As a rising immune checkpoint on tumor cells, CD24 is closely related to tumorigenesis and progression. CD24 can directly regulate the malignant behavior of tumor cells and indirectly inhibit the function of immune cells in the meantime, which promotes the immune escape of tumor cells, induces cancer invasion and causes poor prognosis. The basic principle of cancer treatment is to induce cell death and inhibit cell survival. Resistance to chemoradiotherapy is a critical challenge in oncology, which limits the effectiveness of anti-cancer treatments. Many studies have shown a strong association between CD24 and chemoradiotherapy resistance in tumor cells, but the specific mechanism remains unclear. Understanding the mechanisms that CD24 induces chemoradiotherapy resistance may allow us to develop new promising therapeutic strategies to enhance the efficacy of chemoradiotherapy and improve clinical outcomes in the treatment of cancer patients. In this review, we summarized the basic characteristics and functions of CD24, as well as its role in the development of cancer. We focused on the resistance to radiotherapy and chemotherapy mediated by CD24, deciphered fundamental mechanisms and introduced existing clinical studies, with an attempt to propose potential solutions for future explorations.
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Few studies have investigated the characteristics of non‐BRCA homologous recombination repair (HRR) pathway somatic mutations, and the impact of these mutations on efficacy of treatment in ovarian cancer patients is not clear. Therefore, we conducted this study to analyze the frequency and spectrum of somatic mutations in HRR pathway genes in patients with ovarian cancer and to examine the relationships between somatic mutations in HRR pathway genes and their effects on the efficacy of platinum‐based chemotherapy.
We performed targeted sequencing of 688 genes related to the occurrence, development, treatment, and prognosis of solid tumors. Somatic mutations were identified by paired analysis of tumor tissue and germline DNA in blood cells.
A total of 38 patients with ovarian cancer were included in the study, and 35 (92.1%) patients were diagnosed with high‐grade serous carcinoma. All patients exhibited somatic mutations in the tumor tissue samples. The commonly mutated genes were TP53 (73.7%), BRCA2 (55.3%), NF1 (52.6%), BRCA1 (47.4%), and CDH1 (47.4%). Overall, 71.1% of the patients exhibited mutation in at least one HRR pathway gene. The most frequently altered HRR genes were BRCA2 (55.3%), followed by BRCA1 (47.4%), ATM (44.7%), BARD1 (42.1%), and CHEK1 (36.8%). The median progression‐free survival (PFS) in patients with HRR pathway mutation was 36.0 months compared with 13.6 months in patients with no HRR pathway mutation (hazard ratio [HR], 0.25; 95% confidence interval [CI], 0.08–0.77; p = 0.016). Patients harboring BRCA1/2 and/or CDK12 mutations displayed a longer PFS (median, 36.0 months) compared with patients with no BRCA1/2 or CDK12 mutation (median, 13.6 months; HR, 0.21; 95% CI, 0.07–0.61; p = 0.004). In multivariate analysis Cox proportional hazards models, after adjustment for tumor stage at diagnosis and histology of initial diagnosis, patients with HRR pathway mutation had a longer PFS than patients with HRR wild‐type genes (p = 0.006).
HRR pathway somatic mutations are common in Chinese patients with ovarian cancer. HRR pathway somatic mutations were associated with improved sensitivity to platinum‐based chemotherapy. Large‐scale prospective studies are needed to verify our findings.
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