Objective To understand breast cancer 1 (BRCA1) gene and relationship between BRCA1 gene and breast cancer, and analyze its effect on clinical comprehensive therapy of breast cancer. Method The domestic and international studies relevant BRCA1 and breast cancer in recent years were reviewed and summarized. Results BRCA1, a tumor suppressor gene, its mutations caused structural changes and functional abnormalities, which were closely related to breast cancer. And the expression situation and mutation of BRCA1 were associated with the therapeutic effect. Conclusions Mutation of BRCA1 is closely related to occurrence and development of breast cancer in female. Comprehensive therapy ideas should be found in clinical therapy according to expression or mutation of BRCA1. Further research on BTCA1 is beneficial to explore gold standard for treatment of breast cancer.
ObjectiveThis study is aimed to determine the expression of ubiquitin-specific peptidase 39 (USP39) protein in the colorectal cancer (CRC) tissues, and the effect of silencing USP39 gene on the cell growth and cell cycle distribution of CRC cells.Methods① The expressions of USP39 protein in CRC tissues and its paracancerous tissues were determined by immunohistochemical staining method. ② By lentiviral infection, Lv-shUSP39 (KD-1 and KD-2 group) and Lv-shCon (shCon group) were transferred into SW1116 and HCT116 cells, and cells of blank control group did not received any treatment (Con group). To determine the role of USP39 gene in cell growth, MTT assay was performed to draw growth curve, and cell cycle distribution of CRC cells in the 4 groups were determined by flow cytometer.Results① The expression of USP39 protein was higher in CRC tissues compared to adjacent tissues (P=0.007). ② For SW1116 and HCT116 cells, the cell proliferation ability of KD-1 and KD-2 groups were remarkably decreased than those in corresponding shCon and Con groups on 3, 4, and 5-day (P<0.05). ③ Flow cytometry assay showed that, the percentage of G0/G1 phase cells were decreased obviously (P<0.05), while increased significantly in percentage of G2/M phase and number of sub-G1 phase cells in KD-1 group compared with that in the Con group and shCon group of SW1116 and HCT116 cells (P<0.05).ConclusionsThe expression of USP39 protein is highly expressed in CRC tissues. Knockdowning of USP39 gene can inhibit cell proliferation and promote cell apoptosis.
ObjectiveTo systematically review the role and potential clinical value of nicotinamide N-methyltransferase (NNMT) in gastric cancer, aiming to provide new insights for diagnosis, treatment, and prognosis of gastric cancer. MethodsRelevant literature from recent years on the involvement of NNMT in gastric cancer was thoroughly analyzed. The review focuses on the mechanisms by which NNMT influences cell proliferation, invasion, migration, and metabolic reprogramming in gastric cancer. Additionally, the study explores the potential of NNMT as a diagnostic and therapeutic target. ResultsNNMT was significantly overexpressed in gastric cancer tissues and was closely associated with tumor progression. It promoted malignant behaviors through various pathways, including metabolic regulation, enhancement of cancer cell proliferation and invasion, and alteration of the tumor microenvironment. Furthermore, NNMT played a crucial role in modulating host immune responses, which might impact the clinical prognosis of gastric cancer patients. ConclusionsNNMT exhibits significant biological functions in the development and progression of gastric cancer. As a potential biomarker and therapeutic target, it holds promising clinical value in the diagnosis and targeted treatment of gastric cancer, providing new strategies and evidence for precision therapy and prognosis assessment.
Objective To summarize the research progress of copper and its derivatives in gastrointestinal tumors in recent years, aiming to provide reference for clinical diagnosis and treatment decisions. Method The literatures related to copper homeostasis and copper death in recent years were read and summarized, and the research progress on the role of copper in cancer and copper applications in cancer diagnosis and treatment was reviewed. Results Copper was an essential trace element involved in a variety of basic biological processes. Elevated levels of copper in serum and tissues were associated with the development of tumors. As the mechanisms of copper action in various gastrointestinal tumors were being investigated, the use of copper and related derivatives in the treatment of cancer patients had become a new strategy. Conclusion Copper and its derivatives have a promising future in the treatment of gastrointestinal tumors, but their benefits in clinical patients still need to be demonstrated in numerous clinical trials.
ObjectiveTo understand the latest research progress in the treatment of advanced gastric cancer (AGC) and explore the optimal treatment strategy. Method The latest literature on the treatment of AGC was retrieved and reviewed. Results For patients with AGC, chemotherapy, radiotherapy, targeted therapy, immunotherapy, palliative therapy, nutritional support, and traditional Chinese medicine therapy were currently adopted in clinic, the combination of them were used usually. Some patients obtained good therapeutic effects by new chemotherapy drugs and antibody conjugated drugs. In the era of first-line immunotherapy or targeted therapy, first-line immunotherapy alone, immunotherapy in combination with chemotherapy, double immunotherapy, and immunotherapy combined with anti-angiogenesis targeted drugs for AGC had represented some survival benefits. ConclusionsThe research, development, and widespread application of new anti-tumor drugs have continuously expanded the treatment methods for AGC. The development of tumor molecular biology provides an opportunity for the treatment of AGC, and the precise diagnosis and treatment pattern guided by molecular typing is gradually maturing. However, the treatment of AGC is still facing challenges. In the era of precision medicine, facing the higher heterogeneity of gastric cancer, the dilemma of precise treatment of drugs for AGC, and the research and development of new anti-tumor drugs, the optimal treatment mode of AGC still needs more clinical exploration. It is necessary to comprehensively consider various aspects such as the patient’s physical condition, previous treatment status, and drug accessibility.
ObjectiveTo systematically elucidate the resistance mechanism of targeted drug therapy for breast cancer and to discuss future direction of optimized treatment strategies. MethodA literature review on targeted therapy for breast cancer had been conducted based on recent domestic and international research. ResultsContemporary breast cancer targeted therapies mainly comprised human epidermal growth factor receptor 2 (HER2)-directed agents, CDK4/6 inhibitors, phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of rapamycin pathway blockers, poly (ADP-ribose) polymerase inhibitors, and immune checkpoint modulators, etc. While these agents had conferred subtype-specific survival benefits, resistance developed through target mutations, compensatory signaling, epigenetic alterations, drug efflux pumps, among other mechanisms. Emerging strategies for reversing drug resistance included dual-targeted approaches (such as trastuzumab in combination with pertuzumab), dynamic monitoring of drug-resistant gene mutations by liquid biopsy, epigenetic modulators, etc. ConclusionsDrug resistance remains a key bottleneck limiting long-term efficacy of breast cancer targeted therapy. Future research should integrate multi-omics approaches to decipher tumor heterogeneity, implement combinatorial multi-target inhibition with real-time monitoring of multidimensional interventions, and leverage artificial intelligence to predict resistance evolution. This integrated strategy is expected to enable personalized combination therapies, ultimately overcoming drug resistance and improving patient survival outcomes.
ObjectiveTo understand the latest progress of transcatheter arterial chemoembolization (TACE)-based combination therapies for unresectable liver metastasis from colorectal carcinoma, and to explore the safe and effective combination therapies in order to controlling the rapid progress of disease and improving the quality of life of patients. MethodsThe literatures about TACE-based combination therapies of liver metastasis from colorectal carcinoma and the latest advance in researches of this field at home and abroad were collected, and the application of combination therapies, the advantages and features of the combined treatments were reviewed. ResultsTACE was a safe and effective therapeutic modality in treating primary liver cancer or secondary liver cancer.Compared with a single treatment, TACE-based combination therapies had distinct advantages to patients with liver metastasis from colorectal carcinoma not only improved the quality of life but also prolonged the survival time.With the emerging of various kinds of new drugs and the rapid development of a variety of interventional treatments, it could bring long-term survival benifit for patients with liver metastasis from colorectal carcinoma. ConclusionsDoctors should pay attention to the combined treatments of patients with liver metastasis from colorectal carcinoma, improve the knowledge of personalized medication about advanced tumors and actively promote more usage of combination therapies.
Venous thromboembolism is the third most common cardiovascular disease worldwide, including deep vein thrombosis in the lower extremities and pulmonary embolism, affecting approximately 5% of the global population. It has a high recurrence rate and mortality rate, and poses a significant burden. The traditional Virchow triangle theory laid the foundation for its pathological research. Platelets, as a key component, undergo a complex and multi-dimensional activation process, not only initiating and amplifying the coagulation cascade reaction, but also constructing a thrombogenic network through interactions with immune cells, endothelial cells, etc. This article elaborates on the core mechanism, driving pathways, specific pathological effects, and clinical value of platelet activation in venous thromboembolism, combined with insights from clinical practice and cutting-edge research, with the aim of providing new ideas for the prevention and treatment of venous thromboembolism.
Human tumor necrosis factor-related apoptosis-inducing ligand (hTRAIL) might be developed as a novel anti-tumor drug due to its selective cytotoxicity in tumor cells. The predicted Macaca mulatta TRAIL (mmTRAIL) is highly homologous to hTRAIL in nucleotide acid as well as amino acid sequence, suggesting that mmTRAIL might induce apoptosis of human cancer cells. However, the cytotoxicity of mmTRAIL in human cancer cells has not been investigated. In this paper, it is reported that the gene encoding mmTRAIL has been cloned by using reverse-transcriptase polymerase chain reaction (RT-PCR) from monkey peripheral blood mononuclear cells (PBMCs) in our laboratory. Subsequently, an expression plasmid was constructed by inserting mmTRAIL gene into pQE30 plasmid. After induction by addition of Isopropylβ-D-1-Thiogalactopyranoside (IPTG), mmTRAIL was expressed. MmTRAIL was recovered from supernatant of sonicated bacteria by Ni-NTA agarose affinity chromatography. SDS-PAGE and gel filtration chromatography demonstrated that mmTRAIL forms trimer in solution. In vitro assays indicated that mmTRAIL was cytotoxic to human COLO205 tumor cells but not to normal cells at low concentration of nanomole. In addition, antitumor effect of mmTRAIL was evaluated in mice bearing human COLO205 tumor xenografts. Intratumorally injected mmTRAIL significantly inhibited growth of tumor grafts. These results suggested that mmTRAIL was valuable as candidate drug for cancer-targeted therapy.
ObjectiveTo summarize the research progress of KRAS mutation in pancreatic tumorigenesis and therapy.MethodThe research progress of KRAS mutation in pancreatic tumorigenesis and therapy were summarized by reading the domestic and international literatures published in recent years.ResultsPancreatic cancer had the title of " king of cancer”. More than 90% of pancreatic cancer patients had KRAS mutation. KRAS had a complex relationship with pancreatic cancer through downstream signaling pathways, including Raf (rapidly accelerated fibrosarcoma)-mitogen-activated protein kinase kinase (MEK)-extracellular signal-regulated kinase (ERK), phosphatidylinositol-4, 5-bisphosphate 3-kinase (PI3K)-protein kinase B (AKT), and RalGDS-Ral. Although basic research on pancreatic cancer was deepening, there was still a lack of effective molecular targeted drugs.ConclusionsKRASgene plays an important role in the occurrence of pancreatic cancer. The treatment associated with KRAS mutation provides a more effective prognostic possibility for pancreatic cancer patients.