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[The effect of c-Myc on regulating the immune-related ligands in Y subtype small cell lung cancer through histone deacetylase 1].
Q3 Medicine Pub Date : 2024-11-23 DOI: 10.3760/cma.j.cn112152-20230803-00058
P Y Zhao, X D Sun, H Li, L Tian, Y H Lu, Y Cheng
<p><p><b>Objective:</b> To explore the effect and mechanism of c-Myc on regulating the expression of immune-related ligands in Y subtype small-cell lung cancer (SCLC) characterized by high expression of immune-related molecules. <b>Methods:</b> The Y subtype SCLC cell line H196 was randomly divided into the control group, c-Myc inhibitor 10058-F4 group, histone deacetylase 1 (HDAC1) inhibitor pyroxamide group, and 10058-F4 plus pyroxamide group. The co-culture system with NK-92MI cells was used to determine the effect of H196 cells on the function of natural killer (NK) cells. Western Blotting and co-immunoprecipitation assays were used to detect the effect of c-Myc on class Ⅰ HDAC, and flow cytometry was used to detect the regulatory effect of c-Mycon CD47, programmed cell death ligand 1 (PD-L1), and CD155, which are highly expressed immune checkpoints in Y subtype SCLC, and major histocompatibility complex classⅠ-related chains A and (MICA/B), which is a poorly expressed immune-activating ligand in SCLC, and the role of HDAC. Chromatin immunoprecipitation (ChIP) assay and real-time quantitative polymerase chain reaction (RT-qPCR) were used to determine the regulatory mechanism of c-Myc-HDAC1 on MICA/B expression. <b>Results:</b> Inhibition of c-Myc decreased the mortality of H196 cells in the co-culture system and down-regulated the expression of MICA/B. Compared with the NK+H196 group [(42.54±2.47)%], the proportion of cells killed by NK-92MI cells in the NK+H196+10058-F4 group was lower [(28.48±3.38)%, <i>P</i><0.001]. The mean fluorescence intensity (MFI) of MICA/B on the cells in the 10058-F4 group (36.40±0.82) was lower than that in the control group (91.23±8.60, <i>P</i><0.001). And c-Myc could bind to HDAC1, whose protein level was up-regulated by 10058-F4 while the mRNA level was not. Compared with the cells in the control group (90.10±4.91), the MFI of MICA/B on the cells in the pyroxamide group was significantly increased (145.70±5.86, <i>P</i><0.001), and the MFI of MICA/B on the cells in the 10058-F4+pyroxamide group (54.60±2.88) was significantly increased compared with the cells in the 10058-F4 group (35.97±1.60, <i>P</i><0.001). The percentage of MICA promoter gene fragments in the c-Myc antibody precipitation group (0.125±0.037) was significantly higher than that in the IgG group (0.000 8±0.000 3, <i>P</i>=0.004). MICB had a similar trend, suggesting that the c-Myc-HDAC1 complex could bind to the promoter region of MICA/B. The MFI of CD47 on the cells in the 10058-F4 group (60.07±0.21) was significantly lower than cells in the control group (70.27±1.37, <i>P</i><0.001), but the MFIs of PD-L1 (13.50±0.61) and CD155 (829.70±41.19) were significantly higher than those on the cells in the control group (9.23±0.94, <i>P</i><0.01; 496.00±4.36, <i>P</i><0.001, respectively). <b>Conclusions:</b> c-Myc may promote the expression of MICA/B and CD47 in Y subtype SCLC cells by binding and inhibiting HDAC1, while it may also be involved in i
{"title":"[The effect of c-Myc on regulating the immune-related ligands in Y subtype small cell lung cancer through histone deacetylase 1].","authors":"P Y Zhao, X D Sun, H Li, L Tian, Y H Lu, Y Cheng","doi":"10.3760/cma.j.cn112152-20230803-00058","DOIUrl":"https://doi.org/10.3760/cma.j.cn112152-20230803-00058","url":null,"abstract":"&lt;p&gt;&lt;p&gt;&lt;b&gt;Objective:&lt;/b&gt; To explore the effect and mechanism of c-Myc on regulating the expression of immune-related ligands in Y subtype small-cell lung cancer (SCLC) characterized by high expression of immune-related molecules. &lt;b&gt;Methods:&lt;/b&gt; The Y subtype SCLC cell line H196 was randomly divided into the control group, c-Myc inhibitor 10058-F4 group, histone deacetylase 1 (HDAC1) inhibitor pyroxamide group, and 10058-F4 plus pyroxamide group. The co-culture system with NK-92MI cells was used to determine the effect of H196 cells on the function of natural killer (NK) cells. Western Blotting and co-immunoprecipitation assays were used to detect the effect of c-Myc on class Ⅰ HDAC, and flow cytometry was used to detect the regulatory effect of c-Mycon CD47, programmed cell death ligand 1 (PD-L1), and CD155, which are highly expressed immune checkpoints in Y subtype SCLC, and major histocompatibility complex classⅠ-related chains A and (MICA/B), which is a poorly expressed immune-activating ligand in SCLC, and the role of HDAC. Chromatin immunoprecipitation (ChIP) assay and real-time quantitative polymerase chain reaction (RT-qPCR) were used to determine the regulatory mechanism of c-Myc-HDAC1 on MICA/B expression. &lt;b&gt;Results:&lt;/b&gt; Inhibition of c-Myc decreased the mortality of H196 cells in the co-culture system and down-regulated the expression of MICA/B. Compared with the NK+H196 group [(42.54±2.47)%], the proportion of cells killed by NK-92MI cells in the NK+H196+10058-F4 group was lower [(28.48±3.38)%, &lt;i&gt;P&lt;/i&gt;<0.001]. The mean fluorescence intensity (MFI) of MICA/B on the cells in the 10058-F4 group (36.40±0.82) was lower than that in the control group (91.23±8.60, &lt;i&gt;P&lt;/i&gt;<0.001). And c-Myc could bind to HDAC1, whose protein level was up-regulated by 10058-F4 while the mRNA level was not. Compared with the cells in the control group (90.10±4.91), the MFI of MICA/B on the cells in the pyroxamide group was significantly increased (145.70±5.86, &lt;i&gt;P&lt;/i&gt;<0.001), and the MFI of MICA/B on the cells in the 10058-F4+pyroxamide group (54.60±2.88) was significantly increased compared with the cells in the 10058-F4 group (35.97±1.60, &lt;i&gt;P&lt;/i&gt;<0.001). The percentage of MICA promoter gene fragments in the c-Myc antibody precipitation group (0.125±0.037) was significantly higher than that in the IgG group (0.000 8±0.000 3, &lt;i&gt;P&lt;/i&gt;=0.004). MICB had a similar trend, suggesting that the c-Myc-HDAC1 complex could bind to the promoter region of MICA/B. The MFI of CD47 on the cells in the 10058-F4 group (60.07±0.21) was significantly lower than cells in the control group (70.27±1.37, &lt;i&gt;P&lt;/i&gt;<0.001), but the MFIs of PD-L1 (13.50±0.61) and CD155 (829.70±41.19) were significantly higher than those on the cells in the control group (9.23±0.94, &lt;i&gt;P&lt;/i&gt;<0.01; 496.00±4.36, &lt;i&gt;P&lt;/i&gt;<0.001, respectively). &lt;b&gt;Conclusions:&lt;/b&gt; c-Myc may promote the expression of MICA/B and CD47 in Y subtype SCLC cells by binding and inhibiting HDAC1, while it may also be involved in i","PeriodicalId":39868,"journal":{"name":"中华肿瘤杂志","volume":"46 11","pages":"1009-1018"},"PeriodicalIF":0.0,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142773353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Application of 9-gene panel in assisting fine needle aspiration cytology to diagnose thyroid cancer].
Q3 Medicine Pub Date : 2024-11-23 DOI: 10.3760/cma.j.cn112152-20240225-00084
Y Q Zhang, H Zhao, L L Zhao, Y Sun, C Wang, Z H Zhang, T Qiu, X Yang, T Xiao, H Q Guo
<p><p><b>Objective:</b> To evaluate the utility of the 9-gene panel as a differential diagnostic method for thyroid nodules within determinate cytological diagnosis and as a parallel diagnostic method for thyroid fine-needle aspiration (FNA) cytology. <b>Methods:</b> 579 liquid-based cytology samples from 544 patients were collected after thyroid FNA diagnosis in our hospital from December 2014 to April 2021. Mutations at any site of 9 genes, namely, BRAF, NRAS, HRAS, KRAS, GNAS, RET, TERT, TP53, and PIK3CA as recorded by the Catalogue of Somatic Mutations in Cancer (COSMIC), were analyzed by next-generation sequencing. Taking postoperative histopathology and cytology results with definite benign or malignant diagnosis as the gold standard, the diagnostic efficacy of the 9-gene panel as a reclassified method for thyroid nodules with indeterminate cytological diagnosis and as a parallel diagnostic method for thyroid FNA cytology were evaluated and compared with that of the BRAF V600E single-gene detection method. <b>Results:</b> Of the 579 thyroid nodules, 196 (33.85%) were Bethesda Ⅱ, 11 (1.90%) were Bethesda Ⅲ, 31 (5.35%) were Bethesda Ⅳ, 27 (4.66%) were Bethesda Ⅴ, and 314 (54.23%) were Bethesda Ⅵ, as diagnosed by thyroid FNA cytology. Among these 579 thyroid nodules, 275 were tested positive for 9-gene mutations, with a mutation rate of 47.5%. Of the 329 thyroid nodules surgically removed, 30 (9.12%) were benign, 5 (1.52%) were borderline, and 294 (89.36%) were malignant. Regarding borderline nodules as malignant nodules, the mutation rates of the 9 genes in the 299 malignant thyroid nodules from high to low were BRAF 62.21% (186/299), NRAS 5.02% (15/299), HRAS 1.00% (3/299), PIK3CA 0.67% (2/299), GNAS 0.67% (2/299), KRAS 0.33% (1/299), TP53 0.33% (1/299), TERT 0.33% (1/299) and RET 0.00% (0/299). The malignant risks of the 9 genes from high to low were BRAF 100% (186/186), PIK3CA 100.00% (2/2), GNAS 100.00% (2/2), TERT 100.00% (1/1), TP53 100.00% (1/1), NRAS 78.95% (15/19), HRAS 75.00% (3/4), and KRAS 50.00% (1/2). For thyroid nodules of Bethesda Ⅲ-Ⅳ (indeterminate diagnosis), the sensitivity (SN) of the 9-gene panel in diagnosing thyroid cancer is 34.48% (10/29), the specificity (SP) is 61.54% (8/13), and the accuracy is 42.86% (18/42); whereas the SN of the BRAF V600E detection method is 0%. Therefore, the diagnostic efficiency of the 9-gene panel is significantly better than that of BRAF V600E single gene detection. For thyroid nodules of Bethesda Ⅱ-Ⅵ, the SN of the 9-gene panel in diagnosing thyroid cancer was 68.83% (254/369), the SP was 90.00% (189/210), the accuracy was 76.51% (443/579), and the area under the curve (AUC) was 0.79; whereas the SN of BRAF V600E single-gene detection in diagnosing thyroid cancer was 63.69% (235/369), the SP was 99.52% (209/210), the accuracy was 76.68% (444/579), and the AUC was 0.82. The SP of BRAF V600E detection is higher than that of the 9-gene panel (<i>P</i><0.01), but there is no significant diffe
{"title":"[Application of 9-gene panel in assisting fine needle aspiration cytology to diagnose thyroid cancer].","authors":"Y Q Zhang, H Zhao, L L Zhao, Y Sun, C Wang, Z H Zhang, T Qiu, X Yang, T Xiao, H Q Guo","doi":"10.3760/cma.j.cn112152-20240225-00084","DOIUrl":"https://doi.org/10.3760/cma.j.cn112152-20240225-00084","url":null,"abstract":"&lt;p&gt;&lt;p&gt;&lt;b&gt;Objective:&lt;/b&gt; To evaluate the utility of the 9-gene panel as a differential diagnostic method for thyroid nodules within determinate cytological diagnosis and as a parallel diagnostic method for thyroid fine-needle aspiration (FNA) cytology. &lt;b&gt;Methods:&lt;/b&gt; 579 liquid-based cytology samples from 544 patients were collected after thyroid FNA diagnosis in our hospital from December 2014 to April 2021. Mutations at any site of 9 genes, namely, BRAF, NRAS, HRAS, KRAS, GNAS, RET, TERT, TP53, and PIK3CA as recorded by the Catalogue of Somatic Mutations in Cancer (COSMIC), were analyzed by next-generation sequencing. Taking postoperative histopathology and cytology results with definite benign or malignant diagnosis as the gold standard, the diagnostic efficacy of the 9-gene panel as a reclassified method for thyroid nodules with indeterminate cytological diagnosis and as a parallel diagnostic method for thyroid FNA cytology were evaluated and compared with that of the BRAF V600E single-gene detection method. &lt;b&gt;Results:&lt;/b&gt; Of the 579 thyroid nodules, 196 (33.85%) were Bethesda Ⅱ, 11 (1.90%) were Bethesda Ⅲ, 31 (5.35%) were Bethesda Ⅳ, 27 (4.66%) were Bethesda Ⅴ, and 314 (54.23%) were Bethesda Ⅵ, as diagnosed by thyroid FNA cytology. Among these 579 thyroid nodules, 275 were tested positive for 9-gene mutations, with a mutation rate of 47.5%. Of the 329 thyroid nodules surgically removed, 30 (9.12%) were benign, 5 (1.52%) were borderline, and 294 (89.36%) were malignant. Regarding borderline nodules as malignant nodules, the mutation rates of the 9 genes in the 299 malignant thyroid nodules from high to low were BRAF 62.21% (186/299), NRAS 5.02% (15/299), HRAS 1.00% (3/299), PIK3CA 0.67% (2/299), GNAS 0.67% (2/299), KRAS 0.33% (1/299), TP53 0.33% (1/299), TERT 0.33% (1/299) and RET 0.00% (0/299). The malignant risks of the 9 genes from high to low were BRAF 100% (186/186), PIK3CA 100.00% (2/2), GNAS 100.00% (2/2), TERT 100.00% (1/1), TP53 100.00% (1/1), NRAS 78.95% (15/19), HRAS 75.00% (3/4), and KRAS 50.00% (1/2). For thyroid nodules of Bethesda Ⅲ-Ⅳ (indeterminate diagnosis), the sensitivity (SN) of the 9-gene panel in diagnosing thyroid cancer is 34.48% (10/29), the specificity (SP) is 61.54% (8/13), and the accuracy is 42.86% (18/42); whereas the SN of the BRAF V600E detection method is 0%. Therefore, the diagnostic efficiency of the 9-gene panel is significantly better than that of BRAF V600E single gene detection. For thyroid nodules of Bethesda Ⅱ-Ⅵ, the SN of the 9-gene panel in diagnosing thyroid cancer was 68.83% (254/369), the SP was 90.00% (189/210), the accuracy was 76.51% (443/579), and the area under the curve (AUC) was 0.79; whereas the SN of BRAF V600E single-gene detection in diagnosing thyroid cancer was 63.69% (235/369), the SP was 99.52% (209/210), the accuracy was 76.68% (444/579), and the AUC was 0.82. The SP of BRAF V600E detection is higher than that of the 9-gene panel (&lt;i&gt;P&lt;/i&gt;<0.01), but there is no significant diffe","PeriodicalId":39868,"journal":{"name":"中华肿瘤杂志","volume":"46 11","pages":"1049-1057"},"PeriodicalIF":0.0,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142773325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[A real-world study of first-line albumin-bound paclitaxel in the treatment of advanced pancreatic cancer in China].
Q3 Medicine Pub Date : 2024-11-23 DOI: 10.3760/cma.j.cn112152-20231223-00383
J Du, X Qiu, J Y Ni, Q L Wang, F Tong, H Z Sha, Y H Zhu, L Qi, W Cai, C Gao, X W Wei, M B Chen, Z Y Qian, M H Cai, M Tao, C L Wang, G C Zheng, H Jiang, A W Dai, J Wu, M H Zhao, X Q Li, B Lu, C B Wang, B R Liu
<p><p><b>Objective:</b> To observe and evaluate the clinical efficacy and safety of albumin-bound paclitaxel as first-line treatment for patients with advanced pancreatic cancer in China, and to explore the prognosis-related molecules in pancreatic cancer based on next-generation sequencing (NGS) of tumor tissues. <b>Methods:</b> From December 2018 to December 2020, patients with locally advanced or metastatic pancreatic cancer were recruited to accept albumin-bound paclitaxel as first-line treatment in the oncology departments of 24 hospitals in East China. The primary endpoints were overall survival (OS) and treatment related adverse events, and the secondary endpoint was progression-free survival (PFS). Adverse effects were graded using Common Terminology Criteria for Adverse Events 5.0 (CTCAE 5.0). NGS sequencing on the primary or metastatic tissue samples of pancreatic cancer obtained through surgical resection or biopsy was performed. <b>Results:</b> This study recruited 229 patients, including 70 patients with locally advanced pancreatic cancer (LAPC) and 159 patients with metastatic pancreatic cancer (mPC). The disease control rate was 79.9% and the objective response rate is 36.3%.The common adverse effects during treatment were anaemia (159 cases), leucopenia (170 cases), neutropenia (169 cases), increased aminotransferases (110 cases), and thrombocytopenia (95 cases), and the incidence of grade 3-4 neutropenia is 12.2% (28/229). The median follow-up time was 21.2 months (95% <i>CI</i>: 18.5-23.1 months). The median PFS (mPFS) was 5.3 months (95% <i>CI</i>: 4.37-4.07 months) and the median OS (mOS) was 11.2 months (95% <i>CI</i>: 9.5-12.9 months). The mPFS of patients with LAPC was 7.4 months (95% <i>CI</i>: 6.6-11.2 months), and their mOS was 15.5 months (95% <i>CI</i>: 12.6-NA months). The mPFS of patients with mPC was 3.9 months (95% <i>CI</i>: 3.4-5.1 months), and their mOS was 9.3 months (95% <i>CI</i>: 8.0-10.8 months). Multivariate Cox regression analysis showed that clinical stage (<i>HR</i>=1.47, 95% <i>CI</i>: 1.06-2.04), primary tumor site (<i>HR</i>=0.64, 95% <i>CI</i>: 0.48-0.86), Eastern Cooperative Oncology Group Performance Status (ECOG PS) score (<i>HR</i>=2.66, 95% <i>CI</i>: 1.53-4.65), and whether to combine radiotherapy (<i>HR</i>=0.65, 95% <i>CI</i>: 0.42-1.00) were independent influencing factors for the PFS of these patients. The primary tumor site (<i>HR</i>=0.68, 95% <i>CI</i>: 0.48-0.95), ECOG score (<i>HR</i>=5.82, 95% <i>CI</i>: 3.14-10.82), and whether to combine radiotherapy (<i>HR</i>=0.58, 95% <i>CI</i>: 0.35-0.96) were independent influencing factors of the OS of these patients. The most frequent gene mutations in these advanced stage pancreatic patients were <i>KRAS</i> (89.66%), <i>TP53</i> (77.01%), <i>CDKN2A</i> (32.18%), and <i>SMAD4</i> (21.84%) by NGS of tumor tissues from 87 pancreatic cancer patients with sufficient specimens. Further analysis revealed that mutations in <i>CDKN2B</i>, <i>PTEN</
{"title":"[A real-world study of first-line albumin-bound paclitaxel in the treatment of advanced pancreatic cancer in China].","authors":"J Du, X Qiu, J Y Ni, Q L Wang, F Tong, H Z Sha, Y H Zhu, L Qi, W Cai, C Gao, X W Wei, M B Chen, Z Y Qian, M H Cai, M Tao, C L Wang, G C Zheng, H Jiang, A W Dai, J Wu, M H Zhao, X Q Li, B Lu, C B Wang, B R Liu","doi":"10.3760/cma.j.cn112152-20231223-00383","DOIUrl":"https://doi.org/10.3760/cma.j.cn112152-20231223-00383","url":null,"abstract":"&lt;p&gt;&lt;p&gt;&lt;b&gt;Objective:&lt;/b&gt; To observe and evaluate the clinical efficacy and safety of albumin-bound paclitaxel as first-line treatment for patients with advanced pancreatic cancer in China, and to explore the prognosis-related molecules in pancreatic cancer based on next-generation sequencing (NGS) of tumor tissues. &lt;b&gt;Methods:&lt;/b&gt; From December 2018 to December 2020, patients with locally advanced or metastatic pancreatic cancer were recruited to accept albumin-bound paclitaxel as first-line treatment in the oncology departments of 24 hospitals in East China. The primary endpoints were overall survival (OS) and treatment related adverse events, and the secondary endpoint was progression-free survival (PFS). Adverse effects were graded using Common Terminology Criteria for Adverse Events 5.0 (CTCAE 5.0). NGS sequencing on the primary or metastatic tissue samples of pancreatic cancer obtained through surgical resection or biopsy was performed. &lt;b&gt;Results:&lt;/b&gt; This study recruited 229 patients, including 70 patients with locally advanced pancreatic cancer (LAPC) and 159 patients with metastatic pancreatic cancer (mPC). The disease control rate was 79.9% and the objective response rate is 36.3%.The common adverse effects during treatment were anaemia (159 cases), leucopenia (170 cases), neutropenia (169 cases), increased aminotransferases (110 cases), and thrombocytopenia (95 cases), and the incidence of grade 3-4 neutropenia is 12.2% (28/229). The median follow-up time was 21.2 months (95% &lt;i&gt;CI&lt;/i&gt;: 18.5-23.1 months). The median PFS (mPFS) was 5.3 months (95% &lt;i&gt;CI&lt;/i&gt;: 4.37-4.07 months) and the median OS (mOS) was 11.2 months (95% &lt;i&gt;CI&lt;/i&gt;: 9.5-12.9 months). The mPFS of patients with LAPC was 7.4 months (95% &lt;i&gt;CI&lt;/i&gt;: 6.6-11.2 months), and their mOS was 15.5 months (95% &lt;i&gt;CI&lt;/i&gt;: 12.6-NA months). The mPFS of patients with mPC was 3.9 months (95% &lt;i&gt;CI&lt;/i&gt;: 3.4-5.1 months), and their mOS was 9.3 months (95% &lt;i&gt;CI&lt;/i&gt;: 8.0-10.8 months). Multivariate Cox regression analysis showed that clinical stage (&lt;i&gt;HR&lt;/i&gt;=1.47, 95% &lt;i&gt;CI&lt;/i&gt;: 1.06-2.04), primary tumor site (&lt;i&gt;HR&lt;/i&gt;=0.64, 95% &lt;i&gt;CI&lt;/i&gt;: 0.48-0.86), Eastern Cooperative Oncology Group Performance Status (ECOG PS) score (&lt;i&gt;HR&lt;/i&gt;=2.66, 95% &lt;i&gt;CI&lt;/i&gt;: 1.53-4.65), and whether to combine radiotherapy (&lt;i&gt;HR&lt;/i&gt;=0.65, 95% &lt;i&gt;CI&lt;/i&gt;: 0.42-1.00) were independent influencing factors for the PFS of these patients. The primary tumor site (&lt;i&gt;HR&lt;/i&gt;=0.68, 95% &lt;i&gt;CI&lt;/i&gt;: 0.48-0.95), ECOG score (&lt;i&gt;HR&lt;/i&gt;=5.82, 95% &lt;i&gt;CI&lt;/i&gt;: 3.14-10.82), and whether to combine radiotherapy (&lt;i&gt;HR&lt;/i&gt;=0.58, 95% &lt;i&gt;CI&lt;/i&gt;: 0.35-0.96) were independent influencing factors of the OS of these patients. The most frequent gene mutations in these advanced stage pancreatic patients were &lt;i&gt;KRAS&lt;/i&gt; (89.66%), &lt;i&gt;TP53&lt;/i&gt; (77.01%), &lt;i&gt;CDKN2A&lt;/i&gt; (32.18%), and &lt;i&gt;SMAD4&lt;/i&gt; (21.84%) by NGS of tumor tissues from 87 pancreatic cancer patients with sufficient specimens. Further analysis revealed that mutations in &lt;i&gt;CDKN2B&lt;/i&gt;, &lt;i&gt;PTEN&lt;/","PeriodicalId":39868,"journal":{"name":"中华肿瘤杂志","volume":"46 11","pages":"1038-1048"},"PeriodicalIF":0.0,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142773388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[The clinical pathway in China county for lung cancer diagnosis and treatment (2024 edition)]. [中国县域肺癌诊治临床路径(2024 年版)"。
Q3 Medicine Pub Date : 2024-11-06 DOI: 10.3760/cma.j.cn112152-20240710-00283

Standardizing the diagnosis and treatment of lung cancer is a key measure to improve the survival rate of lung cancer patients and reduce the mortality rate. However, county hospitals generally face the problem of inaccessibility to advanced diagnostic and treatment technologies. Therefore, when developing quality control standards and clinical diagnosis and treatment specifications, it is necessary to combine the actual situation of county hospitals and formulate specific recommendations. The recommendations of treatment measures also need to consider the approval status of indications and whether it is included in the National Reimbursement Drug List (NRDL), to ensure the access to medicines. To address the above issues, based on the existing guidelines at home and abroad and the clinical work characteristics of county hospitals, the " the clinical pathway in China county for lung cancer diagnosis and treatment (2024 edition)" has been updated on the basis of the first edition. This pathway elaborated on the imaging diagnosis, pathological diagnosis, molecular testing, precision medicine, and developed different diagnosis and treatment processes for different types of lung cancer patients. Consistent with the first pathway, this update still divides the recommendations for diagnosis and treatment of clinical scenarios into basic strategies and optional strategies for elaboration. The basic strategies are the standards that county hospitals must meet, while the optional strategies provide more choices for hospitals, which are convenient for county doctors to put into clinical practice. All the recommended diagnostic and treatment plans strictly refer to existing guidelines and consensus. Compared to the first edition, based on the latest high-level evidence-based medicine and the approval status of indications, the pathway has updated the diagnosis and treatment recommendations for lung cancer under different pathological types, TNM classification, and molecular classification in basic and optional strategies.

规范肺癌诊治是提高肺癌患者生存率、降低死亡率的关键措施。然而,县级医院普遍面临着先进诊疗技术难以普及的问题。因此,在制定质量控制标准和临床诊疗规范时,要结合县级医院的实际情况,制定具体的建议。诊疗措施建议还需考虑适应症的审批情况,是否纳入国家报销药品目录,确保药品可及性。针对上述问题,根据国内外现有指南,结合县级医院临床工作特点,在第一版的基础上更新了《中国县域肺癌诊疗临床路径(2024年版)》。该路径从影像诊断、病理诊断、分子检测、精准医疗等方面进行了阐述,并针对不同类型的肺癌患者制定了不同的诊疗流程。与第一版路径一致,本次更新仍将临床场景的诊断和治疗建议分为基本策略和可选策略进行阐述。基本策略是县级医院必须达到的标准,而可选策略则为医院提供了更多选择,便于县级医院医生在临床实践中运用。所有推荐的诊疗方案均严格参考现有指南和共识。与第一版相比,《路径》根据最新的高水平循证医学证据和适应症审批情况,更新了基本策略和可选策略中不同病理类型、TNM分型、分子分型下肺癌的诊疗建议。
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引用次数: 0
[Chinese multidisciplinary expert consensus on the rational use of surufatinib in clinical practice(2024 edition)]. [中国多学科专家关于在临床实践中合理使用舒伐替尼的共识(2024 年版)"。
Q3 Medicine Pub Date : 2024-10-23 DOI: 10.3760/cma.j.cn112152-20240524-00216

Neuroendocrine neoplasms are a group of heterogeneous tumors originating from the neuroendocrine system, which can occur in any part of the body. Pulmonary and gastroenteropancreatic neuroendocrine tumors are the most common. In recent years, the global incidence of neuroendocrine tumors has increased more significantly than other types of tumors, especially in the past 40 years. The drug treatment of neuroendocrine tumors includes somatostatin analogues, anti-angiogenesis targeting drugs, nuclide therapy and chemotherapy. Surufatinib is an oral tyrosine kinase receptor inhibitors that targets for vascular endothelial growth factor receptor (VEGFR1-3), fibroblast growth factor receptor 1 (FGFR1), and colony-stimulating factor-1 receptor (CSF-1R), has received approval in 2020 and 2021 for the treatment of locally advanced or metastatic, progressive nonfunctional, well-differentiated (G1, G2) neuroendocrine tumors (NETs) of both pancreatic and extrapancreatic origin that are unresectable. Ongoing exploratory studies are investigating its potential application in other tumor types. Common adverse reactions observed during surufatinib treatment include hypertension, proteinuria, bleeding events, and hepatic lab test abnormal and diarrhea. Chinese multidisciplinary expert consensus on the rational use of surufatinib in clinical practice (2024 edition) aims to provide standardized guidance for its rational use and enhance patient compliance to maximize therapeutic benefits.

神经内分泌肿瘤是一组起源于神经内分泌系统的异质性肿瘤,可发生在身体的任何部位。肺和胃肠胰神经内分泌肿瘤最为常见。近年来,全球神经内分泌肿瘤的发病率比其他类型的肿瘤有了更显著的增长,尤其是在过去 40 年中。神经内分泌肿瘤的药物治疗包括体生长激素类似物、抗血管生成靶向药物、核素治疗和化疗。舒罗伐替尼是一种口服酪氨酸激酶受体抑制剂,靶向血管内皮生长因子受体(VEGFR1-3)、成纤维细胞生长因子受体1(FGFR1)和集落刺激因子-1受体(CSF-1R)、已于 2020 年和 2021 年获得批准,用于治疗无法切除的局部晚期或转移性、进展性无功能、分化良好(G1、G2)的胰腺和胰腺外神经内分泌肿瘤(NET)。目前正在进行的探索性研究正在调查其在其他肿瘤类型中的潜在应用。在舒法替尼治疗期间观察到的常见不良反应包括高血压、蛋白尿、出血事件、肝脏实验室检查异常和腹泻。中国多学科专家共识(2024年版)》旨在为索非替尼的临床合理应用提供规范化指导,提高患者依从性,最大限度地提高治疗效果。
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引用次数: 0
[A case of primary giant gastrointestinal stromal tumor of the liver]. [肝脏原发性巨大胃肠道间质瘤一例]。
Q3 Medicine Pub Date : 2024-10-23 DOI: 10.3760/cma.j.cn112152-20230809-00070
W L Wang, A Hu, G Luo, Y P Luo, Y M Ou
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引用次数: 0
[Clinical predictive value of PD-1/PD-L1-induced electrocardiogram changes for cardiotoxicity]. [PD-1/PD-L1诱导的心电图变化对心脏毒性的临床预测价值]。
Q3 Medicine Pub Date : 2024-10-23 DOI: 10.3760/cma.j.cn112152-20231024-00230
N Xue, L L Peng, D W Wu, X J Li

Objective: To observe the electrocardiogram (ECG) changes of programmed death receptor 1 (PD-1)/programmed death receptor-ligand 1 (PD-L1) immune checkpoint inhibitors before and after immunotherapy of patients during clinical antitumor process, and to explore the occurrence and influencing factors of cardiotoxicity of immune checkpoint inhibitors. Methods: A total of 93 patients with locally advanced or metastatic solid tumors confirmed by pathological diagnosis in Cancer Hospital of Chinese Academy of Medical Sciences from October 1, 2019 to September 30, 2020 were selected and treated with PD-1/PD-L1 inhibitor monotherapy. Groups were divided according to immunotherapy regimen: Group A (drug code: 609A), 16 patients were given 1 mg/kg of the drug for 21 days; Group B (drug code: HX008), 23 patients were treated with 200mg for 21 days; Group C (drug code: GB226), 28 patients were treated with 3mg/kg for 14 days; Group D (drug code: LP002), 26 patients were treated with 900mg for 14 days. The patients were monitored and followed up for 10 cycles. The ECG results of each group were recorded, and the correlation between ECG abnormality and cardiotoxicity was analyzed. Results: A total of 75 patients showed abnormal ECG that met the diagnostic criteria. There was no significant difference in abnormal ECG rate after immunotherapy in group A (P>0.05), while the incidence of adverse cardiac events increased after immunotherapy in group B (P<0.05), and the abnormal ECG rate increased significantly after chemotherapy in group C and group D. There was statistical difference before and after immunotherapy (P<0.001). The number of abnormal cases in group A (8 cases, 50.0%, 8/16) was significantly lower than that of group B (20 cases, 87.0%, 20/23). The number of abnormal cases in group C and group D was 24 (85.7%) and 23 (88.4%), respectively, without statistical difference (P>0.05), but their abnormal rates of ECG were higher than that in group A. The incidence of electrical adverse events in immunotherapy center of patients with underlying diseases was 1.93 times higher than that of patients without underlying diseases. The incidence of central electrical adverse events during immunotherapy in group B, C and D was 6.667, 6.000 and 7.667 times higher than that in group A, respectively. Conclusions: The high sensitivity of early ECG changes induced by immune checkpoint inhibitors enables early prediction of related cardiotoxicity. The presence or absence of comorbid underlying disease and drug dosage are correlated with the occurrence of adverse cardiac events, and these early changes provide a evidence for clinical treatment and prevention.

目的观察临床抗肿瘤过程中患者免疫治疗前后程序性死亡受体1(PD-1)/程序性死亡受体配体1(PD-L1)免疫检查点抑制剂的心电图(ECG)变化,探讨免疫检查点抑制剂心脏毒性的发生及影响因素。研究方法选取中国医学科学院肿瘤医院2019年10月1日至2020年9月30日经病理诊断确诊的局部晚期或转移性实体瘤患者共93例,采用PD-1/PD-L1抑制剂单药治疗。根据免疫治疗方案进行分组:A组(药物代码:609A),16例患者给予1mg/kg的药物,治疗21天;B组(药物代码:HX008),23例患者给予200mg的药物,治疗21天;C组(药物代码:GB226),28例患者给予3mg/kg的药物,治疗14天;D组(药物代码:LP002),26例患者给予900mg的药物,治疗14天。对患者进行了 10 个周期的监测和随访。记录各组的心电图结果,并分析心电图异常与心脏毒性之间的相关性。结果共有 75 名患者的心电图异常符合诊断标准。A组免疫治疗后心电图异常率无明显差异(P>0.05),B组免疫治疗后心脏不良事件发生率增加(P<0.05),C组和D组化疗后心电图异常率明显增加,免疫治疗前后有统计学差异(P<0.001)。A 组异常病例数(8 例,50.0%,8/16)明显低于 B 组(20 例,87.0%,20/23)。C组和D组异常例数分别为24例(85.7%)和23例(88.4%),无统计学差异(P>0.05),但其心电图异常率均高于A组。B组、C组和D组免疫治疗期间中心电不良事件的发生率分别是A组的6.667倍、6.000倍和7.667倍。结论免疫检查点抑制剂诱发的早期心电图变化具有很高的灵敏度,可以及早预测相关的心脏毒性。有无合并基础疾病和药物剂量与心脏不良事件的发生相关,这些早期变化为临床治疗和预防提供了证据。
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引用次数: 0
[CT measurement of blood perfusion in hepatocellular carcinoma: from basic principle, measurement methods to clinical application]. [肝细胞癌血液灌注 CT 测量:从基本原理、测量方法到临床应用]。
Q3 Medicine Pub Date : 2024-10-23 DOI: 10.3760/cma.j.cn112152-20240605-00240
Y K Li, Q B Wang, Y B Liang, Y Ke

Hepatocellular carcinoma (HCC) is one of the common and fatal malignant tumors worldwide, and the burden of HCC is particularly severe in China. Physiologically, the blood supply to healthy liver is mainly from the portal vein, supplemented by the hepatic artery. While in the development of HCC, the main source of blood supply to HCC is changed from the portal vein to the hepatic artery. The characteristics of HCC vascularization are important for imaging, surgery, interventional therapy, targeted therapy, etc. Even in the future, with the development of radiation therapy technology, such as proton and heavy ion therapy and artificial intelligence technology, the dynamic changes in HCC blood perfusion can be used as a new biomarker of tumor activity to provide accurate information on the intensity modulation of radiotherapy, so that accurate measurements of HCC blood perfusion is of great significance in guiding the diagnosis and treatment of HCC. The technologies for measurement of HCC blood perfusion have developed from invasive techniques, such as inert gas scavenging, electromagnetic flowmeter, and radionuclide-labeled erythrocyte elution in the middle of the last century to the present non-invasive techniques of CT. With the development of CT imaging technology in the last 30 years, the CT-based imaging technology can assess the status of organ and tissue perfusion relatively easily and accurately. In this paper, the various CT measurement techniques of blood perfusion in HCC were categorized into three types: semi-quantitative technique, relative quantitative technique, and absolute quantitative technique. Their basic principle, scanning methods, and clinical applications were discussed to provide a reference for the diagnosis and treatment of HCC.

肝细胞癌(HCC)是全球常见的致命性恶性肿瘤之一,在中国的发病率尤为严重。从生理学角度讲,健康肝脏的血液供应主要来自门静脉,辅以肝动脉。而在 HCC 的发展过程中,HCC 的主要供血来源由门静脉转变为肝动脉。HCC 血管化的特点对于成像、手术、介入治疗、靶向治疗等都非常重要。甚至在未来,随着质子、重离子治疗等放射治疗技术和人工智能技术的发展,HCC 血液灌注的动态变化可作为肿瘤活性的新生物标志物,为放疗强度调控提供准确信息,因此准确测量 HCC 血液灌注对指导 HCC 的诊断和治疗具有重要意义。HCC 血液灌注测量技术从上世纪中期的惰性气体清除、电磁流量计、放射性核素标记红细胞洗脱等有创技术发展到现在的 CT 无创技术。随着近 30 年 CT 成像技术的发展,以 CT 为基础的成像技术可以比较容易和准确地评估器官和组织的灌注状况。本文将 HCC 血液灌注的各种 CT 测量技术分为三类:半定量技术、相对定量技术和绝对定量技术。并对其基本原理、扫描方法和临床应用进行了探讨,以期为 HCC 的诊断和治疗提供参考。
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引用次数: 0
[TRAF4 promotes lung cancer development by activating tyrosine kinase of EGFR]. [TRAF4通过激活表皮生长因子受体的酪氨酸激酶促进肺癌发展]
Q3 Medicine Pub Date : 2024-10-23 DOI: 10.3760/cma.j.cn112152-20231024-00240
X M Nie, D F Dong, J F Lin, B Y Wu, G Cai
<p><p><b>Objective:</b> To explore the role of tumor necrosis factor receptor-associated factor 4 (TRAF4) in promoting the abnormal activation of epidermal growth factor receptor (EGFR) and its effect on lung cancer cell proliferation, migration and invasion. <b>Methods:</b> Tumor tissues from patients who underwent lung adenocarcinoma resection at The First Affiliated Hospital of Second Military Medical University, from January 2015 to May 2017 were collected, and the expressions of TRAF4 and Ki-67 in lung cancer tissues were detected by immunohistochemistry, the mRNA levels of Cyclin D and Vimentin were detected by real-time fluorescence quantitative PCR (qRT-PCR). The effect of TRAF4 on the tumor growth ability of lung cancer A549 cells was investigated by the xenograft model, the effect of TRAF4 or EGFR on the tumor proliferation ability was detected by using cell counting kit 8 (CCK8) and BrdU assay, and the migration and invasion abilities of tumor cells were detected by Transwell assay. Different structural domain deletion expression vectors of TRAF4 and EGFR were constructed to transfect cells, and the interaction mode of TRAF4 and EGFR was investigated by immunoprecipitation assay. <b>Results:</b> The expression of TRAF4 in non-small cell lung cancer (NSCLC) tissues was positively correlated with the expressions of Ki-67, cyclin D, and vimentin (<i>r</i><sup>2</sup>: 0.438, 0.695, and 0.736, respectively, all <i>P</i><0.01). Immunohistochemical assay of tumor tissues from NSCLC patients showed that tissues with high expression of TRAF4 were also high in Ki-67. Patients with high TRAF4 expression (TRAF4 positivity >30%) had a shorter progression-free survival (PFS) time than that of patients with low TRAF4 expression (TRAF4 positivity ≤30%) (median PFS of 12 and 19 months, respectively; <i>P</i>=0.034). Traf4<sup>-/-</sup> cells had a weakened proliferative capacity than <i>traf4</i><sup>+/+</sup> cells and formed tumors with smaller size (<i>P</i><0.05). The expression level of Ki-67 in the tumor tissues formed by <i>traf4<sup>-/-</sup></i> cells [(45.6±8.7)%] was lower than that in the tumor tissues formed by <i>traf4</i><sup>+/+</sup> cells [(62.3±10.3)%, <i>P</i>=0.015], the mRNA levels of cyclin D (1.01±0.15) and vimentin (1.01±0.12) in the <i>traf4<sup>-/-</sup></i> cells were lower than those of the <i>traf4</i><sup>+/+</sup> cells (3.41±0.32 and 3.12±0.18, respectively, both <i>P</i><0.05).The western blot results showed that, with the elevated intracellular expression level of TRAF4, phosphorylation level of EGFR was significantly increased in both wild-type EGFR and activation mutant EGFR-expression cells. The capacities of proliferation, migration and invasion of A549 cells was weakened after EGFR knockdown (all <i>P</i><0.01). Immunoprecipitation experiments showed that TRAF4 binds to the peptide segment of the near-membrane region of EGFR through the TRAF structural domain, and the mutual binding between EGFR molecules was en
目的探讨肿瘤坏死因子受体相关因子 4(TRAF4)在促进表皮生长因子受体(EGFR)异常活化中的作用及其对肺癌细胞增殖、迁移和侵袭的影响。研究方法收集2015年1月至2017年5月在第二军医大学第一附属医院接受肺腺癌切除术患者的肿瘤组织,采用免疫组化方法检测肺癌组织中TRAF4和Ki-67的表达,采用实时荧光定量PCR(qRT-PCR)方法检测细胞周期蛋白D和Vimentin的mRNA水平。异种移植模型研究了TRAF4对肺癌A549细胞肿瘤生长能力的影响,细胞计数试剂盒8(CCK8)和BrdU检测了TRAF4或EGFR对肿瘤增殖能力的影响,Transwell检测了肿瘤细胞的迁移和侵袭能力。构建了不同结构域缺失的TRAF4和EGFR表达载体转染细胞,并通过免疫沉淀实验研究了TRAF4和EGFR的相互作用模式。结果显示非小细胞肺癌(NSCLC)组织中TRAF4的表达与Ki-67、细胞周期蛋白D和波形蛋白的表达呈正相关(r2分别为0.438、0.695和0.736,均P<0.01)。对 NSCLC 患者肿瘤组织的免疫组化检测显示,TRAF4 高表达的组织 Ki-67 也高。TRAF4高表达(TRAF4阳性率>30%)患者的无进展生存期(PFS)比TRAF4低表达(TRAF4阳性率≤30%)患者短(中位PFS分别为12个月和19个月;P=0.034)。与Traf4+/+细胞相比,Traf4-/-细胞的增殖能力更弱,形成的肿瘤更小(P<0.05)。traf4-/-细胞形成的肿瘤组织中Ki-67的表达水平[(45.6±8.7)%]低于traf4+/+细胞形成的肿瘤组织中Ki-67的表达水平[(62.3±10.3)%,P=0.015],traf4-/-细胞中细胞周期蛋白D(1.01±0.15)和波形蛋白(1.01±0.12)的mRNA水平低于traf4+/+细胞(3.Western印迹结果显示,随着TRAF4在细胞内表达水平的升高,野生型表皮生长因子受体和活化突变型表皮生长因子受体表达细胞的表皮生长因子受体磷酸化水平均显著升高。敲除表皮生长因子受体后,A549细胞的增殖、迁移和侵袭能力减弱(均P<0.01)。免疫沉淀实验表明,TRAF4通过TRAF结构域与表皮生长因子受体近膜区的肽段结合,在TRAF4过表达条件下,表皮生长因子受体分子间的相互结合增强。TRAF4 表达的增加促进了表皮生长因子受体分子磷酸化和下游信号的激活。结论:TRAF4在NSCLC组织和肿瘤细胞中表达升高,促进肿瘤增殖、迁移和侵袭。TRAF4可直接与表皮生长因子受体分子结合,增强自身磷酸化,并通过促进表皮生长因子受体分子间的相互作用激活下游信号通路。
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引用次数: 0
[Results of the cancer screening program in urban areas in Shaanxi province of China, 2019-2020]. [2019-2020年中国陕西省城市地区癌症筛查项目结果]。
Q3 Medicine Pub Date : 2024-10-23 DOI: 10.3760/cma.j.cn112152-20231020-00208
Y Chen, B H Song, G Li, P Chen, S P Huang, Z J Liao, R Xu, Y R Li

Objective: Analyze the cancer screening status of the cancer screening program in urban areas in Shaanxi province in 2019-2020. Methods: The early diagnosis and early treatment project for urban cancers carried out high-risk population screening for 5 types of high-incidence malignant tumors (breast cancer, lung cancer, upper gastrointestinal cancer, liver cancer, and colorectal cancer) in urban areas. Three prefecture-level cities in Shaanxi province with a population of over 1 million (Xi'an, Baoji, and Shangluo) were selected, and 4 communities with a relatively good working foundation were selected in each city. The general population aged 45-74 years was surveyed on the principles of informed consent and voluntariness, and high-risk groups identified through the questionnaire were further subjected to free endoscopy, ultrasound, CT, and other clinical screenings. The high-risk rates, screening compliance rates, and positive detection rates of the above 5 types of malignant tumors were analyzed. Results: A total of 19 632 people completed the survey effectively, with the proportion of male participants (40.0%) lower than that of females (60.0%). A total of 10 102 high-risk groups were identified, with an initial screening high-risk rate of 51.5%, and the high-risk rates for the 5 types of cancers were 24.1% for breast cancer, 28.6% for lung cancer, 9.1% for upper gastrointestinal cancer, 4.0% for liver cancer, and 20.0% for colorectal cancer. Among the 14 960 person-time initially assessed as high-risk, 5 129 person-time received clinical screening, with a screening compliance rate of 34.3%. The number of people receiving clinical screening and the screening compliance rates for the 5 types of cancers were 1 192 (41.9%) for breast cancer, 2 081 (37.1%) for lung cancer, 574 (32.0%) for upper gastrointestinal cancer, 404 (51.3%) for liver cancer, and 878 (22.3%) for colorectal cancer, with positive detection numbers and rates of 179 (15.0%) for breast, 289 (13.9%) for lung, 9 (1.6%) for upper gastrointestinal, 14 (3.5%) for suspected liver, and 67 (7.6%) for colorectal, respectively. Conclusion: The cancer screening status of the cancer screening program in urban areas in Shaanxi province is beneficial for the detection of precancerous lesions and early cancer patients, and improving the early diagnosis and treatment rate of patients, but the public participation rate is not high, and the project management model and technical plan need to be further improved.

目的分析2019-2020年陕西省城市地区癌症筛查项目的筛查情况。方法:开展城市癌症早诊早治项目:城市癌症早诊早治项目在城市地区开展5种高发恶性肿瘤(乳腺癌、肺癌、上消化道癌、肝癌、结直肠癌)高危人群筛查。选择陕西省三个人口超过 100 万的地级市(西安、宝鸡、商洛),每个城市选择 4 个工作基础较好的社区。本着知情同意和自愿的原则,对 45-74 岁的普通人群进行问卷调查,并对通过问卷调查确定的高危人群进一步进行免费的内镜、超声、CT 等临床筛查。对上述 5 种恶性肿瘤的高风险率、筛查符合率和阳性检出率进行了分析。结果显示共有 19 632 人有效完成了调查,其中男性参与者比例(40.0%)低于女性(60.0%)。共发现 10 102 名高风险人群,初筛高风险率为 51.5%,5 种癌症的高风险率分别为:乳腺癌 24.1%、肺癌 28.6%、上消化道癌 9.1%、肝癌 4.0%、结直肠癌 20.0%。在初步评估为高风险的 14 960 人次中,有 5 129 人次接受了临床筛查,筛查达标率为 34.3%。在 5 种癌症中,接受临床筛查的人数和筛查达标率分别为:乳腺癌 1 192 人(41.9%)、肺癌 2 081 人(37.1%)、上消化道癌 574 人(32.0%)、肝癌 404 人(51.3%)、结肠癌 8 人(34.3%)。阳性检出人数和阳性检出率分别为:乳腺癌 179 人(15.0%)、肺癌 289 人(13.9%)、上消化道癌 9 人(1.6%)、疑似肝癌 14 人(3.5%)和结直肠癌 67 人(7.6%)。结论陕西省城市地区癌症筛查项目的癌症筛查现状有利于发现癌前病变和早期癌症患者,提高患者的早诊早治率,但公众参与率不高,项目管理模式和技术方案有待进一步完善。
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中华肿瘤杂志
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