KGM significantly decreased the viability of HepG2/5-FU cells in the presence of 5-FU. KGM downregulated the mRNA and protein expression of MDR and P-gp, and inhibited the mRNA and protein expression of cyclin A, cyclin B1 and CDK2. In addition, KGM significantly suppressed BCL-2 expression and increased the expression of cleaved caspase-3 and Bax, resulting in a higher apoptotic rate of HepG2/5-FU cells. Furthermore, KGM suppressed AKT phosphorylation and upregulated p53 expression. Notably, KGM significantly inhibited the growth of HepG2/5-FU in nude mice. KGM may be a promising agent against the resistance of HepG2/5-FU cells to 5-FU by suppressing AKT signaling and increasing p53 expression.Cancer cells usually show different metabolic patterns compared with healthy cells due to the reprogramming of metabolic processes. The process of lipid metabolism undergoes notable changes, leading to the accumulation of lipid droplets in cells. Additionally, this phenotype is considered an important marker of cancer cells. Lipid droplets are a highly dynamic type of organelle in the cell, which is composed of a neutral lipid core, a monolayer phospholipid membrane and lipid droplet-related proteins. Lipid droplets are involved in several biological processes, including cell proliferation, apoptosis, lipid metabolism, stress, immunity, signal transduction and protein trafficking. Epidermal growth factor receptor (EGFR)-activating mutations are currently the most effective therapeutic targets for non-small cell lung cancer. Several EGFR tyrosine kinase inhibitors (EGFR-TKIs) that target these mutations, including gefitinib, erlotinib, afatinib and osimertinib, have been widely used clinically. However, the development of acquired resistance has a major impact on the efficacy of these drugs. A number of previous studies have reported that the expression of lipid droplets in the tumor tissues of patients with lung cancer are elevated, whereas the association between elevated numbers of lipid droplets and drug resistance has received little attention. The present review describes the potential association between lipid droplets and drug resistance. Furthermore, the mechanisms and implications of lipid droplet accumulation in cancer cells are analyzed, as wells as the mechanism by which lipid droplets suppress endoplasmic reticulum stress and apoptosis, which are essential for the development and treatment of lung cancer.Immunotherapy is an emerging clinical approach that has gained traction over the past decade as a novel treatment option for lung cancer and melanoma. Notably, researchers have made marked improvements in the treatment of endometrial cancer (EC), and potential immune responses have been identified in patients with EC, thereby offering the possibility of exploring immunotherapy for EC. Nevertheless, various needs remain unmet, and immunotherapy applications in EC have yielded limited success, as only a minority of patients exhibited a clinical response. Therefore, further understanding of immune dysfunction associated with EC is still required. The present review describes recent findings regarding the immunosuppressive microenvironment of EC, with emphasis on immune evasion mechanisms and immunotherapy in EC.Cervical cancer is a malignant tumour that occurs in the cervix and is classified into two histological types, adenocarcinoma and squamous cell carcinoma (SCC); SCC is more common and accounts for 70% of all cases. In 2018 there were ~569,000 new cases of cervical cancer diagnosed worldwide and ~311,000 deaths were attributed to cervical cancer. Of these, between 84 and 90% occurred in low- and middle-income countries (LMICs) such as South Africa, India, China and Brazil. The most common cause of cervical cancer is persistent infection caused by the sexually transmitted human papilloma virus. Other factors that contribute to the incidence of cervical cancer include geography, traditional practices and beliefs, the screening levels, socioeconomic status, healthcare access, public awareness, use of oral contraceptives, smoking and co-infection with HIV. An estimated 11 million women from LMICs will be diagnosed with cervical cancer in the next 10-20 years. The aim of this review was to explore various types of genetic and epigenetic factors that influence the development, progression or suppression of cervical cancer.An intriguing relationship between menstrual cycle phase at the time of breast cancer surgery and clinical outcomes was first proposed in the late 1980s. Despite a number of clinical studies conducted to address this, as well as meta-analyses and systematic reviews, there remains significant controversy surrounding the effect of menstrual cycle phase at time of surgery on the prognosis of premenopausal breast cancer. While some studies have suggested that surgery performed during the luteal phase results in the most favourable outcome, other studies report the follicular phase is more favourable, and others show no association. Given the conflicting results, there remains insufficient evidence to determine whether there is an optimal time of the month to perform surgery. This issue has dogged breast cancer surgery for decades; knowledge of an optimal time of the month to conduct surgery would be a simple approach to improving patient outcomes. This review explores the potential biological mechanisms through which the hormonal milieu might contribute to differences in prognosis, and why clinical findings are so variable. It is concluded that a significant problem with current clinical research is the lack of insight from mechanistic studies. While there are a number of plausible biological mechanisms that could lead to altered survival, supporting evidence is limited. There are also variable approaches to defining the menstrual cycle phase and hormone receptor status of the tumour and few studies controlled for prognostic factors such as tumour size and stage, or addressed the impact of adjuvant treatments. Elucidation of the specific confounding factors, as well as biological mechanistic pathways that could explain the potential relationship between timing of surgery and survival, will greatly assist in designing robust well-controlled prospective clinical studies to evaluate this paradigm.The aim of the present study was to evaluate the effectiveness of interventional treatment of primary tracheal tumors through flexible bronchoscopy. The clinical data of 38 patients with primary tracheal tumours who underwent flexible bronchoscopy intervention therapy between January 2011 and January 2017 were retrospectively analyzed. The average time interval from onset of symptoms to the appearance of actual clinical manifestations in the 38 patients ranged from 0 to 60 months, with an average of 8.1±11.6 months and a median of 4.2 months. The rate of misdiagnosis at the first visit was 36.8% (14/38). After interventional treatment, the overall efficiency (complete + partial response) of airway stenosis recanalization in the 38 patients was 89.5%. In 3 patients with benign tumors, the anhelation score was reduced following treatment (1.00±0.77 vs. 3.13±1.21 at the pre-treatment stage; P less then 0.001). The overall survival rates of the 35 patients at 1, 3 and 5 years were 69.3, 48.7 and 20.3%, respectively. Therefore, flexible bronchoscopic intervention may effectively smoothen the airways of patients and relieve the symptoms of anhelation. Combining radiotherapy and chemotherapy may improve patient prognosis and safety.Endothelial cell injury in vascular arterial walls plays a crucial role in the pathological process of atherosclerosis. Pterostilbene, a stilbenoid chemically related to resveratrol, has anti-inflammatory, anti-apoptosis and antioxidant properties. However, the underlying mechanisms mediated by pterostilbene in regards to endothelial cell injury in vascular arterial walls are not fully understood. The purpose of the present study was to investigate the benefits of pterostilbene in a rat model of atherosclerosis. The possible mechanism of pterostilbene was also analyzed in regards to endothelial cell injury in vascular arterial walls in vitro. A rat model of atherosclerosis was established using endothelial injury of the iliac arteries. CCK-8 assay, TUNEL, immunofluorescence, western blot analysis and hematoxylin and eosin (H&E) staining were used to analyze the role of pterostilbene in the pathological processes of atherosclerosis. In vivo results showed that pterostilbene decreased cholesterol (CHO), high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) in plasma and attenuated interleukin (IL)-1, tumor necrosis factor (TNF)-α and IL-6 and oxidative stress injury in serum in the experimental animals. Pterostilbene treatment reduced atherogenesis, aortic plaques, macrophage infiltration and apoptosis of vascular arterial walls in the atherosclerosis rat model. In vitro assay demonstrated that pterostilbene administration increased viability of the endothelial cells, attenuated oxidative stress injury and apoptosis of endothelial cells. The results found that pterostilbene regulated endothelial cell apoptosis via the Nrf2-mediated TLR-4/MyD88/NF-κB pathway. In conclusion, data from the present study revealed that pterostilbene protects rats against atherosclerosis by regulation of the Nrf2-mediated TLR-4/MyD88/NF-κB pathway.The mortality and disability rate of patients with ruptured anterior communicating artery (AComA) aneurysm after bleeding is high. Even with the most advanced treatment methods, the incidence of complications remains high. The purpose of the present study was to determine the efficacy of microsurgery via supraorbital eyebrow keyhole approach (SOEK) in clipping ruptured AComA aneurysms. Between September 2010 and October 2018, 543 patients with intracranial aneurysms were admitted to the Department of Neurosurgery of the Third Affiliated Hospital of Sun Yat-Sen University (Guangzhou, China). Among them, 85 patients with ruptured AComA aneurysm and subarachnoid hemorrhage (SAH) underwent microsurgical clipping via the SOEK approach. In those patients, the clipping rate, complications and clinical efficacy of treatment were evaluated. The average age of the patients was 52.69±9.94 years (range, 28-78 years). The proportions of small, medium and large aneurysms were 83.5, 15.3 and 1.2%, respectively. Procedural complications occurred in 9 cases (10.5%). The occlusion rate of the aneurysms was 98.8%. The average follow-up period was 37.9 (±24.5) months. A total of 81.2% of the patients with SAH had a good clinical prognosisat 1 year (modified Rankin scale score, ≤2). In conclusion, for a skilled and experienced surgeon, SOEK was indicated to be a safe procedure for the treatment of ruptured AComA aneurysms; it provided sufficient intra-operative exposure and a high clipping rate.The antitumor enzyme L-asparaginase (L-Asp) has commonly been used for the treatment of acute lymphoblastic leukemia. However, the effects of L-Asp on acute myeloid leukemia (AML) and their underlying mechanisms have not been fully elucidated. In the present study, the effects of L-Asp on cell proliferation and apoptosis were investigated using the AML cell lines U937, HL-60 and KG-1a. The effects of combining L-Asp with mitoxantrone (MIT) and cytarabine (Ara-c) were also analyzed. The combination of MIT and Ara-C is known as MA therapy, and is a widely used therapeutic regimen for the treatment of elderly patients with refractory AML. When applied alone, L-Asp inhibited cell proliferation and induced apoptosis in each of the cell lines tested. Furthermore, the combined use of L-Asp with MA therapy further potentiated the inhibition of cell proliferation while increasing the induction of apoptosis. These findings provide evidence for the potential antitumor effect of L-Asp in AML, and indicate that improved efficacy maybe achieved by combining L-Asp with MIT and Ara-c.