Abstract
In the era of precision medicine, radiotherapy strategies should be determined based on genetic profiles that predict tumor radiosensitivity. Accordingly, pre-clinical research aimed at discovering clinically applicable genetic profiles is needed. However, how a given genetic profile affects cancer cell radiosensitivity is unclear. To address this issue, we performed a pilot in vitro study by utilizing EGFR mutational status as a model for genetic profile. Clonogenic assays of EGFR mutant (n = 6) and wild-type (n = 9) non-small cell lung carcinoma (NSCLC) cell lines were performed independently by two oncologists. Clonogenic survival parameters SF2, SF4, SF6, SF8, mean inactivation dose (MID), D10, D50, α, and β were obtained using the linear quadratic model. The differences in the clonogenic survival parameters between the EGFR mutant and wild-type cell lines were assessed using the Mann–Whitney U test. As a result, for both datasets, the p values for SF2, SF4, D50, α, and α/β were below 0.05, and those for SF2 were lowest. These data indicate that a genetic profile of NSCLC cell lines might be predictive for their radiation response; i.e., EGFR mutant cell lines might be more sensitive to low dose- and low fraction sized-irradiation.
Highlights
Radiation therapy is one of the most important treatments for cancer
In the pre-clinical setting, Amornwichet et al [14] found that radiosensitivity determined by D10 from clonogenic assays was significantly higher for EGFR mutant cells than for EGFR wild-type cells in a panel of non-small cell lung carcinoma (NSCLC) cell lines, as well as in genetically engineered isogenic
In the pre-clinical setting, Amornwichet et al [14] found that radiosensitivity determined by D10 from clonogenic assays was significantly higher for EGFR mutant cells than for EGFR wild-type cells in a panel of NSCLC cell lines, as well as in genetically engineered isogenic NSCLC cells
Summary
Radiation therapy is one of the most important treatments for cancer. In the clinical practice of definitive radiation therapy, the doses required for clinical tumor control vary widely even for tumors arising in the same anatomical sites. An integrated analysis of 50 single-institution studies performed by Okunieff et al revealed that the dose required for 50% clinical tumor control ranged from 21.4 to 90.3 Gy for breast cancer, 50.4 to 83.4 Gy for supraglottic cancer, and 24.3 to 64.4 Gy for cervical cancer [1] These data highlight the need to establish predictive biomarkers of tumor radioresponsiveness that could advance personalization of radiation therapy. Given genetic affects cancer cell radiosensitivity as assessed by by various various clonogenic clonogenic survival survival parameters parameters is unclear. To address address this this issue, issue, we we performed performed aa pilot pilot study study by by utilizing utilizing EGFR.
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