Radiation techniques for esophageal cancer

Zhang, Minsi; Wu, Abraham J.

doi:10.21037/cco.2017.06.33

Cited by 16 publications

(12 citation statements)

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“…Radiotherapy is a standardized treatment for thoracic tumours such as lung cancer, 1 oesophageal cancer, 2 malignant lymphoma 3 and breast cancer 4 . Clinical data show that the incidence of radiation‐induced lung injury (RILI) is 5%–25% after radiation therapy in patients with lung cancer, followed by those with mediastinal lymphoma (5%–10%) and breast cancer (1%–5%) 5 .…”

Section: Introductionmentioning

confidence: 99%

Pirfenidone modulates macrophage polarization and ameliorates radiation‐induced lung fibrosis by inhibiting the TGF‐β1/Smad3 pathway

Ying

Fang

Hang

et al. 2021

J Cellular Molecular Medi

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Radiation‐induced lung injury (RILI) mainly contributes to the complications of thoracic radiotherapy. RILI can be divided into radiation pneumonia (RP) and radiation‐induced lung fibrosis (RILF). Once RILF occurs, patients will eventually develop irreversible respiratory failure; thus, a new treatment strategy to prevent RILI is urgently needed. This study explored the therapeutic effect of pirfenidone (PFD), a Food and Drug Administration (FDA)‐approved drug for (IPF) treatment, and its mechanism in the treatment of RILF. In vivo, C57BL/6 mice received a 50 Gy dose of X‐ray radiation to the whole thorax with or without the administration of PFD. Collagen deposition and fibrosis in the lung were reversed by PFD treatment, which was associated with reduced M2 macrophage infiltration and inhibition of the transforming growth factor‐β1 (TGF‐β1)/Drosophila mothers against the decapentaplegic 3 (Smad3) signalling pathway. Moreover, PFD treatment decreased the radiation‐induced expression of TGF‐β1 and phosphorylation of Smad3 in alveolar epithelial cells (AECs) and vascular endothelial cells (VECs). Furthermore, IL‐4–induced M2 macrophage polarization and IL‐13–induced M2 macrophage polarization were suppressed by PFD treatment in vitro, resulting in reductions in the release of arginase‐1 (ARG‐1), chitinase 3‐like 3 (YM‐1) and TGF‐β1. Notably, the PFD‐induced inhibitory effects on M2 macrophage polarization were associated with downregulation of nuclear factor kappa‐B (NF‐κB) p50 activity. Additionally, PFD could significantly inhibit ionizing radiation‐induced chemokine secretion in MLE‐12 cells and consequently impair the migration of RAW264.7 cells. PFD could also eliminate TGF‐β1 from M2 macrophages by attenuating the activation of TGF‐β1/Smad3. In conclusion, PFD is a potential therapeutic agent to ameliorate fibrosis in RILF by reducing M2 macrophage infiltration and inhibiting the activation of TGF‐β1/Smad3.

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Section: Introductionmentioning

confidence: 99%

Pirfenidone modulates macrophage polarization and ameliorates radiation‐induced lung fibrosis by inhibiting the TGF‐β1/Smad3 pathway

Ying

Fang

Hang

et al. 2021

J Cellular Molecular Medi

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“…Radiation has an established role in de nitive, palliative and neoadjuvant environments, having a vital effect on the treatment of local EC [19]. To date, multiple drugs have been introduced to overcome radioresistance in EC, including Anlotinib.…”

Section: Discussionmentioning

confidence: 99%

Anlotinib induces tumor blood vessel normalization to strengthen the anticancer effect of radiotherapy on esophageal cancer by inhibiting EphA2

Zhu

Huang

et al. 2021

Preprint

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Background Anlotinib has anti-tumor activity in diverse solid tumors. Given that, our study was designed to unearth the mechanism of Anlotinib in radioresistant esophageal cancer (EC) cells by modulating Ephrin type-A receptor 2 (EphA2). Methods EC cells (TE-1 and KYSE-150) were induced to radioresistant EC cells (TE-1R and KYSE-150R). EphA2 expression in TE-1R and KYSE-150R cells was measured. Then, TE-1R and KYSE-150R cells were treated with Anlotinib and/or transfected with the plasmids that altered EphA2 expression. Otherwise, TE-1R and KYSE-150R cells were transfected with si-EphA2 or OE-EphA2 plasmids independently. In vitro experiments were conducted to monitor cell proliferation, angiogenesis, migration and invasion. In vivo experiment was also implemented to observe tumor growth. Results EphA2 expression was raised in TE-1R and KYSE-150R cells. Anlotinib inhibited proliferation, angiogenesis, migration and invasion of TE-1R and KYSE-150R cells in vitro, as well as tumor growth and MVD in vivo. Inhibiting EphA2 enhanced Anlotinib-mediated effects on TE-1R and KYSE-150R cells. Down-regulating EphA2 restrained proliferation, angiogenesis, migration and invasion of TE-1R and KYSE-150R cells. Conclusion It is concluded that Anlotinib suppresses EC development under radiotherapy by inhibiting EphA2, providing another perspective to overcome radioresistance in EC.

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“…Threefourths of affected patients are male. Patients diagnosed with esophageal cancer have a very poor survival rate [1]. There is evidence that neoadjuvant chemoradiotherapy (CRT) will shrink tumor size, which increases the success rate of surgery.…”

Section: Introductionmentioning

confidence: 99%

Phantom simulation of liver metastasis on a positron emission tomography with computed tomography scan after neoadjuvant chemoradiotherapy for distal esophageal cancer: a case report

et al. 2020

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Background: Neoadjuvant chemoradiotherapy is currently the gold standard treatment for esophageal cancer prior to surgery. This radiation therapy will sometimes lead to liver damage parallel to esophageal lesions, which mimics liver metastasis visualized by 18 F-fluorodeoxyglucose positron emission tomography with computed tomography. In this report, we publish virtual radiation-induced liver damage images obtained during surgery, along with the coherent pathology, in order to confirm the false-positive result through an optimally decisive radiological examination. Case presentation: We report a case of a Asian male patient with distal esophageal cancer who had undergone neoadjuvant chemoradiotherapy (5000 cGy). Subsequently, a new lesion was discovered during a positron emission tomography with computed tomography scan 6 weeks later, near the left caudate lobe of the liver during tumor restaging. To exclude the possibility of liver metastasis, serial imaging was conducted, which included liver sonography, computed tomography, and magnetic resonance imaging for a more intimate probe. The patient's condition was verified as being liver inflammation change, as seen by the liver magnetic resonance imaging presentation. Thoracoscopic esophagectomy was performed with cervical esophagogastrostomy via the retrosternal route, along with a feeding jejunostomy. The procedure was performed smoothly, with an intraoperative liver biopsy also being conducted 2 weeks later, after positron emission tomography with computed tomography restaging. The pathology report revealed esophageal cancer in the form of poorly differentiated squamous cell carcinoma, pT3N1M0. The liver biopsy revealed obvious inflammation change after radiation therapy, which elucidated sinusoidal congestion with the attenuated hepatic cords and filled with erythrocytes. There was no evidence of liver metastasis. The patient recovered uneventfully and was discharged with his oral intake performing smoothly, and a stable condition was observed during 12 months of outpatient department follow-up.

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Radiation techniques for esophageal cancer

Cited by 16 publications

References 0 publications

Pirfenidone modulates macrophage polarization and ameliorates radiation‐induced lung fibrosis by inhibiting the TGF‐β1/Smad3 pathway

Pirfenidone modulates macrophage polarization and ameliorates radiation‐induced lung fibrosis by inhibiting the TGF‐β1/Smad3 pathway

Anlotinib induces tumor blood vessel normalization to strengthen the anticancer effect of radiotherapy on esophageal cancer by inhibiting EphA2

Phantom simulation of liver metastasis on a positron emission tomography with computed tomography scan after neoadjuvant chemoradiotherapy for distal esophageal cancer: a case report

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