Objective To investigate the effect and related mechanism of Marsdenia tenacissima combined with XELOX solution on disulfide apoptosis in human colorectal cancer HCT116 cells. Methods The human colorectal cancer HCT116 cells were cultured in vitro and treated with different concentrations of capecitabine （0， 0.3， 0.6， 1.2， 2.4， 4.8 μg/ml）， oxaliplatin （0， 10， 20， 40， 80， 160 μg/ml）， Marsdenia tenacissima （0， 15， 30， 60， 120， 240 mg/ml）， and the glucose inhibitor BAY-876 （0， 4， 8， 16， 32， 64 μg/ml）， respectively. Furthermore， the HCT116 cells were pre-treated with 25 μg/ml of BAY-876， followed by exposure to the specified concentrations of each drug group. HCT116 cells were divided into the following groups： negative control group （no treatment）， capecitabine group （4.0 μg/ml）， oxaliplatin group （90 μg/ml）， Marsdenia tenacissima group （140 mg/ml）， XELOX solution group （4.0 μg/ml capecitabine+90 μg/ml oxaliplatin）， and Marsdenia tenacissima combined with XELOX solution group （140 mg/ml Marsdenia tenacissima+4.0 μg/ml capecitabine+90 μg/ml oxaliplatin）. BAY-876 treatment groups refer to the groups which the glucose inhibitor BAY-876 25 μg/ml was added to each of the above groups. The cell proliferation was assessed using the MTT assay. Apoptosis was determined through Annexin Ⅴ- FITC/PI double staining. The concentration of glucose was quantified using the o-toluidine method. NADPH levels were measured by colorimetry. Cystine uptake fluorescence assay was utilized to quantify the fluorescence intensity of cystine， and cysteine content was determined using cysteine colorimetry. Results After 0， 0.3， 0.6， 1.2， 2.4， 4.8 μg/ml concentration of capecitabine， 0， 10， 20， 40， 80， 160 μg/ml concentration of oxaliplatin， 0， 4， 8， 16， 32， 64 μg/ml concentration of BAY-876， and after pre-treatment with 25 μg/ml glucose inhibitor BAY-876， HCT116 cells were treated with the above drugs and concentrations， there were statistically significant differences in cell survival rate （F=644.60， P<0.001； F=417.30， P<0.001； F=1 028.00， P<0.001； F=1 066.00， P<0.001； F=847.70， P<0.001）， and with the increase of each drug concentration， the activity of HCT116 cells decreased gradually （all P<0.05）. After 0， 15， 30， 60， 120， 240 mg/ml concentration of Marsdenia tenacissima， and after pre-treatment with 25 μg/ml glucose inhibitor BAY-876， HCT116 cells were treated with the above drugs， there were statistically significant differences in cell survival rate （F=107.50， P<0.001； F=619.70， P<0.001）， and with the increase of drug concentration， the activity of HCT116 cells increased first and then decreased （all P<0.05）. Annexin Ⅴ- FITC/PI staining showed that the intensity of green， red and yellow fluorescence was weaker in the negative control group. The expression of green fluorescence and red fluorescence was enhanced in each drug group. In capecitabine group， the red fluorescence and yellow fluorescence were larger. The proportion of green fluorescence in oxaliplatin group and Marsdenia tenacissima group was smaller. The proportion of green fluorescence and yellow fluorescence in XELOX solution group was higher than that in capecitabine group and oxaliplatin group. Marsdenia tenacissima combined with XELOX solution group had the highest proportion of green and red fluorescence. After pre-treatment with the glucose inhibitor BAY-876， the green and yellow fluorescence of the cells in each group increased significantly. The green and yellow fluorescence of capecitabine group and oxaliplatin group increased significantly. The fluorescence of XELOX solution group was significantly higher than that of capecitabine group and oxaliplatin group. In Marsdenia tenacissima combined with XELOX solution group， the proportion of fluorescence expressing three colors was the largest. In the negative control group， capecitabine group， oxaliplatin group， Marsdenia tenacissima group， XELOX solution group， Marsdenia tenacissima combined with XELOX solution group， and the groups after BAY-876 pre-treatment， the glucose concentration of HCT116 was （19.91±0.13）， （22.82±0.88）， （11.87±0.14）， （17.93±0.14）， （10.53±0.10）， （7.56±0.08）， （11.44±0.10）， （11.73±0.72）， （8.98±0.40）， （14.25±0.33）， （6.77±1.50）， and （1.56±0.17） μg/ml， respectively， with statistically significant differences （F=762.60， P<0.001； F=118.80， P<0.001）. Compared with the untreated groups， the intracellular glucose concentration of HCT116 cells treated with BAY-876 was significantly decreased （t=86.50， P<0.001； t=16.90， P<0.001； t=11.83， P<0.001； t=17.79， P<0.001； t=4.35， P=0.012； t=54.34， P<0.001）. NADPH levels in each group were （131.80±2.61）， （93.87±1.00）， （136.50±3.69）， （105.70±0.84）， （146.90±2.94）， （105.00±2.25）， （92.33±0.23）， （88.63±0.31）， （97.33±2.02）， （81.77±1.33）， （102.80±1.61）， and （85.13±0.45） nmol/gProt， respectively， with statistically significant differences （F=225.60， P<0.001； F=125.50， P<0.001）； Compared with the untreated groups， the intracellular NADPH levels of HCT116 cells treated with BAY-876 was significantly decreased （t=26.11， P<0.001； t=8.62， P<0.001； t=16.13， P<0.001； t=26.38， P<0.001； t=22.78， P<0.001； t=14.97， P<0.001）. The fluorescence intensity of cystine in each group was 607.30±8.76， 655.70±6.57， 647.10±19.35， 737.80±6.34， 756.00±8.65， 846.60±11.70， 929.60±6.88， 1 049.00±22.35， 1 021.00±29.49， 1 094.00±16.17， 1 137.00±10.08， and 1 230.00±46.57， respectively， with statistically significant differences （F=188.00， P<0.001； F=48.32， P<0.001）. Compared with the untreated groups， the intracellular fluorescence intensity of cystine of HCT116 cells was significantly increased after treatment with BAY-876 （t=50.09， P<0.001； t=29.26， P<0.001； t=18.34， P<0.001； t=35.53， P<0.001； t=49.66， P<0.001； t=13.83， P<0.001）. The contents of cysteine in each group were （457.00±30.69）， （581.20±30.69）， （326.40±5.49）， （374.20±5.54）， （565.30±5.54）， （246.80±30.69）， （100.30±16.57）， （472.90±19.10）， （262.70±28.65）， （348.70±9.55）， （533.40±11.03）， （30.23±5.49） μmol/L， respectively， with statistically significant differences （F=110.00， P<0.001； F=423.50， P<0.001）. Compared with the untreated groups， the intracellular contents of cysteine of HCT116 cells treated with BAY-876 was significantly decreased （t=17.71， P<0.001； t=5.19， P=0.006； t=3.78， P=0.019； t=4.00， P=0.016； t=4.47， P=0.011； t=12.03， P<0.001）. Conclusion Marsdenia tenacissima combined with XELOX solution can promote HCT116 cell death through disulfide apoptosis.

Objective To explore the prognostic value of epidermal growth factor receptor （EGFR） co-mutation status in patients with advanced lung adenocarcinoma. Methods Clinical data of patients with stage ⅢB-Ⅳ lung adenocarcinoma who were first diagnosed in the Department of Respiratory and Critical Care Medicine， First Affiliated Hospital of Hebei North University from January 2019 to December 2022 were collected prospectively. Patients were divided into EGFR mutation group （n=82） and EGFR co-mutation group （n=74） according to whether EGFR was combined with other gene mutations. The level of circulating tumor DNA （ctDNA） in peripheral blood was measured by real time fluorescence quantitative PCR. Objective response rate （ORR）， disease control rate （DCR）， the levels of ctDNA in peripheral blood， and progression-free survival （PFS） were compared between two groups of patients before and after 1 month of treatment. The univariate and multivariate analyses were conducted by Cox proportional hazards regression model. Results In the EGFR mutation group， there were 45 cases of EGFR19 deletion mutation and 37 cases of EGFR21 mutation. In the EGFR co-mutation group， there were 41 cases of EGFR19 deletion mutation， 33 cases of EGFR21 mutation， 46 cases of TP53 mutation， 16 cases of RB1 mutation， 6 cases of PTEN mutation， 2 cases of MET amplification， 1 case of ERBB2 mutation， 1 case of KRAS mutation， 1 case of RET rearrangement， and 1 case of ALK rearrangement. There were statistically significant differences between the EGFR mutation group and the EGFR co-mutation group in the maximum tumor diameter （χ²=5.04， P=0.025） and stage （χ²=3.92， P=0.048）. The ORRs of the two groups were 64.63% （53/82） and 37.84% （28/74）， respectively， with a statistically significant difference （χ²=11.19， P<0.001）. The DCRs were 96.34% （79/82） and 86.49% （64/74）， respectively， with a statistically significant difference （χ²=4.95， P=0.026）. The ctDNA levels in the EGFR mutation group and EGFR co-mutation group after one month of treatment decreased compared to before treatment [2.63 （1.83， 3.30） ng/μl vs. 4.73 （3.92， 5.49） ng/μl， Z=-7.06， P<0.001； 4.26 （2.26， 6.07） ng/μl vs. 5.28 （4.37， 6.09） ng/μl， Z=-5.15， P<0.001]， the ctDNA levels in the EGFR co-mutation group were higher than those in the EGFR mutation group before treatment and after 1 month of treatment （Z=-2.47， P=0.013； Z=-4.29， P<0.001）. In the EGFR co-mutation group， the ctDNA levels in peripheral blood of patients who were effectively treated with targeted therapy decreased after 1 month of treatment compared to before treatment [（2.03±0.63） ng/μl vs. （3.92±0.82） ng/μl， t=42.94， P<0.001]， the levels of ctDNA in peripheral blood of ineffectively treated patients before and after 1 month of treatment were higher than those of effectively treated patients [（5.84±0.57） ng/μl vs. （3.92±0.82） ng/μl， t=-11.91， P<0.001； （5.87±1.64） ng/μl vs. （2.03±0.63） ng/μl， t=-14.43， P<0.001]. The median PFS of the EGFR mutation group and the EGFR co-mutation group of patients were 10.4 and 8.3 months， respectively， with a statistically significant difference （χ²=22.28， P<0.001）. Univariate analysis suggested that the maximum tumor diameter （HR=0.10， 95%CI： 0.06-0.16， P<0.001）， performance status （PS） score （HR=0.09， 95%CI： 0.06-0.15， P<0.001）， stage （HR=0.09， 95%CI： 0.05-0.14， P<0.001）， pre-treatment ctDNA level （HR=12.04， 95%CI： 8.21-17.65， P<0.001）， ctDNA level after 1 month of treatment （HR=3.75， 95%CI： 3.10-4.54， P<0.001） and EGFR co-mutations （HR=2.21， 95%CI： 1.57-3.12， P<0.001） were found to be significant factors affecting the PFS of stage ⅢB -Ⅳ lung adenocarcinoma patients receiving targeted therapy； Multivariate analysis demonstrated that PS score （HR=0.25， 95%CI： 0.14-0.47， P<0.001）， stage （HR=0.49， 95%CI： 0.24-0.98， P=0.044）， pre-treatment ctDNA level （HR=4.73， 95%CI： 3.08-7.28， P<0.001）， ctDNA level after 1 month of treatment （HR=2.15， 95%CI： 1.65-2.80， P<0.001）， and EGFR gene co-mutation （HR=2.26， 95%CI： 1.40-3.64， P<0.001） were independent risk factors for PFS in stage ⅢB -Ⅳ lung adenocarcinoma patients receiving targeted therapy. Conclusion Both the EGFR mutation group and EGFR co-mutation group show a decrease in ctDNA levels after targeted therapy for one month compared to before treatment. The median PFS of EGFR co-mutation patients is shorter than that of patients with a single EGFR mutation. PS score， stage， ctDNA levels before and after treatment， and EGFR gene co-mutation are all independent factors affecting PFS in stage ⅢB-Ⅳ lung adenocarcinoma patients after targeted therapy.

Objective To analyze the early predictive value of serum soluble CD163 （sCD163）， interferon-γ （IFN-γ）， and transforming growth factor-β1 （TGF-β1） for radiation pneumonitis （RP） in non-small cell lung cancer （NSCLC） patients after radiation therapy. Methods One hundred and thirty-two NSCLC patients with clinical stage Ⅲ-Ⅳ receiving radiotherapy at Wuhan Hospital of Traditional Chinese Medicine from December 2020 to November 2023 were selected. Serum sCD163， IFN-γ and TGF-β1 levels were detected by enzyme-linked immunosorbent assay. The occurrence of RP after radiotherapy was analyzed； serum sCD163， IFN-γ， and TGF-β1 levels were compared between NSCLC patients receiving radiotherapy who had RP and those who did not， as well as patients with different levels of RP. Multivariate logistic regression was used to analyze the factors affecting the occurrence of RP in NSCLC patients； the predictive value of serum sCD163， IFN-γ combined with TGF-β1 for the occurrence of RP in patients undergoing radiotherapy for NSCLC was analyzed using reciver operator characteristic （ROC） curves. Results The incidence of RP in NSCLC patients receiving radiotherapy was 24.24% （32/132）. There were 18 cases of grade Ⅱ， 12 cases of grade Ⅲ， 2 cases of grade Ⅳ. Serum sCD163 levels in patients with RP [（94.30±15.78） pg/ml vs. （75.43±13.16） pg/ml， t=6.72， P<0.001]， IFN-γ [（6.52±1.54） pg/ml vs. （4.79±0.94） pg/ml， t=7.65， P<0.001]， TGF-β1 [（9.40±2.63） μg/L vs. （6.30±1.55） μg/L， t=8.18， P<0.001] were significantly higher than those of patients without RP， and there were statistically significant differences. And levels of serum sCD163 [（104.44±15.97） pg/ml vs. （86.41±15.63） pg/ml， t=3.21， P=0.003]， IFN-γ [（7.47±1.56） pg/ml vs. （5.78±1.52） pg/ml， t=3.09， P=0.004] and TGF-β1 [（11.27±2.68） μg/L vs. （7.94±2.59） μg/L， t=3.55， P=0.001] in RP patients with grade Ⅲ-Ⅳ were higher than those in RP patients with grade Ⅱ， and there were statistically significant differences. There were statistically significant differences in radiation dose （χ²=9.25， P=0.002）， V₂₀ （t=6.39， P<0.001） and mean lung dose （MLD） （t=3.57， P<0.001） between patients with and without RP. Multivariate analysis showed that radiation dose （OR=3.98， 95%CI： 2.22-7.15， P<0.001）， V₂₀ （OR=4.75， 95%CI： 2.03-11.15， P<0.001）， MLD （OR=3.15， 95%CI： 1.63-6.09， P=0.001）， sCD163 （OR=4.53， 95%CI： 1.63-12.58， P=0.004）， IFN-γ （OR=5.11， 95%CI： 2.07-12.65， P<0.001）， and TGF-β1 （OR=5.55， 95%CI： 2.99-10.31， P<0.001） were the independent influencing factors for developing RP in patients receiving radiotherapy for NSCLC. The area under the curve （AUC） of sCD163， IFN-γ， and TGF-β1 alone for predicting the occurrence of RP in patients receiving radiotherapy for NSCLC was 0.81 （95%CI： 0.72-0.89）， 0.83 （95%CI： 0.75-0.92） and 0.84 （95%CI： 0.76-0.92）， and the AUC of the above three combined for predicting the occurrence of RP in NSCLC patients receiving radiotherapy was 0.93 （95%CI： 0.88-0.99）， and the combined predictive value of the three was higher than that of sCD163 （Z=2.57， P=0.005）， IFN-γ （Z=2.02， P=0.021）， and TGF-β1 （Z=1.94， P=0.026） alone. Conclusion Serum sCD163， IFN-γ， and TGF-β1 levels are significantly elevated in NSCLC patients undergoing radiotherapy who develop RP， and the combination of the three is of high value in predicting the development of RP in NSCLC patients after radiation therapy.

Objective To explore the pattern of lymph node metastasis in the lung lobes of stage Ⅱa non-small cell lung cancer （NSCLC） and the lymph node dissection method during complete video-assisted thoracoscopic lobectomy surgery （cVATS）. Methods A total of 244 patients with NSCLC who underwent cVATS treatment at Nanjing Tongren Hospital Affiliated to Southeast University School of Medicine from January 2015 to November 2018 were selected. Patients admitted from January 2015 to April 2018 were defined as the training set （n=183）， and patients admitted from May 2018 to November 2018 were defined as the validation set （n=61）. The training set was used to build the model， and the validation set was used to evaluate the performance of the model. In the training set， patients were divided into systematic meditational lymphadenectomy （SML） group （n=93） and lobe-specific systematic node dissection （LSND） group （n=90） based on lymph node dissection methods.The lymph node metastasis rate of patients in the training set was calculated， and the clinical data of patients with （n=55） and without （n=128） lymph node metastasis were compared. Multivariate logistic regression was used to analyze the influencing factors of lymph node metastasis， and a nomogram prediction model was constructed based on the results of the multivariate analysis， and the model was validated. Clinical data， perioperative clinical indicators， overall survival （OS）， and incidence of postoperative complications were compared between the SML group and LSND group in the training set. Results In the training set， the lymph node metastasis rate of 183 patients with NSCLC was 30.05% （55/183）， with a total of 328 metastatic lymph nodes； from the 2nd to the 13th groups of lymph nodes， the 10th （15.60%， 44/282）， the 11th （22.79%， 98/430）， and the 12th to the 13th （15.25%， 61/400） groups had the highest lymph node metastasis rate. Multivariate analysis showed that maximum tumor diameter （OR=2.71， 95%CI： 1.82-4.09， P<0.001）， CT imaging features （OR=2.49， 95%CI： 1.59-6.99， P=0.001）， degree of differentiation （OR=2.06， 95%CI： 1.11-3.81， P=0.010）， serum carcinoembryonic antigen （CEA） （OR=1.87， 95%CI： 1.42-2.58， P=0.015）， and pleural invasion （OR=1.81， 95%CI： 1.07-3.07， P=0.021） were all independent influencing factors for the occurrence of lymph node metastasis in Ⅱa NSCLC patients. The C-index of the training set and the validation set were 0.91 （95%CI： 0.88-0.97） and 0.89 （95%CI： 0.84-0.96）， respectively， and the calibration curves of the two sets were well fitted to the ideal curves. Receiver operating characteristic curve analysis showed that， the area under curve of the nomogram prediction model used for differential diagnosis of patients in the training and validation sets were 0.92 （95%CI： 0.87-0.96） and 0.91 （95%CI： 0.85-0.98）， respectively. There were statistically significant differences in surgical time [（203.08±38.26） min vs. （177.14±22.18） min， t=5.59， P<0.001]， intraoperative blood loss [（458.14±65.04） ml vs. （426.08±26.58） ml， t=4.34， P<0.001]， thoracic drainage volume [（1 200.14±226.58） ml vs. （1 114.38±164.34） ml， t=2.92， P=0.004]， extubation time [（6.57±1.28） d vs. （5.02±1.12） d， t=8.71， P<0.001]， hospital stay [（15.02±1.29） d vs. （12.08±1.57） d， t=13.86， P<0.001） between the SML group and the LSND group in the training set. There was no statistically significant difference in OS rate between two groups of patients at 1 year （96.77% vs. 96.67%）， 3 years （84.95% vs. 86.67%）， and 5 years （75.27% vs. 77.78%） （χ²=0.16， P=0.689）. There was a statistically significant difference in the overall incidence of adverse reactions [18.28%（17/93） vs. 7.78%（7/90）] between two groups of patients （χ²=4.43， P=0.035）. Conclusion Intrapulmonary segment lymph node accounts for a considerable proportion in the metastasis process of NSCLC， with the highest degree of lymph node metastasis rate in groups 10， 11， and 12-13. Maximum tumor diameter， CT imaging features， degree of differentiation， serum CEA， and pleural invasion are all independent influencing factors for the occurrence of lymph node metastasis in NSCLC patients. Compared with SML， LSND has less trauma and a lower incidence of adverse reactions.

Objective To compare the clinical efficacy of helical tomotherapy in the treatment of esophageal cancer， explore its influence on nutrition status， blood routine indexes， inflammatory factors and immune function， and analyze its safety. Methods A total of 124 patients with esophageal cancer treated in Liyang People's Hospital of Jiangsu Province from May 2021 to April 2023 were selected as the study objects， and the patients were divided into the helical tomotherapy group （n=62） and the modulated arc therapy group （n=62） according to random number table method. The clinical efficacy， nutritional status [transferrin （TRF）， prealbumin （PAB）， serum albumin （ALB）]， blood routine indexes [hemoglobin （HGB）， neutrophils count， white blood cells （WBC） count， platelets count]， the inflammatory factors [C-reactive protein （CRP）， interleukin （IL）-6， IL-18， tumor necrosis factor-α （TNF-α）]， immune function indexes [CD3⁺ T cells， CD4⁺ T cells， CD4⁺ T cells /CD8⁺ T cells ratio， natural killer （NK） cells]， and the rate of adverse reactions were statistically analyzed. Results The disease control rate of treatment in the helical tomotherapy group （88.71%， 55/62） was significantly higher than that in the modulated arc therapy group （74.19%， 46/62）， with a statistically significant difference （χ²=4.32， P=0.038）. After treatment， TRF [（178.42±19.24） µg/dl vs. （171.27±18.19） µg/dl， t=2.13， P=0.035]， PAB [（0.37±0.11） g/L vs. （0.31±0.09） g/L， t=3.32， P=0.001]， ALB [（4.25±0.52） g/dl vs. （4.01±0.58） g/dl， t=2.43， P=0.017] in the helical tomotherapy group were higher than those in the modulated arc therapy group， with statistically significant differences. After treatment， HGB [（125.49±13.87） g/dl vs. （112.37±14.49） g/dl， t=5.21， P<0.001] in the helical tomotherapy group were higher than those in the modulated arc therapy group； neutrophils count [（4.91±0.75）×10⁹/L vs. （5.37±0.84）×10⁹/L， t=3.22， P=0.002]， WBC count [（4.96±0.52）×10⁹/L vs. （5.26±0.61）×10⁹/L， t=2.95， P=0.004]， platelets count [（227.15±25.38）×10⁹/L vs. （241.37±26.91）×10⁹/L， t=3.03， P=0.003] in the helical tomotherapy group were lower than those in the modulated arc therapy group， with statistically significant differences. After treatment， CRP [（7.76±0.84） mg/dl vs. （8.11±1.01） mg/dl， t=2.10， P=0.038]， IL-6 [（6.47±0.81） µg/L vs. （7.16±0.93） µg/L， t=4.41， P<0.001]， IL-18 [（191.01±23.14） µg/L vs. （201.62±22.96） µg/L， t=2.56， P=0.012，） and TNF-α [（3.65±0.41） µg/L vs. （3.82±0.43） µg/L， t=2.25， P=0.026] in the helical tomotherapy group were lower than those in the modulated arc therapy group， with statistically significant differences. After treatment， the proportion of CD3⁺ T cells [（41.27±5.45） % vs.（35.48±5.17） %， t=6.07， P<0.001]， the proportion of CD4⁺ T cells [（36.11±4.49） % vs. （29.24±9.52） %， t=9.48， P<0.001]， CD4⁺ T cells /CD8⁺ T cells ratio （1.35±0.19 vs. 1.21±0.13， t=4.79， P<0.001）， the proportion of NK cells [（14.68±2.79） % vs. （12.37±1.86） %， t=5.42， P<0.001] in the helical tomotherapy group were higher than those in the modulated arc therapy group， with statistically significant differences. The rate of adverse reactions in the helical tomotherapy group （80.65%， 50/62） was significantly lower than that in the modulated arc therapy group （93.55%， 58/62）， with a statistically significant difference （χ²=4.59， P=0.032）. Conclusion Helical tomotherapy is more effective than modulated arc therapy in the treatment of esophageal cancer， which can improve nutrition levels， reduce immunity decline， and has high safety.

Vav guanine nucleotide exchange factor 3 （Vav3） protein is one of the guanine nucleotide exchange factors of the Rho family GTPases. It is encoded by the proto-oncogene Vav3 and is involved in the regulation of cell proliferation and apoptosis， differentiation， migration， etc. In recent years， Vav3 has been closely related to the development of a variety of malignant tumors. In glioma， breast cancer， non-small cell lung cancer， gastric cancer， pancreatic cancer， colorectal cancer， prostate cancer， ovarian cancer， osteosarcoma and acute leukemia， the expression of Vav3 is elevated to varying degrees， and it participates in regulating multiple signaling pathways， which promotes the progression of tumors and affects the prognosis of patients. Therefore， Vav3 is expected to be a potential therapeutic target for these malignant tumors.

The pregnane X receptor （PXR） is a crucial regulator of cytochrome P-450 （CYP450） expression. It is involved in oxidative stress， steroid and bile acid metabolism， inflammatory response， apoptosis， cell proliferation and other biological behaviors， and also participates in the metabolism， transport and clearance of chemotherapy drugs. After activation， PXR can affect chemotherapy drug resistance of breast cancer through genetic variation and epigenetic modification， regulation of apoptosis， and participation in phosphorylation/dephosphorylation. It may be a potential therapeutic target for patients with breast cancer resistance.

Gastric cancer and esophagogastric junction cancer （EGJC） are one of the world's most common types of malignant tumors. Traditional treatment methods mainly include radiotherapy， chemotherapy， and surgery， but the patients' prognosis is limited. In recent years， with the development in treatment methods， immunotherapy and targeted therapy are gradually recognized as the first-line treatment methods. In immunotherapy， nivolumab and pabolizumab have shown clear efficacy in patients with programmed death-ligand 1 positive， while other immunotherapies （such as tumor vaccine， engineered T cells， and non-specific immunomodulators） are still being tested or developed. In addition， targeted therapy has only shown comparatively large therapeutic potential in certain specific populations or in second-line treatment. For instance， tratuzumab has a clear curative effect on patients with positive human epidermal growth factor receptor 2， but has suboptimal efficacy in patients with amplification of other molecular targets. An in-depth discussion of the research progress of immunotherapy and targeted therapy in gastric cancer and EGJC will help to improve the prognosis of patients and provide a reference for accurate treatment of tumors.

Colorectal cancer is a common malignant tumor of the digestive system， with the characteristics of insidious onset， high risk of recurrence and metastasis， and poor prognosis. In recent years， clinical researches related to targeted therapy for colorectal cancer of different molecular subtypes such as RAS， BRAF， MMR/MSI， HER2， MET， NTRK， and POLE/POLD1 have all achieved certain results. Besides， the exploration of the combined application of molecular targeted therapy for colorectal cancer and other therapies is also continuously carried out. Clarifying the mechanism of action and clinical application progress of molecular targeted therapy for colorectal cancer can provide a more reliable basis for formulating clinical treatment plans for colorectal cancer patients.