Objective:To investigate the efficacy and application value of vacuum sealing drainage (VSD) in high-risk incision after bone and soft tissue tumor surgery.Methods:From January 2020 to September 2022, 22 patients with high-risk incisions after bone and soft tissue tumor resection in Shengjing Hospital, China Medical University were treated with VSD. The postoperative negative pressure was set at 0.025 MPa (188 mmHg, 1 mmHg = 0.133 kPa), and the VSD device was removed on the 7th day after operation. After removal, the wound healing and the incidence of related complications were observed.Results:After removing the VSD, 20 patients with high-risk incisions reached the standard of grade A healing, the rate of grade A healing was 90.91%, and 2 patients had incision wound necrosis, and the incision healed were improved after dressing change. The patients were followed up for 6 - 12 months, with an average time of 10 months. The wound healing of all patients reached the standard of grade A healing, and no long-term complications occurred.Conclusions:VSD technique has good clinical effect and can be applied to various high-risk incisions after bone and soft tissue tumor surgery, which can effectively prevent the occurrence of incision complications.

Osteosarcoma is the most common primary malignant bone tumor, yet treatment modalities and patient outcomes have remained relatively stagnant over the past three decades. Recently, with increasing insights into the molecular characteristics of osteosarcoma, targeted therapies, such as tyrosine kinase inhibitors and cell cycle-related inhibitors, have shown significant progress in both preclinical studies and clinical trials. Checkpoint kinase 1 (CHEK1), a key player in DNA damage response, is involved in various critical biological functions, and the development of its specific inhibitors has gained attention in multiple fields of cancer treatment. Osteosarcoma, comprising multiple subtypes with distinct alterations in cell cycle and DNA damage response mechanisms, particularly exhibits increased sensitivity to CHEK1 inhibitors in p53 mutant cells. Targeting the CHEK1-associated pathway holds promise for improving patient outcomes. Inhibition of ataxia telangiectasia mutated (ATM) and/or ataxia telangiectasia and Rad3-related (ATR) pathways impairs DNA damage repair in osteosarcoma cells, identifying downstream molecules linked to CHEK1 as potential therapeutic targets. Suppression of CHEK1 activity leads to downregulation of related protein expression and inhibits cell proliferation and repair processes, an effect that is notably enhanced when combined with chemotherapeutic agents. Although single-agent chemotherapy often produces limited results, the use of CHEK1 inhibitors such as Prexasertib enhances cytotoxic effects against osteosarcoma cells, either as monotherapy or in combination regimens, demonstrating robust efficacy. Co-administration of CHEK1 inhibitors with other cell cycle modulators or downstream target antagonists could further optimize treatment outcomes. Furthermore, modulating DNA damage response pathways may have implications for immunotherapy. This review systematically summarizes recent research on the CHEK1-related pathway in osteosarcoma and emphasizes that targeting the DNA damage response pathway related to CHEK1 may be a promising strategy for osteosarcoma treatment with broad prospects.