New Molecular Targeted Therapies Integrated With Radiation Therapy in Lung Cancer

Provencio, Mariano; Sánchez, Antonio; Garrido, P.; Valcárcel, Francisco

doi:10.3816/clc.2010.n.012

Cited by 57 publications

(34 citation statements)

References 55 publications

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“…The combination of bevacizumab with re-irradiation increases the therapeutic ratio through increased antitumor and antivascular effects [99]. Preclinical data suggest that vascular endothelial growth factor (VEGF) is upregulated following radiation exposure, and therefore combination of anti-angiogenic agents with radiation may sensitize both tumors and associated tumor vasculature to RT [100].…”

Section: Re-irradiation For Recurrent Glioblastomamentioning

confidence: 99%

Radiation Therapy of Glioblastoma

Barani

Larson

2014

Cancer Treatment and Research

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Glioblastoma multiforme (GBM) is the most common malignant brain tumor that affects approximately 17,000 patients annually. Clear survival advantages have been demonstrated with postoperative radiation therapy (RT) to doses of 5,000-6,000 cGy but dose-escalation attempts beyond 6,000 cGy have resulted in increased toxicity but no additional survival benefit. To improve local control and limit toxicity to normal brain tissue with these infiltrating tumors, novel imaging techniques are actively being explored to better define tumor extent and associated RT treatment fields. Hyperfractionated RT has been associated with a survival detriment. Current standard-of-care treatment involves concurrent use of temozolomide and RT to 6,000 cGy over 30 days followed by adjuvant temozolomide treatment for 6 months. Brachytherapy and stereotactic radiosurgery are effective therapies for relapsed GBM but tend to be associated with notable toxicity. More recently, re-irradiation strategies employ concurrent use of bevacizumab to limit treatment-related injury while still permitting delivery of meaningful doses. These clinical trials are ongoing and merits of these strategies are not yet clear but appear promising.

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Section: Re-irradiation For Recurrent Glioblastomamentioning

confidence: 99%

Radiation Therapy of Glioblastoma

Barani

Larson

2014

Cancer Treatment and Research

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“…These authors revealed a significant association between somatic mutations in the tyrosine kinase domain of the epidermal-growth-factor receptor (EGFR) and the responsiveness of non-small-cell lung cancer to gefitinib. Since then, several groups have confirmed these findings [60][61][62][63][64][65][66].…”

Section: Cell-free Circulating Dna As a Diagnos-tic Marker In Lung Camentioning

confidence: 83%

Circulating DNA as a Biomarker for Early Detection of Cancer: A Brief Update with an Emphasis on Lung Cancer~!2010-06-09~!2010-08-03~!2010-09-06~!

Cabral¹

2010

TOLCJ

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Abstract:In most cases, early detection and treatment of cancer are prerequisites for full recovery. However, its early detection continues to be extremely difficult since its characteristic symptoms rarely manifest at the onset of disease. The development of highly sensitive, specific biomarkers also capable of reflecting pathological changes is, therefore, of the upmost importance. Lung cancer, for example, is most frequently diagnosed during the late metastatic stage so that, as a result, malignant neoplasms in the lung are among the leading causes of cancer-related deaths worldwide. Circulating DNA is a non-invasive diagnostic assay that has been greatly improved for the purposes of diagnosis, prognosis, and treatment of cancer. In the current review, we discuss recent data concerning circulating tumor-derived DNA as a tool for early detection, diagnosis, and follow-up. Given the scope of this review, the focus will be on lung cancer, one of the most prolific and lethal cancers affecting humanity today.

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“…Radioresistance is a huge impediment to radiotherapy (52). Cancer cells resistant to radiotherapy can result in therapy failure and the local recurrence (53,54). Several pathways and genes have been reported to be involved in radioresistance including nuclear factor-κB (NF-κB), signal transducer and activator of transcription 3 (STAT3), DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and ataxia telangiectasia-mutated gene (ATM) (14)(15)(16)(17)(18).…”

Section: Discussionmentioning

confidence: 99%

Betulinic acid increases radiosensitization of oral squamous cell carcinoma through inducing Sp1 sumoylation and PTEN expression

Yuan

Meng

et al. 2017

Oncology Reports

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Abstract. Radiotherapy is one of the most effective nonsurgical treatments for oral squamous cell carcinoma. However, radioresistance remains a major impediment to radiotherapy. Although BetA (Betulinic acid) can induce radiosensitization, the underlying mechanism and whether it could induce radiosensitization in oral squamous cell carcinoma are not fully understood. In this study, we showed that BetA increased radiosensitization in CAL-27 and Tca-83 cells. Radiation-triggered Sp1 overexpression was responsible for radioresistance of OSCC (oral squamous cell carcinoma) cells. Treatment with BetA downregulated Sp1 and upregulated PTEN through inducing Sp1 sumoylation and correspondingly increased radiosensitization. Moreover, Sumoylation of Sp1 upregulated PTEN protein expression by downregulating Sp1 as well as inhibiting Sp1 DNA binding activity, thereby leading to the activation of PTEN transcription. Our results suggested that BetA was able to enhance radiosensitization at least partially by downregulating Sp1 and upregulating PTEN through inducing Sp1 sumoylation. BetA is suggested to be a promising drug for increasing radiosensitization in oral squamous cell carcinoma radiotherapy.

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New Molecular Targeted Therapies Integrated With Radiation Therapy in Lung Cancer

Cited by 57 publications

References 55 publications

Radiation Therapy of Glioblastoma

Radiation Therapy of Glioblastoma

Circulating DNA as a Biomarker for Early Detection of Cancer: A Brief Update with an Emphasis on Lung Cancer~!2010-06-09~!2010-08-03~!2010-09-06~!

Betulinic acid increases radiosensitization of oral squamous cell carcinoma through inducing Sp1 sumoylation and PTEN expression

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