Nasopharyngeal carcinoma is rare in children and adolescents， but the prognosis is relatively good. More and more studies focus on the growth and development， as well as the quality of life of patients after treatment. Certain progress has been made in the research of nasopharyngeal carcinoma in children and adolescents， covering multiple aspects such as etiology， clinical characteristics， treatment regimens and prognosis. The factors causing nasopharyngeal carcinoma include viral infection， genetic susceptibility and environmental factors， etc. The main treatment methods are radiotherapy， chemotherapy， targeted therapy， immunotherapy and surgery. In addition， traditional Chinese medicine has also shown its unique efficacy and potential in the adjuvant therapy of nasopharyngeal carcinoma， providing more treatment options for patients. Further exploration of the factors influencing the occurrence of nasopharyngeal carcinoma in children and adolescents， and analysis of the effects and applications of different treatment methods， can provide new perspectives and references for future research.

Objective To investigate the effects of metformin on esophageal squamous cell carcinoma cell growth， migration and angiogenesis by regulating the expression of ALKBH3. Methods Human esophageal cancer TE-1 cells were treated with different concentrations （0， 0.5， 1.0， 2.0， 4.0， 8.0 mmol/L） of metformin， and they were divided into a blank control group， low- （0.5 mmol/L）， medium- （1.0 mmol/L）， and high- （2.0 mmol/L） concentration metformin groups， a metformin （2.0 mmol/L）+pcDNA-NC group， and a metformin （2.0 mmol/L）+pcDNA-ALKBH3 group. The cell viability was determined by the CCK-8 method. The cell proliferation ability was detected by the clone formation assay. The cell migration and invasion abilities were examined by the Transwell assay. The cell apoptosis was detected by flow cytometry. The tube formation ability of cells was detected by the angiogenesis assay. A xenograft tumor model was constructed using 4- to 6-week-old male BALB/c thymus-less nude mice， which were divided into a model control group， a metformin group， a metformin+pcDNA-NC group， and a metformin+pcDNA-ALKBH3 group using a random number table method， and with six in each group. And the volume and weight of the tumor were measured. The protein expression levels of apoptosis-related proteins Bcl-2， Bax， ALKBH3 and vascular endothelial growth factor A （VEGF-A） were detected by Western blotting. The expression of CD31 protein was detected by immunohistochemistry. Results After treating TE-1 cells with 0， 0.5， 1.0， 2.0， 4.0， and 8.0 mmol/L metformin for 48 hours， the cell viability was （100.00±0.00）%， （90.31±5.23）%， （81.25±8.65）%， （63.52±6.80）%， （54.64±5.35）%， and （31.48±4.21）%， respectively， with a statistically significant difference （F=98.11， P<0.001）. There were statistically significant differences in cell viability between 0.5， 1.0， 2.0， 4.0， 8.0 mmol/L and 0 mmol/L （all P<0.05）. The IC₅₀ of metformin for TE-1 cells was 4.46 mmol/L. The numbers of colony formations of TE-1 cells in the blank control group， low-， medium-， and high-concentration metformin groups， metformin+pcDNA-NC group， and metformin+pcDNA-ALKBH3 group were 153.15±13.55， 134.80±11.62， 116.24±10.43， 93.17±8.85， 89.39±8.46， 110.26±7.21， respectively， with a statistically significant difference （F=34.28， P<0.001）； the numbers of colony formations of TE-1 cells in the metformin groups at different concentrations decreased significantly with the increase in metformin concentration （both P<0.05）； compared with the metformin+pcDNA-NC group， the number of colony formations of cells in the metformin+pcDNA-ALKBH3 group increased （P<0.05）. The numbers of migration of TE-1 cells of 6 groups were 152.13±13.40， 133.85±10.72， 115.28±8.64， 91.16±7.89， 85.39±7.23， 116.85±8.36， the numbers of invasion were 135.22±10.77， 112.07±9.53， 86.30±7.45， 69.53±6.74， 65.81±5.65， 79.80±6.32， respectively， with statistically significant differences （F=41.35， P<0.001； F=69.06， P<0.001）； the numbers of migrated and invaded cells in the metformin groups at different concentrations decreased significantly with the increase in metformin concentration （all P<0.05）； compared with the metformin+pcDNA-NC group， the numbers of migrated and invaded cells in the metformin+pcDNA-ALKBH3 group increased significantly （both P<0.05）. The apoptosis rates of TE-1 cells in 6 groups were （3.22±1.13）%， （13.82±1.90）%， （22.67±2.53）%， （29.18±3.24）%， （26.84±2.75）%， and （16.36±1.63）%， respectively， with a statistically significant difference （F=103.66， P<0.001）； the apoptosis rates of cells in the metformin groups at different concentrations gradually increased with the increase in metformin concentration （both P<0.05）； compared with the metformin+pcDNA-NC group， the apoptosis rate of cells in the metformin+pcDNA-ALKBH3 group was relatively lower （P<0.05）. The tubular structure of cells in blank control group was intact， and there were different degrees of damage to the tubular structure of cells in the low-， medium-， high- concentration metformin groups， the degree of damage to the tubular structure of cells in the metformin+pcDNA-ALKBH3 group was reduced. The numbers of cellular tubular structures of TE-1 cells in the 6 groups were 38.35±3.20， 27.15±2.64， 15.92±3.14， 7.39±1.50， 8.61±1.37， and 29.33±4.20， respectively， with a statistically significant difference （F=113.92， P<0.001）； the number of cellular tubular structures in the low-， medium-， and high- concentration metformin groups gradually decreased （both P<0.05）； the number of cellular tubular structures in the metformin+pcDNA-ALKBH3 group was more than that in the metformin+pcDNA-NC group （P<0.05）. There were statistically significant differences in the protein expressions of Bcl-2， Bax， ALKBH3， and VEGF-A in TE-1 cells among 6 groups （F=56.36， P<0.001； F=57.26， P<0.001； F=159.30， P<0.001； F=132.89， P<0.001）； compared with the blank control group， the protein expressions of Bcl-2， ALKBH3， and VEGF-A in the metformin groups at different concentrations decreased， while the protein expression of Bax increased （all P<0.05）； compared with the metformin+pcDNA-NC group， the protein expressions of Bcl-2， ALKBH3， and VEGF-A in the metformin+pcDNA-ALKBH3 group increased， and the expression level of Bax decreased （all P<0.05）. The weights of tumors in the model control group， metformin group， metformin+pcDNA-NC group， and metformin+pcDNA-ALKBH3 group were （1.16±0.12）， （0.46±0.05）， （0.50±0.06）， （1.19±0.14） g， the volumes of tumors were （878.36±108.93）， （413.59±50.23）， （439.78±51.39）， （793.75±96.98） mm³， with statistically significant differences （F=96.61， P<0.001； F=51.90， P<0.001）； the weight of tumors were lower and the volume of tumors were smaller in the metformin group than those in the model control group （both P<0.05）， the weight of tumors were higher and the volume of tumors were bigger in the metformin+pcDNA-ALKBH3 group than those in the metformin group and the metformin+pcDNA-NC group （all P<0.05）. CD31 was mainly distributed in the cytoplasm and cell membrane of tumor cells. There were statistically significant differences in the positive rates of CD31 and the protein expression levels of VEGF-A in transplanted tumor tissues among 4 groups （F=7.12， P=0.002； F=48.81， P<0.001）； the positive rate of CD31 and the protein expression level of VEGF-A in the metformin group were lower than those in the model control group； the positive rate of CD31 and the protein expression level of VEGF-A in the metformin+pcDNA-ALKBH3 group were higher than those in the metformin group and the metformin+pcDNA-NC group （all P<0.05）. Conclusions Metformin may inhibit the proliferation， migration， and tumor angiogenesis of esophageal squamous cell carcinoma by reducing ALKBH3 expression.

Objective To investigate the efficacy of rapamycin arterial perfusion combined with ¹³¹I-fibroblast activation protein （FAP） loaded dextran microspheres in the treatment of rabbits with liver transplantation tumor. Methods Fifty male New Zealand white rabbits were selected. Forty white rabbits were used to establish liver transplantation tumor models and were randomly divided into a negative control （based on arterial perfusion with the same volume of normal saline， MO） group， rapamycin arterial perfusion （RA） group， ¹³¹I-FAP loaded dextran microspheres for interventional embolization therapy （IF） group， and rapamycin arterial perfusion combined with ¹³¹I-FAP-loaded dextran microspheres interventional embolization therapy （RI） group by the random number table method， with 10 rabbits in each group. The remaining 10 unmodeled white rabbits were classified as the normal （based on arterial perfusion with the same volume of normal saline， NO） group. The pathological morphology of tumor tissues was detected by HE staining， liver function was detected by automatic biochemical analyzer， apoptosis of tumor cells was detected by TUNEL method， and the protein expression of vascular endothelial growth factor （VEGF） and vascular endothelial growth factor receptor （VEGFR） in liver tissues was detected by Western blotting. Results The tumor mass of MO group， RA group， IF group and RI group was （20.33±2.39）， （14.62±1.23）， （14.34±1.22）， （8.28±0.84） g， respectively. Tumor volumes were （0.87±0.13）， （0.51±0.09）， （0.53±0.08）， （0.32±0.02） cm³， respectively. Tumor necrosis rates were （21.11±2.14）%， （32.18±3.25）%， （32.29±3.28）%， （48.53±4.37）%， respectively. Tumor suppression rates were （0.00±0.00）%， （24.66±2.47）%， （24.13±2.46）%， （45.55±4.51）%， respectively. There were statistically significant differences （F=316.40， P<0.001； F=159.50， P<0.001； F=356.10， P<0.001； F=571.30， P<0.001）； there were statistically significant differences in RA， IF and RI groups compared with the MO group （all P<0.05）； there were statistically significant differences between RI group and IF group （all P<0.05）. Tumor cells of MO group showed infiltrating growth， with more mitotic images， no obvious necrosis， and a large number of inflammatory cell infiltration. Cancer nests in RA group， IF group and RI group became significantly smaller， tumor cells showed swelling， nuclear contraction and a large number of necrosis， and inflammatory cell infiltration was significantly reduced， among which the improvement was most obvious in RI group. The albumin （ALB） level of NO group， MO group， RA group， IF group and RI group was （40.55±4.38）， （17.34±1.02）， （22.65±2.18）， （22.37±2.17）， （29.01±2.83） g/L， respectively. The alanine aminotransferase （ALT） level was （19.68±1.34）， （92.17±9.24）， （78.71±7.39）， （78.35±7.40）， （50.30±5.12） U/L， respectively. The aspartate aminotransferase （AST） level was （74.27±7.48）， （182.21±20.23）， （165.78±16.05）， （165.26±16.09）， （102.33±11.11） U/L， respectively. The total bilirubin （TBIL） level was （22.42±2.58）， （82.24±8.35）， （61.86±6.17）， （61.53±6.16）， （46.45±4.53） μmoL/L， respectively. There were statistically significant differences （F=105.90， P<0.001； F=189.00， P<0.001； F=99.57， P<0.001； F=142.10， P<0.001）； there were statistically significant differences in MO， RA， IF， RI groups compared with the NO group （all P<0.05）； there were statistically significant differences in RA， IF， RI groups compared with the MO group （all P<0.05）； there were statistically significant differences between IF group and RI group （all P<0.05）. The apoptosis rates in MO group， RA group， IF group and RI group were （9.01±1.23）%， （15.65±1.68）%， （15.72±1.69）% and （24.34±2.12）%， respectively， and there was a statistically significant difference （F=135.30， P<0.001）； there were statistically significant differences in RA， IF and RI groups compared with the MO group （all P<0.05）； there was a statistically significant difference between RI group and IF group （P<0.05）. VEGF expression level in NO group， MO group， RA group， IF group and RI group was 1.33±0.13， 2.28±0.21， 1.88±0.19， 1.86±0.18 and 1.50±0.14， respectively. VEGFR expression level was 1.32±0.09， 2.14±0.28， 1.91±0.18， 1.89±0.17， 1.62±0.15， respectively. There were statistically significant differences （F=45.84， P<0.001； F=29.05， P<0.001）； there were statistically significant differences in MO， RA， IF， RI groups compared with the NO group （all P<0.05）； there were statistically significant differences in RA， IF， RI groups compared with the MO group （all P<0.05）； there were statistically significant differences between IF group and RI group （both P<0.05）. Conclusions Rapamycin arterial perfusion combined with ¹³¹I-FAP-loaded dextran microspheres interventional embolization therapy in the treatment of rabbits with liver transplantation tumor can effectively inhibit tumor growth， enhance the tumor necrosis rate， tumor inhibition rate and apoptotic ability， improve liver function indicators， and has a significant therapeutic effect on rabbits with liver transplantation tumor.

Objective To investigate the predictive value of serum matrix metalloproteinase-9 （MMP-9）， fatty acid-binding protein 5 （FABP5） combined with MRI for the efficacy and recurrence of primary liver cancer after percutaneous radiofrequency ablation. Methods A total of 192 patients with primary liver cancer who underwent percutaneous radiofrequency ablation treatment at the First Affiliated Hospital of Air Force Medical University from June 2022 to May 2023 were selected as the research subjects. MRI examination was performed within one week before the treatment， and the apparent diffusion coefficient （ADC） value was recorded. The enzyme-linked immunosorbent assay （ELISA） was used to determine the levels of MMP-9 and FABP5 in the serum. According to the results of MRI examination， the ablation status of the lesions was determined， and the patients were divided into a complete ablation group （n=157） and a residual lesion group （n=35）. Patients with completely ablated lesions were regularly followed up for one year， and their recurrence status was recorded. According to the recurrence of the patients， the patients were divided into a non-recurrence group （n=115） and a recurrence group （n=42）. The levels of MMP-9 and FABP5 and the ADC values of the patients in the complete ablation group and the residual lesion group， as well as those in the non-recurrence group and the recurrence group， were compared. The receiver operator characteristic （ROC） curve was used to evaluate the predictive value of serum MMP-9 and FABP5 combined with MRI for the postoperative efficacy and recurrence of the patients. Results The levels of serum MMP-9 and FABP5， and the ADC value of patients in the complete ablation group were （181.05±29.68） ng/ml， （7.95±1.82） μg/L， and （1.32±0.45）×10^-3 mm²/s， respectively， while those in the residual lesion group were （202.18±35.06） ng/ml， （9.56±2.39） μg/L， and （0.75±0.23）×10^-3 mm²/s， respectively. The levels of MMP-9 and FABP5 in the complete ablation group were significantly lower than those in the residual lesion group， and the ADC value was significantly higher than that in the residual lesion group， with statistically significant differences （t=3.68， P<0.001； t=4.45， P<0.001； t=7.27， P<0.001）. The areas under the curve （AUC） of serum MMP-9， FABP5， and ADC value alone in predicting the postoperative efficacy of patients were 0.68 （95%CI： 0.61-0.75）， 0.75 （95%CI： 0.68-0.81）， and 0.90 （95%CI： 0.85-0.94）， respectively. The AUC of the combined prediction of these three was 0.94 （95%CI： 0.89-0.97）， and the combined prediction of these three was superior to the individual prediction of MMP-9， FABP5， and ADC value （Z=5.72， P<0.001； Z=4.84， P<0.001； Z=2.29， P=0.022）. The levels of serum MMP-9 and FABP5， and the ADC value of patients in the non-recurrence group were （176.52±30.28） ng/ml， （8.69±1.92） μg/L， and （1.35±0.29）×10^-3 mm²/s， respectively， while those in the recurrence group were （201.85±28.72） ng/ml， （11.05±2.86） μg/L， and （1.14±0.12）×10^-3 mm²/s， respectively. The levels of serum MMP-9 and FABP5 of patients in the non-recurrence group were significantly lower than those in the recurrence group， and the ADC value was significantly higher than that in the recurrence group， with statistically significant differences （t=4.70， P<0.001； t=5.93， P<0.001； t=4.55， P<0.001）. The AUCs of serum MMP-9， FABP5， and ADC value alone in predicting the postoperative recurrence of patients were 0.74 （95%CI： 0.66-0.81）， 0.90 （95%CI： 0.84-0.94）， and 0.74 （95%CI： 0.66-0.80）， respectively. The AUC of the combined prediction of these three was 0.95 （95%CI： 0.90-0.98）， and the combined prediction of these three was superior to the individual prediction of MMP-9， FABP5， and ADC value （Z=5.00， P<0.001； Z=3.03， P=0.002； Z=5.33， P<0.001）. Conclusions The levels of serum MMP-9 and FABP5 in patients with primary liver cancer treated by percutaneous radiofrequency ablation in the complete ablation group are significantly lower than those in the residual lesion group， and the ADC value is significantly higher than that in the residual lesion group. The levels of serum MMP-9 and FABP5 of patients in the non-recurrence group are also significantly lower than those in the recurrence group， and the ADC value is also significantly higher than that in the recurrence group. The combined detection of serum MMP-9， FABP5 and MRI has a relatively high clinical value in predicting the efficacy and recurrence of patients after percutaneous radiofrequency ablation for liver cancer.

Objective To investigate the efficacy of the combination of sintilimab and docetaxel in the treatment of cervical cancer and its impact on laboratory indicators. Methods A total of 86 patients with advanced cervical cancer treated at Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine from July 2019 to June 2022 were selected as the study subjects. The patients were divided into a study group （n=43） and a control group （n=43） according to the treatment method. The study group was treated with a combination of sintilimab and docetaxel， while the control group was treated with docetaxel. After 6 cycles of treatment， the clinical efficacy， vascular endothelial growth factor receptor （VEGFR） levels， tumor marker levels， immune function indicators， programmed death-1 （PD-1）， programmed death-ligand 1 （PD-L1） levels， and adverse reactions during treatment between the two groups were compared. 1-year progression-free survival （PFS） rate and overall survival （OS） rate between the two groups of patients were compared. Results After 6 cycles of treatment， the objective response rates （ORR） of the study group and the control group were 48.84% （21/43） and 30.23% （13/43）， respectively， with no statistically significant difference （χ²=3.11， P=0.078）； the disease control rates （DCR） of the two groups were 86.05% （37/43） and 62.79% （27/43）， respectively， with a statistically significant difference （χ²=6.11， P=0.013）. Before treatment， the levels of VEGFR2 and VEGFR3 in the study group were （223.42±57.89）， （3.25±1.22） ng/L， respectively， while those in the control group were （220.56±58.45）， （3.31±1.17） ng/L， respectively， with no statistically significant differences （t=0.23， P=0.820； t=0.23， P=0.817）. After treatment， the VEGFR2 and VEGFR3 levels in the study group were （123.21±36.97）， （0.81±0.21） ng/L， respectively， while those in the control group were （151.22±37.34）， （1.33±0.37） ng/L， respectively， with statistically significant differences （t=3.50， P=0.001； t=8.02， P<0.001）. However， the levels of VEGFR2 and VEGFR3 in both groups of patients decreased after treatment compared to before treatment （all P<0.05）. Before treatment， the levels of carcinoembryonic antigen （CEA）， carbohydrate antigen 125 （CA125）， and squamous cell carcinoma antigen （SCC-Ag） in the study group were （8.73±1.02） ng/ml， （29.73±5.88） U/ml， and （7.23±1.34） ng/ml， respectively， while those in the control group were （8.41±1.23） ng/ml， （30.12±5.93） U/ml， and （7.37±1.43） ng/ml， respectively， with no statistically significant differences （t=1.31， P=0.193； t=0.31， P=0.760； t=0.47， P=0.641）. After treatment， the CEA， CA125， and SCC-Ag levels in the study group were （3.52±0.78） ng/ml， （13.28±1.82） U/ml， and （2.33±0.49） ng/ml， respectively， while those in the control group were （3.87±0.62） ng/ml， （14.12±1.72） U/ml， and （2.65±0.54） ng/ml， respectively， with statistically significant differences （t=2.30， P=0.024； t=2.20， P=0.031； t=2.88， P=0.005）. However， the levels of CEA， CA125， and SCC-Ag in both groups of patients decreased after treatment compared to before treatment （all P<0.05）. Before treatment， the T cell subsets CD4⁺， CD8⁺， and CD4⁺/CD8⁺ in the study group were （27.53±2.23） %， （29.34±3.78） %， and 0.93±0.33， respectively， while those in the control group were （28.32±2.31） %， （30.03±3.27） %， and 0.94±0.42， respectively， with no statistically significant differences （t=1.61， P=0.110； t=0.91， P=0.368； t=0.12， P=0.903）. After treatment， the T cell subsets CD4⁺， CD8⁺， and CD4⁺/CD8⁺ in the study group were （35.33±3.36） %， （44.32±4.33） %， and 0.80±0.22， respectively， while those in the control group were （30.31±3.23） %， （42.21±4.31） %， and 0.71±0.19， respectively， with statistically significant differences （t=7.06， P<0.001； t=2.27， P=0.026； t=2.03， P=0.046）. After treatment， the CD4⁺ and CD8⁺ T cell subsets in both groups were higher than before treatment， while the CD4⁺/CD8⁺ was lower than before treatment （all P<0.05）. Before treatment， the levels of PD-1 and PD-L1 mRNA in peripheral blood mononuclear lymphocytes of the study group were 1.21±0.21 and 0.73±0.15， respectively， while those in the control group were 1.23±0.25 and 0.79±0.14， respectively， with no statistically significant differences （t=0.40， P=0.689； t=1.92， P=0.059）. After treatment， the levels of PD-1 and PD-L1 mRNA in peripheral blood mononuclear lymphocytes of the study group were 0.77±0.13 and 0.52±0.13， respectively， while those in the control group were 0.93±0.19 and 0.66±0.17， respectively， with statistically significant differences （t=4.56， P<0.001； t=4.29， P<0.001）. However， the levels of PD-1 and PD-L1 mRNA in both groups of patients decreased after treatment compared to before treatment （all P<0.05）. The 1-year PFS rate and OS rate of the study group patients were 60.47% and 72.09%， respectively； while those in the control groups were 51.16% and 65.12%， respectively， with no statistically significant differences （χ²=1.31， P=0.253； χ²=0.82， P=0.365）. The incidences of digestive system response， abnormal liver and kidney function， hematuria， bone marrow suppression， and rash in the study group were 39.53% （17/43）， 13.95% （6/43）， 13.95% （6/43）， 23.26% （10/43）， and 37.21% （16/43）， respectively， while those in the control group were 32.56% （14/43）， 9.30% （4/43）， 11.63% （5/43）， 18.60% （8/43）， and 30.23% （13/43）， respectively， with no statistically significant differences （χ²=0.45， P=0.500； χ²=0.45， P=0.501； χ²=0.10， P=0.747； χ²=0.28， P=0.596； χ²=0.47， P=0.494）. Conclusions Compared with monotherapy with docetaxel， the combination of sintilimab and docetaxel has a higher DCR in the treatment of advanced cervical cancer. To a certain extent， it effectively reduces the expression levels of VEGFR， serum tumor markers， and PD-1， PD-L1 in peripheral blood mononuclear lymphocytes， improves the immune function of patients， and has comparable drug safety. However， the two treatment options have comparable 1-year survival rates.

Brain metastases are relatively common in anaplastic lymphoma kinase （ALK）-positive non-small cell lung cancer （NSCLC） patients. Although first-to third-generation ALK-tyrosine kinase inhibitors （TKI） have been widely used in the treatment of ALK-positive patients with brain metastases， some patients still experience inadequate intracranial control. First-generation ALK-TKI cannot penetrate the blood-brain barrier， and the addition of brain radiotherapy significantly improves intracranial control. In contrast， second- and third-generation ALK-TKI can cross the blood-brain barrier， offering better intracranial control. However， the beneficiary population and optimal timing for combining radiotherapy remain controversial. The optimal approach for combining ALK-TKI with cranial radiotherapy remains inconclusive. It should be determined by comprehensively considering factors such as prior radiotherapy history， the type of targeted drugs， the number of brain metastases， the interval time of ALK-TKI， and others. Close monitoring for radiotherapy-related adverse effects， such as brain necrosis， is also essential.

Breast cancer organoids faithfully reflect the structural and functional characteristics of primary tumors， demonstrating broad application potential. Clinically， organoids have been utilized for drug sensitivity testing， significantly enhancing the precision of personalized treatment strategies. Organoids play a crucial role in accelerating new drug development， uncovering drug resistance mechanisms， and improving the efficacy of immunotherapy. In-depth analysis of the application of breast cancer organoid technology in clinical and transformation can provide new ideas for clinical diagnosis and treatment of breast cancer.

The epidermal growth factor receptor （EGFR） exon 20 insertion （ex20ins） mutation is a rare subtype of mutations in non-small cell lung cancer （NSCLC）. Patients with advanced NSCLC carrying the EGFR ex20ins mutation tend to have poor responses to traditional EGFR tyrosine kinase inhibitors （TKIs）， chemotherapy， and immunotherapy， leading to a poor clinical prognosis. Significant progress has been made in the development of new drugs targeting the EGFR ex20ins mutation. The research on new drugs targeting EGFR ex20ins mutations has made significant progress. The main ones include new EGFR-TKIs （such as sunvozertinib， mobocertinib， and furmetinib， etc.）， bispecific antibodies （such as amivantamab， JMT101， and GB263T， etc.）， and emerging drugs such as AUY922. These agents have demonstrated promising efficacy in clinical trials， improving the objective response rate and progression-free survival of patients， and are expected to improve overall survival. An in-depth analysis of the mechanism of action and clinical trial progress of these novel targeted drugs for EGFR ex20ins-mutated NSCLC can offer new therapeutic strategies for patients with EGFR ex20ins-mutated NSCLC.

Liver metastasis from colorectal cancer is a complex biological process， involving the interaction of multiple mechanisms and cell types， including the self-renewal and dynamic acquisition of the traits of cancer stem cells. Characteristic metabolic changes occur in colorectal cancer cells to meet the energy demands during the metastasis process. Epithelial-mesenchymal transition promotes the migration of primary colorectal cancer cells into the circulatory system， where they become circulating tumor cells， and then extravasate into the portal venous system to complete the processes of seeding， proliferation， and the formation of metastatic foci. Resident cells and immune cells in the hepatic microenvironment coordinate the immune response， inducing the occurrence of metastatic liver tumors. Further research on the molecular mechanisms related to liver metastasis from colorectal cancer is expected to develop novel therapeutic drugs targeting these molecular mechanisms， so as to improve the prognosis outcomes of patients.