PARP was an enzyme found in the nucleus of eukaryotic cells that played a crucial role in repairing damaged DNA. Recently, PARP inhibitors have demonstrated great potential in cancer treatment. Thus, the FDA has approved several small-molecule PARP inhibitors for cancer maintenance therapy. The combination of PARP inhibitors and radiotherapy relies on synthetic lethality, taking advantage of the flaws in DNA repair pathways to target cancer cells specifically. Studies conducted prior to clinical trials have suggested that the combination of PARP inhibitors and radiotherapy can enhance the sensitivity of cancer cells to radiation, intensify DNA damage, and trigger cell death. Combining radiotherapy with PARP inhibitors in clinical trials has enhanced the response rate and progression-free survival of diverse cancer patients. The theoretical foundation of PARP inhibitors combined with radiotherapy is explained in detail in this article, and the latest advances in preclinical and clinical research on these inhibitors for tumor radiotherapy are summarized. The problems in the current field are recognized in our research and potential therapeutic applications for tumors are suggested. Nevertheless, certain obstacles need to be tackled when implementing PARP inhibitors and radiotherapies in clinical settings. Factors to consider when using the combination therapy are the most suitable schedule and amount of medication, identifying advantageous candidates, and the probable adverse effects linked with the combination. The combination of radiotherapy and PARP inhibitors can greatly enhance the effectiveness of cancer treatment.

With the advancement of radiotherapy equipment, stereotactic radiotherapy (SRT) has been increasingly used. Among the many radiotherapy devices, Halcyon shows promising applications. This article reviews the dosimetric performance such as plan quality, plan complexity, and gamma passing rates of SRT plans with Halcyon to determine the effectiveness and safety of Halcyon SRT plans. This article retrieved the last 5 years of PubMed studies on the effectiveness and safety of the Halcyon SRT plans. Two authors independently reviewed the titles and abstracts to decide whether to include the studies. A search was conducted to identify publications relevant to evaluating the dosimetric performance of SRT plans on Halcyon using the key strings Halcyon, stereotactic radiosurgery, SRT, stereotactic body radiotherapy, and stereotactic ablative radiotherapy. A total of 18 eligible publications were retrieved. Compared to SRT plans on the TrueBeam, the Halcyon has advantages in terms of plan quality, plan complexity, and gamma passing rates. The high treatment speed of SRT plans on the Halcyon is impressive, while the results of its plan evaluation are also encouraging. As a result, Halcyon offers a new option for busy radiotherapy units while significantly improving patient comfort in treatment. For more accurate results, additional relevant publications will need to be followed up in subsequent studies.

Background: Absent in melanoma 1-like (AIM1L), also known as crystalline beta gamma domain containing 2. The relationship between AIM1L and tumors has not been fully investigated, and the biological function of AIM1L in different tumors is unknown, so we bioinformatically explored a possible relationship between AIM1L and esophageal squamous cell carcinoma (ESCC). Methods: AIM1L mRNA expression was detected by the Gene Expression Omnibus database (GSE20347, GSE161533, and GSE53625), and protein level expression was detected by immunohistochemistry. The correlation between AIM1L expression and clinical pathological characteristics was evaluated by the Wilcoxon signed rank test or chi-square test. Kaplan–Meier analysis and Cox proportional risk regression model were used to determine the prognostic value of AIM1L in ESCC patients and establish and verify a nomogram. Find genes highly related to the expression of AIM1L, conduct GO and Kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis, and conduct GSEA analysis on the gene set. The “CIBERSORT” R package was used to explore the relationship between AIM1L and immune infiltration, and the “OncoPredict” R package was used to explore the relationship between AIM1L and drug sensitivity. Results: Compared with the matched adjacent non-cancer tissues, the expression of AIM1L was down-regulated in ESCC tissues, and correlated with tumor grade. Kaplan–Meier survival analysis and Cox analysis showed that the low expression of AIM1L was related to the poor prognosis of ESCC patients. Enrichment analysis explained the possible function of AIM1L, GSEA determined the highly correlated signal pathway of AIM1L low expression phenotype, immune infiltration analysis determined that AIM1L was related to activated NK cells and macrophage M2, and drug sensitivity analysis determined that the low expression of AIM1L might be related to EGFR targeted drug resistance. Conclusion: AIM1L may be a candidate tumor suppressor gene for ESCC and an independent molecular biomarker for the prognosis of ESCC patients.

Objective: This study aims to explore the impact of APE1 gene knockout on the transcriptome of esophageal cancer cells and conduct a preliminary screening of APE1-regulated target genes to provide a basis for understanding APE1 target genes and finding new anti-esophageal cancer therapeutic targets.Methods: We collected 100 patients with esophageal squamous cell carcinoma (ESCC), analyzed the expression of APE1 in ESCC by immunohistochemical, and analyzed the overall survival. TE-1 cells with APE1 knockout were used for transcriptome sequencing (RNA sequencing, RNA-Seq) detection, and GO and KEGG enrichment analysis of differentially expressed genes was conducted. Protein-protein interaction (PPI) network analysis was performed on the genes in the intersection of differential genes between the two sequencing datasets. The qRT-PCR and Western blotting experiments were employed to confirm the effect of APE1 knockdown on the expression levels of FN1, TNF, and IL-6 in esophageal cancer cells.Results: APE1 highly expressed in ESCC tissue, and its high expression leads the worse OS. The stable transfected TE-1 cell line with knockdown of the APE1 gene was successfully constructed, with a knockdown efficiency of 100%. RNA-seq analysis revealed that 2,060 differential genes were detected between APE1-KO stably transfected cells and their corresponding APE1-YD cells, with 1,063 upregulated genes and 997 downregulated genes. RNA-seq analysis found that differentially expressed genes after APE1 knockout in TE-1 cells were primarily enriched in pathways related to metabolism, extracellular matrix, inflammatory response, and angiogenesis. PPI network analysis demonstrated that FN1, TNF, and IL-6 may be essential target genes of APE1. The three core genes of FN1, TNF, and IL-6 were confirmed using qRT-PCR and Western blotting, and the results were consistent with the transcriptome sequencing results.Conclusion: Knocking out APE1 can affect the function, related pathways, and downstream target gene expression of ESCC cells. APE1 can promote the transcriptional expressions of FN1 and IL6 genes while inhibiting the TNF gene. FN1, TNF, and IL-6 may be potential target genes regulated by APE1 in esophageal cancer.

Nucleotide binding and oligomeric domain‑like receptor X1 (NLRX1), a member of the NLR family, is associated with the physiological and pathological processes of inflammation, autophagy, immunity, metabolism and mitochondrial regulation, and has been demonstrated to have pro‑ or antitumor effects in various tumor types. However, the biological function of NLRX1 in esophageal squamous cell carcinoma (ESCC) has remained elusive. In the present study, by using bioinformatics methods, the differential expression of NLRX1 at the mRNA level was examined. Overall survival, clinical correlation, receiver operating characteristic curve, Cox regression, co‑expression, enrichment, immune infiltration and drug sensitivity analyses were carried out. A nomogram and a calibration curve were constructed. Changes in protein expression levels were investigated by immunohistochemistry and western blotting. The impact of NLRX1 on i) cell proliferation was evaluated by Cell Counting Kit‑8 assays; ii) migration was examined by wound‑healing assays; iii) migration and invasion were evaluated by Transwell assays; and iv) apoptosis was assessed by Annexin V/PI staining and flow cytometry. The results revealed that, compared to normal adjacent tissue, NLRX1 was lowly expressed in ESCC, and patients with low NLRX1 expression had a shorter survival time. NLRX1 was an independent prognostic factor for ESCC and was associated with tumor grading. Patients in the low‑NLRX1 group showed a decrease in the infiltration of activated natural killer cells, monocytes and M0 macrophages, and these immune‑cell infiltration levels were positively correlated with NLRX1 expression. Knocking down NLRX1 promoted the proliferation of KYSE450 cells, while overexpression of NLRX1 inhibited the proliferation of ECA109 cells. NLRX1 negatively regulated the PI3K/AKT signaling pathway in ESCC. These findings indicate that, through several mechanisms, NLRX1 suppresses tumor growth in ESCC, which offers new insight for investigating the causes and progression of ESCC, as well as for identifying more efficient therapeutic approaches.

Background: This study aimed to investigate the impact of ovary-sparing intensity-modulated radiotherapy (IMRT) on plan quality, treatment time, and gamma passing rates for stage I/II cervical cancer patients. Methods: Fifteen stage I/II cervical cancer patients were retrospectively enrolled, and a pair of clinically suitable IMRT plans were designed for each patient, with (Group A) and without (Group B) ovary-sparing. Plan factors affecting plan quality, treatment time, and gamma passing rates, including the number of segments, monitor units, percentage of small-area segments (field area < 20 cm²), and percentage of small-MU segments (MU < 10), were compared and statistically analyzed. Key plan quality indicators, including ovarian dose, target dose coverage (D_98%, D_95%, D_50%, D_2%), conformity index, and homogeneity index, were evaluated and statistically assessed. Treatment time and gamma passing rates collected by IBA MatriXX were also compared. Results: The median ovarian dose in Group A and Group B was 7.61 Gy (range 6.71–8.51 Gy) and 38.52 Gy (range 29.84–43.82 Gy), respectively. Except for monitor units, all other plan factors were significantly lower in Group A than in Group B (all P < .05). Correlation coefficients between plan factors, treatment time, and gamma passing rates that were statistically different were all negative. Both Groups of plans met the prescription requirement (D_95% ≥ 45.00 Gy) for clinical treatment. D_98% was smaller for Group A than for Group B (P < .05); D_50% and D_2% were larger for Group A than for Group B (P < .05, P < .05). Group A plans had worse conformity index and homogeneity index than Group B plans (P < .05, P < .05). Treatment time did not differ significantly (P > .05). Gamma passing rates in Group A were higher than in Group B with the criteria of 2%/3 mm (P < .05) and 3%/2 mm (P < .05). Conclusion: Despite the slightly decreased quality of the treatment plans, the ovary-sparing IMRT plans exhibited several advantages including lower ovarian dose and plan complexity, improved gamma passing rates, and a negligible impact on treatment time.