Objective To explore the molecular mechanism by which the mitogen-activated extracellular signal-regulated kinase （MEK） inhibitor PD98059 regulates the MEK/extracellular signal-regulated kinase （ERK） signaling pathway and reverses the multiple drug resistance （MDR） of human glioma stem cells （GSCs）. Methods According to the instructions of CD133 immunomagnetic isolation kit， human glioma SHG44 cells with CD133 positive were isolated， and they were cultured with serum-free stem cell culture media. Then， GSCs were divided into control group （normal culture）， inhibitor group （200 μmol/L PD98059）， activation group （25 μmol/L erucin） and MDR1 knockout group （200 μmol/L PD98059+MDR1 gene knockout）. The proliferation of GSCs after treatment with PD98059 （0， 25， 50， 100， 200， 300， 400 μmol/L） was detected by CCK-8. The apoptosis of GSCs after being treated with doxorubicin or vincristine respectively was detected by TUNEL staining. Levels of MEK， ERK and MDR1 mRNA in GSCs were quantitatively analyzed by real-time PCR， expressions of p-MEK/MEK， p-ERK/ERK and MDR1 proteins were detected by Western blotting， and sensitivity of cells to chemotherapy drugs was analyzed by CCK-8. Results In GSCs after treatment with PD98059 （0， 25， 50， 100， 200， 300， 400 μmol/L）， there were statistically significant differences in absorbance （A）₄₅₀ values at different time points （24， 48， 72， 96 h） （F=56.22， P<0.001； F=42.69， P<0.001； F=34.19， P<0.001； F=60.28， P<0.001）， there were statistically significant differences in the A₄₅₀ values at concentrations of 25， 50， 100， 200， 300， and 400 μmol/L compared with 0 μmol/L （all P<0.05）， while there were no statistically significant differences when comparing 200 μmol/L with 300 and 400 μmol/L concentrations （both P>0.05）. After treatment with doxorubicin， apoptosis rates of GSCs in control group， inhibitor group， activation group and MDR1 knockout group were （18.21±0.33）%， （27.73±1.86）%， （20.11±2.06）% and （25.77±2.61）%， while which were （22.07±1.51）%， （33.89±3.12）%， （25.41±2.65）% and （30.19±3.08）% after treatment with vincristine， with statistically significant differences （F=36.46， P<0.001； F=40.14， P<0.001）. The above indexes in inhibitor group， activation group and MDR1 knockout group were significantly higher than those in control group （all P<0.05）， these indexes in activation group were significantly lower than those in inhibitor group （both P<0.05）， and which in MDR1 knockout group were significantly higher than those in activation group （both P<0.05）. The expressions of MEK mRNA in GSCs in the four groups were 1.00±0.00， 0.29±0.05， 0.68±0.07， 0.33±0.03， the expressions of ERK mRNA were 1.00±0.00， 0.35±0.06， 0.74±0.07， 0.38±0.04， the expressions of MDR1 mRNA were 1.00±0.00， 0.51±0.08， 0.89±0.09， 0.56±0.06， respectively， with statistically significant differences （F=30.26， P<0.001； F=22.59， P<0.001； F=18.75， P<0.001）. The above indexes in inhibitor group， activation group and MDR1 knockout group were significantly lower than those in control group （all P<0.05）， these indexes in activation group were significantly higher than those in inhibitor group （all P<0.05）， and which in MDR1 knockout group were lower than those in activation group （all P<0.05）. The levels of p-MEK/MEK proteins in GSCs in the four groups were 0.90±0.09， 0.29±0.05， 0.47±0.05， 0.32±0.04， the levels of p-ERK/ERK proteins were 1.19±0.13， 0.37±0.06， 0.55±0.06， 0.40±0.04， the levels of MDR1 proteins were 1.08±0.12， 0.62±0.07， 0.73±0.07， 0.65±0.06， respectively， with statistically significant differences （F=51.74， P<0.001； F=42.30， P<0.001； F=36.58， P<0.001）. The above indexes in inhibitor group， activation group and MDR1 knockout group were significantly lower than those in control group （all P<0.05）， these indexes in activation group were significantly higher than those in inhibitor group （all P<0.05）， and which in MDR1 knockout group were significantly lower than those in activation group （all P<0.05）. The half maximal inhibitory concentration （IC₅₀） values of GSCs to doxorubicin in the four groups were 0.88， 0.23， 0.79， 0.56 mg/L， the IC₅₀ values to vincristine were 0.84， 0.18， 0.75， 0.51 mg/L， with statistically significant differences （H=17.84， P<0.001； H=15.43， P<0.001）. The above indexes in inhibitor group were lower than those in control group （both P<0.05）， these indexes in activation group were higher than those in inhibitor group （both P<0.05）， and which in MDR1 knockout group were lower than those in activation group （both P<0.05）. Conclusions The MEK inhibitor PD98059 can reduce the MDR1 mRNA level in GSCs by inhibiting the MEK/ERK signaling pathway， thereby enhancing the sensitivity to chemotherapeutic drugs such as doxorubicin and vincristine.

Objective To investigate the relationship between body mass index （BMI） and survival prognosis of invasive breast cancer patients with different menopausal status and molecular subtypes. Methods A total of 2 823 patients with invasive breast cancer who received treatment at the Affiliated Cancer Hospital of Xinjiang Medical University from January 1， 2015 to December 31， 2019 were selected as the study subjects. Patients were divided into four grades according to the clinical classification standard of BMI： underweight （BMI<18.5 kg/m²， n=57）， normal weight （18.5 kg/m²≤BMI<24.0 kg/m²， n=1 289）， overweight （24.0 kg/m²≤BMI<28.0 kg/m²， n=1 061）， and obesity （BMI≥28.0 kg/m²， n=461）. Kaplan-Meier survival curve was drawn to compare the difference of the 5-year overall survival （OS） rates of breast cancer patients with different BMI， and the effect of BMI on the prognosis of breast cancer patients with different menopausal statuses and molecular subtypes was investigated by Cox proportional risk regression model. The dose-response relationship between BMI levels and the risk of all-cause death was further investigated using a RCS function. Results The 5-year OS rates of the invasive breast cancer patients with underweight， normal weight， overweight， obesity were 92.98%， 96.59%， 94.88%， 90.67%， respectively， with a statistically significant difference （χ²=22.11， P<0.001）； the 5-year OS rate of patients with normal weight was better than that of obese patients， with a statistically significant difference （χ²=15.15， P<0.001）. Univariate analysis showed that， obesity was a factor influencing OS of all patients （HR=2.63， 95%CI： 1.73-4.00， P<0.001）， postmenopausal patients （HR=2.47， 95%CI： 1.52-4.02， P<0.001）， Luminal B subtype patients （HR=3.02， 95%CI： 1.64-5.59， P<0.001）， and Luminal B subtype postmenopausal invasive breast cancer patients （HR=2.65， 95%CI： 1.27-5.50， P=0.009）. Multivariate analysis showed that， obesity was an independent factor influencing OS of all patients （HR=1.79， 95%CI： 1.17-2.76， P=0.008）， postmenopausal patients （HR=1.98， 95%CI： 1.20-3.26， P=0.008）， Luminal B subtype patients （HR=2.36， 95%CI： 1.27-4.42， P=0.007）， and Luminal B subtype postmenopausal invasive breast cancer patients （HR=2.39， 95%CI： 1.12-5.11， P=0.024）. When BMI was used as a continuous variable， it showed a U-shaped dose-response relationship with OS of all patients and postmenopausal patients， and the lowest risk points were 24.04， 24.43 kg/m²， respectively. Conclusions Compared with BMI normal weight， obesity significantly reduces the OS rates of all invasive breast cancer patients. Obesity is an independent influencing factor for the OS of all patients， postmenopausal patients， Luminal B subtype and Luminal B subtype postmenopausal invasive breast cancer patients. There is a U-shaped dose-response relationship between BMI and the OS of all patients and postmenopausal patients. When the BMI level of patients exceeds the lowest risk value， the risk of patient death increases with the rise of BMI levels.

Objective To explore the diagnostic value of emission computed tomography （ECT） combined with serum fibroblast growth factor 23 （FGF23） and angiopoietin-like protein 2 （Angptl-2） for bone metastasis in lung cancer patients. Methods A total of 127 patients suspected of having bone metastasis from lung cancer at First Affiliated Hospital of Xi'an Jiaotong University from June 2023 to June 2025 were included as the study subjects. ELISA method was used to measure the levels of serum FGF23 and Angptl-2. The Bayesian log-binomial regression model was used to evaluate the effects of the levels of FGF23 and Angptl-2 on bone metastasis in lung cancer patients. Receiver operator characteristic （ROC） curve was used to analyze the diagnostic efficacy of serum FGF23 and Angptl-2 levels for bone metastasis in lung cancer patients； Four grid table method was used to analyze the diagnostic value of ECT combined with serum FGF23 and Angptl-2 levels for bone metastasis in lung cancer patients. Results Taking the pathological results of bone biopsy as the gold standard， among 127 patients with suspected bone metastasis of lung cancer， 53 cases had bone metastasis and 74 cases didn't have bone metastasis. The levels of serum FGF23 and Angptl-2 in patients with bone metastasis were （123.46±22.18） pg/ml and （32.46±5.13） ng/ml， respectively， while those in patients without bone metastasis were （98.37±16.21） pg/ml and （26.52±4.15） ng/ml， respectively. Compared with patients without bone metastasis， the levels of serum FGF23 and Angptl-2 in patients with bone metastasis were both relatively higher， with statistically significant differences （t=7.37， P<0.001； t=7.20， P<0.001）. The risk of bone metastasis in patients with high levels of serum FGF23 and Angptl-2 was 2.96 times and 2.66 times that of patients with low levels， respectively. The ROC curve analysis showed that， the area under the curve （AUC） of serum FGF23 and Angptl-2 levels in diagnosing bone metastasis in lung cancer patients was 0.77 and 0.81， respectively， the sensitivities were 69.81% and 66.04%， respectively， the specificities were 82.43% and 87.84%， respectively， and the accuracies were 77.17% and 78.74%， respectively. The sensitivity of ECT in diagnosing bone metastasis in lung cancer patients was 79.25%， the specificity was 83.78%， and the accuracy was 81.89%. The sensitivity of ECT combined with serum FGF23 and Angptl-2 in diagnosing bone metastasis in lung cancer patients was 98.11%， the specificity was 81.08%， and the accuracy was 88.19%. The sensitivity of combined diagnosis was higher than that of serum FGF23， Angptl-2 and ECT alone （χ²=15.76， P<0.001； χ²=18.53， P<0.001； χ²=9.40， P=0.002）， and the accuracy of combined diagnosis was higher than that of serum FGF23 and Angptl-2 alone （χ²=5.39， P=0.020； χ²=4.11， P=0.043）. Conclusions Patients with lung cancer bone metastasis have higher levels of serum FGF23 and Angptl-2. ECT combined with serum FGF23 and Angptl-2 levels has a higher diagnostic value for bone metastasis in lung cancer patients compared to the individual detection of each indicator.

Objective To investigate the factors influencing the prognosis of patients with postoperative peritoneal metastasis of gastric cancer. Methods The clinical data of 141 patients with postoperative peritoneal metastasis of gastric cancer admitted to the 909th Hospital （Dongnan Hospital of Xiamen University） from January 2022 to December 2023 were analyzed retrospectively. All patients were followed up for 1 year， and the clinical characteristics of patients with different outcomes were analyzed. The Cox proportional hazards regression model was used to analyze factors influencing patients' prognosis， Kaplan-Meier survival curves were plotted， and the log-rank test was employed to compare 1-year overall survival （OS） rates among patients with different influencing factors. Results Among 141 patients with peritoneal metastasis after gastric cancer surgery， 51 died. The 1-year OS rate of the patients was 70.20%， and the median OS was 13 months. There were statistically significant differences in terms of lymph node metastasis （χ²=9.17， P=0.002）， vascular invasion （χ²=11.78， P=0.001）， cancer nodules （χ²=10.04， P=0.002）， Borrmann type （χ²=6.81， P=0.009）， TNM stage （χ²=22.22， P<0.001）， systemic treatment （χ²=6.47， P=0.011）， and intraperitoneal perfusion chemotherapy （χ²=10.28， P=0.001） between deceased and surviving patients. Multivariate analysis showed that， lymph node metastasis （HR=2.15， 95%CI： 1.44-6.53， P=0.010）， vascular invasion （HR=1.98， 95%CI： 1.28-6.91， P=0.023）， cancer nodules （HR=1.98， 95%CI： 1.26-7.98， P=0.042）， TNM stage （HR=2.09， 95%CI： 1.37-8.03， P=0.025）， and intraperitoneal perfusion chemotherapy （HR=2.19， 95%CI： 1.53-6.30， P=0.008） were all factors influencing the prognosis of patients with postoperative peritoneal metastasis of gastric cancer. Survival curve analysis showed that， the 1-year OS rates of patients with and without lymph node metastasis were 50.0% and 74.7%， respectively， with a statistically significant difference （χ²=9.77， P=0.002）； the 1-year OS rates of patients with and without vascular invasion were 47.5% and 75.6%， respectively， with a statistically significant difference （χ²=12.51， P<0.001）； the 1-year OS rates of patients with and without cancer nodules were 34.8% and 69.5%， respectively， with a statistically significant difference （χ²=11.80， P=0.001）； the 1-year OS rates of patients with TNM stage Ⅰ and Ⅱ were 80.2% and 41.7%， respectively， with a statistically significant difference （χ²=20.64， P<0.001）； and the 1-year OS rates of patients without and with intraperitoneal perfusion chemotherapy were 52.5% and 78.7%， respectively， with a statistically significant difference （χ²=9.83， P=0.002）. Conclusions Lymph node metastasis， vascular invasion， cancer nodules， TNM stage Ⅱ， and no intraperitoneal perfusion chemotherapy are all risk factors for the prognosis of patients with postoperative peritoneal metastasis of gastric cancer.

Objective To explore the predictive value of a nomogram model based on multimodal MRI quantitative parameters for the efficacy of neoadjuvant chemotherapy in rectal cancer. Methods The case data of 106 patients with advanced rectal cancer who received neoadjuvant chemotherapy with the XELOX regimen （oxaliplatin+capecitabine） at the Department of Gastrointestinal Surgery， Nanping First Hospital Affiliated to Fujian Medical University from May 2022 to March 2025 were retrospectively collected. The tumor regression grade （TRG） was evaluated according to the Modified Ryan grading system. The general clinical data and multimodal MRI quantitative indicators T1 value， T2 value， apparent diffusion coefficient （ADC）， volume transport constant （K^trans）， flux rate constant （K_ep）， volume fraction of extravascular extra vascular space （V_e） of patients with different chemotherapy efficacy were compared. A multivariate logistic regression was used to screen the independent influencing factors of the efficacy of neoadjuvant chemotherapy in patients with rectal cancer. A nomogram model was constructed based on the results of multivariate analysis. The predictive efficacy of the model was evaluated using the receiver operator characteristic （ROC） curve， the consistency between the predicted values and the actual values was verified using the calibration curve， and the net benefit and practicability of the model in clinical practice were evaluated through the decision curve. Results Among 106 rectal cancer patients， there were 3 cases of TRG grade 0， 10 cases of grade 1， 32 cases of grade 2， and 61 cases of grade 3. The treatment inefficiency rate was 57.55% （61/106）. There were statistically significant differences in age, TNM stage and degree of differentiation between the ineffective and effective patients （t=3.14， P=0.002； χ²=4.62， P=0.032； χ²=5.17， P=0.023）. The ADC values of patients with ineffective and effective treatment were （1.06±0.14）×10^-3 and （1.18±0.14）×10^-3 mm²/s， respectively， while the K^trans values were （0.24±0.08） and （0.18±0.06） /min， the K_ep values were （1.12±0.34）， （0.88±0.12） /min， and the V_e values were 0.29±0.11 and 0.21±0.06， respectively， with statistically significant differences （t=4.32， P<0.001； t=4.18， P<0.001； t=5.05， P<0.001； t=4.58， P<0.001）. Multivariate analysis showed that， ADC （OR=0.01， 95%CI： 0.01-0.08， P=0.001）， K^trans （OR=1.12， 95%CI： 1.03-1.22， P=0.008）， K_ep （OR=9.09， 95%CI： 5.08-7.12， P<0.001）， V_e （OR=1.11， 95%CI： 1.04-1.19， P=0.003） were independent factors affecting the efficacy of neoadjuvant chemotherapy in patients with rectal cancer. Based on this， a nomogram model was constructed， and the ROC curve analysis showed that the areas under the curve （AUCs） for predicting the efficacy of neoadjuvant chemotherapy in rectal cancer patients by ADC， K^trans， K_ep， V_e， and the nomogram model were 0.73， 0.70， 0.76， 0.71， 0.88， respectively. The predictive value of the nomogram model was higher than that of ADC， K^trans， K_ep， and V_e alone （Z=2.24， P=0.025； Z=2.51， P=0.012； Z=3.49， P<0.001； Z=2.07， P=0.039）. The internal validation of the Bootstrap method showed that the consistency index of the nomogram model for predicting the efficacy of neoadjuvant chemotherapy for rectal cancer was 0.875， and the calibration curve showed that the predictive probability of the model was close to the actual probability. The decision curve showed that the nomogram model could provide a higher clinical net rate of return and had certain clinical practicability. Conclusions The ADC， K^trans， K_ep， and V_e parameters of multimodal MRI are independent influencing factors of the efficacy of neoadjuvant chemotherapy in rectal cancer patients. A nomogram model based on these four parameters has a certain predictive power for the efficacy of neoadjuvant chemotherapy in patients， and shows good predictive performance within this study.

Objective To explore the diagnostic value of MRI combined with serum allograft inflammatory factor-1 （AIF-1） and N-myc downstream regulated gene 4 （NDRG4） for cervical cancer. Methods A total of 108 patients with primary cervical cancer admitted at People's Hospital of Xinjiang Uygur Autonomous Region from May 2022 to October 2024 were considered as study objects （cervical cancer group）， among which 67 cases were in stage Ⅰ-Ⅱ according to FIGO classification and 41 cases were in stage Ⅲ. In addition， 175 patients who underwent MRI at the same time and were diagnosed as having cervical benign cervical lesions through pathological checkups were included （cervical benign lesion group）. A total of 108 healthy individuals who underwent the same-time physical examination were enrolled （normal cervical group）. Enzyme linked immunosorbent assay was used to measure the serum levels of AIF-1 and NDRG4 in each group and in patients with different FIGO stages of cervical cancer. The receiver operator characteristic curve was used to evaluate the value of MRI， AIF-1， NDRG4 and their combination in the diagnosis of cervical cancer. Results The serum AIF-1 levels of the normal cervical group， the cervical benign lesion group， and the cervical cancer group were （122.75±23.69）， （183.50±28.33）， and （212.73±36.14） pg/ml， respectively， with a statistically significant difference （F=263.60， P<0.001）， and the AIF-1 levels increased successively （both P<0.05）. The serum NDRG4 levels of the 3 groups were （134.25±12.33）， （97.48±10.95）， and （86.62±10.27） pg/ml， respectively， with a statistically significant difference （F=581.83， P<0.001）， and the NDRG4 levels decreased successively （both P<0.05）. The serum AIF-1 levels of FIGO stage Ⅰ-Ⅱ， stage Ⅲ cervical cancer patients were （200.35±34.14） and （232.96±36.22） pg/ml， the serum NDRG4 levels of the 2 groups were （91.73±9.21） and （78.26±8.93） pg/ml， with statistically significant differences （t=4.71， P<0.001； t=7.46， P<0.001）. The area under the curve （AUC） for the individual diagnosis of cervical cancer by MRI， AIF-1， and NDRG4 was 0.78， 0.76， and 0.76， respectively. The AUC for the combined diagnosis of the three was 0.85. The diagnostic value of the combined diagnosis was higher than that of MRI， AIF-1， and NDRG4 alone （Z=2.98， P=0.015； Z=3.83， P<0.001； Z=3.83， P<0.001）. Conclusions MRI combined with serum AIF-1 and NDRG4 has higher diagnostic value for cervical cancer.

The V-domain immunoglobulin suppressor of T cell activation （VISTA） is a novel immune checkpoint protein belonging to the B7 family. VISTA is highly expressed in various malignant tumors， and its expression level is closely associated with tumor clinical characteristics and patient prognosis. By binding to its ligand in the tumor microenvironment， VISTA mediates multiple immune escape mechanisms， promoting the progression of virous malignancies and immune resistance， making it a novel target for tumor immunotherapy. Currently， several VISTA inhibitors have entered clinical trial phases， including monotherapy with VISTA inhibitors and combination strategies with other immunomodulatory agents. These developments collectively demonstrate that VISTA is a next-generation immunotherapy target with significant clinical potential.

HOXC10 is a homeobox gene that is closely related to the occurrence and development of digestive system neoplasms. In esophageal cancer， gastric cancer， liver cancer and colorectal cancer， the expression of HOXC10 shows varying degrees of increase， which is closely related to the biological processes such as tumor cell proliferation， metastasis and invasion， apoptosis， and drug resistance， and it participates in tumor regulation through various pathways， which exerts a carcinogenic effect and affects the prognosis of patients. HOXC10 is expected to be a potential molecular target for digestive system neoplasms.

The pathological progression of cervical cancer is closely related to iron metabolism regulation and oxidative stress. Ferroptosis， as a form of iron-dependent programmed cell death， has a significant association with the occurrence and development of cervical cancer. Unlike traditional cell death pathways such as apoptosis and necrosis， ferroptosis shows distinct specificity. Its main characteristics include lipid peroxidation， iron accumulation， and inhibition of the antioxidant system. Ferroptosis has shown excellent efficacy in antitumor treatment and has promising application prospects. When combined with traditional methods such as radiotherapy and chemotherapy， it demonstrates potential for synergistic enhancement. Further exploration of the molecular basis and research advances in the relationship between ferroptosis and cervical cancer， and delving into its underlying mechanism of action， can provide a theoretical foundation and practical guidance for innovative treatment strategies for cervical cancer.

The tumor microenvironment （TME） is a complex ecosystem comprising infiltrating cells and their secretory products， extracellular matrix components， and other non-cellular elements. The pathogenesis of lymphomas involves intricate interactions between neoplastic cells and the TME. While tumor morphology， immunophenotype， and molecular features remain well-established factors for prognostic prediction and therapeutic guidance， the role of non-tumor cell microenvironment components has gained increasing significance with advancing understanding of the biological mechanisms of lymphoma. Consequently， further exploration is warranted into lymphoma subtypes where TME plays a pivotal role in disease development， as well as novel therapeutic approaches and combination strategies targeting non-tumor cells and tumor-non-tumor cell interactions. Such efforts hold promise for providing unique insights into lymphoma management.