effect of first-line chemotherapy on the lymphatic endothelium has been poorly investigated. In this study, we determined that paclitaxel, the anti-cancer drug approved for the treatment of metastatic or locally advanced breast cancer, induces lymphatic endothelial cell (LEC) autophagy to increase metastases. While paclitaxel treatment was largely efficacious in inhibiting LEC adhesion, it had no effect on cell survival. Paclitaxel inhibited LEC migration and branch point formation by inducing an autophagy mechanism independent of Akt phosphorylation. In vivo, paclitaxel mediated a higher permeability of lymphatic endothelium to tumor cells and this effect was reversed by chloroquine, an autophagy-lysosome inhibitor. Despite a strong effect on reducing tumor size, paclitaxel significantly increased metastasis to the sentinel lymph nodes. This effect was restricted to a lymphatic dissemination, as chemotherapy did not affect the blood endothelium. Taken together, our findings suggest that the lymphatic system resists to chemotherapy through an autophagy mechanism to promote malignant progression and metastatic lesions. This study paves the way for new combinative therapies aimed at reducing the number of metastases.


2019 ◽  
Vol 44 (2) ◽  
pp. 183-189 ◽  
Author(s):  
Gijs J. van der Veen ◽  
Tomas Janssen ◽  
Amber Duijn ◽  
Simon van Kranen ◽  
Rob J. de Graaf ◽  
...  

2020 ◽  
Author(s):  
Jing Zhang ◽  
Chunhua Xiao ◽  
Zhenbo Feng ◽  
Yun Gong ◽  
Baohua Sun ◽  
...  

Abstract Purpose Increasing evidence has shown that the transcription factor SOX4 is closely associated with the development and progression of many malignant tumors. However, the effect of SOX4 on breast cancer is unclear. In this study, we purposed to investigate the role of SOX4 in the growth and metastasis in breast cancer and the underlying mechanism. Moreover, the effect of SOX4 on cancer cell resistance to chemotherapeutic agents was also evaluated in vitro and in vivo . Methods We used lentivirus technique to ectopically express SOX4 in MDA-MB-231 and SUM149 cells or knockdown SOX4 in BT474 cells, and examined the effect of these changes on various cellular functions. MTT assay was used to determine the cell viability as well as resistance to chemotherapeutic agents. The regulation of SOX4 on epithelial-mesenchymal transition (EMT)-related genes was analyzed using qRT-PCR. The binding of SOX4 to the CXCR7 gene was demonstrated using chromatin immunoprecipitation assay and dual-luciferase reporter activity assay. The effect of SOX4/CXCR7 axis on metastasis was examined using Transwell migration and Matrigel invasion assays. The expression of SOX4/CXCR7 in primary tumors and metastatic foci in lymph nodes was assessed using immunohistochemistry. Cellular morphology was investigated under phase contrast microscope and transmission electron microscopy. Moreover, the effect of SOX4 on tumor growth, metastasis, and resistance to chemotherapy was also studied in vivo by using bioluminescent imaging. Results SOX4 increased breast cancer cell viability, migration, and invasion in vitro and enhanced tumor growth and metastasis in vivo . It regulated EMT-related genes and bound to CXCR7 promoter to upregulate CXCR7 transcription. Both SOX4 and CXCR7 were highly expressed in human primary tumors and metastatic foci in lymph nodes. Treatment of breast cancer cells with the CXCR7 inhibitor CCX771 reversed the SOX4 effect on cell migration and invasion. Ectopic expression of SOX4 increased the susceptibility of cells to paclitaxel. Conclusions SOX4 plays an important role in the growth and metastasis of breast cancer. SOX4/CXCR7 may serve as potential therapeutic targets for the treatment. Paclitaxel may be a good therapeutic option if the expression level of SOX4 is high.


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