Rahul Kumar Pandey, Saumya Shukla, Rahat Hadi, Nuzhat Husain, Mohammad Hayatul Islam, Ashish Singhal, Surya Kant Tripathi, Rajiv Garg
{"title":"大鼠Kirsten肉瘤病毒蛋白在肺腺癌中的过表达:与临床病理和组织形态学特征的关系","authors":"Rahul Kumar Pandey, Saumya Shukla, Rahat Hadi, Nuzhat Husain, Mohammad Hayatul Islam, Ashish Singhal, Surya Kant Tripathi, Rajiv Garg","doi":"10.4103/jcar.JCar_11_20","DOIUrl":null,"url":null,"abstract":"<p><strong>Context: </strong>Lung cancer is the leading cause of cancer-related deaths worldwide. The constitutive activation of multiple signaling pathways is the major cause of carcinogenesis.</p><p><strong>Aims: </strong>The study evaluates the frequency of Kirsten rat sarcoma virus (KRAS) protein overexpression and correlates with clinicopathological and histomorphological features in non-small cell lung carcinoma (NSCLC)-adenocarcinoma.</p><p><strong>Settings and design: </strong>Tertiary hospital-based retrospective and prospective case series included 100 cases of NSCLC-adenocarcinoma.</p><p><strong>Materials and methods: </strong>The basic panel of Immunohistochemistry including Napsin-A, thyroid transcription factor-1 (TTF-1), and markers for squamous differentiation, p-40 was used in formalin-fixed paraffin-embedded tissue blocks. The KRAS monoclonal antibody (9.13, Thermo Fisher Scientific, USA) was used.</p><p><strong>Statistical analysis used: </strong>The IBM-Statistical Package for the Social Sciences (SPSS) (SPSS, International Business Machines Corporation, New York, NY, USA) analysis software, version 16 was used for all statistical calculations.</p><p><strong>Results: </strong>KRAS protein expressed in 28.0% (28/100) cases. Cases were grouped as KRAS positive and negative. TTF-1 and Napsin-A were expressed in 89.25% (<i>n</i> = 25) and 92.86% (<i>n</i> = 26) cases, respectively. Stage IV clinical disease was identified in 55% of cases, and 36.84% of cases had a mean survival between 6 and 12 months. In KRAS positive group, the most common pattern of cellular arrangement was acinar/loose clusters pattern present in 64.29% (<i>n</i> = 21) and 75.0% (<i>n</i> = 18) cases followed by the solid pattern present in 42.86% of cases (<i>n</i> = 12), respectively. Necrosis was identified in 57.14% (<i>n</i> = 16) cases. Mucin pattern was present in 32.14% of cases (<i>n</i> = 9), which was significantly different when compared with the KRAS negative group (<i>P</i> = 0.036).</p><p><strong>Conclusions: </strong>This finding may imply that KRAS mutations may not be entirely triggered by alterations induced by carcinogens in smoke. KRAS gene is frequently mutated in pulmonary tumors. It should be tested in NSCLC owing to its predictive and prognostic effects.</p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2020-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7921778/pdf/","citationCount":"2","resultStr":"{\"title\":\"Kirsten rat sarcoma virus protein overexpression in adenocarcinoma lung: Association with clinicopathological and histomorphological features.\",\"authors\":\"Rahul Kumar Pandey, Saumya Shukla, Rahat Hadi, Nuzhat Husain, Mohammad Hayatul Islam, Ashish Singhal, Surya Kant Tripathi, Rajiv Garg\",\"doi\":\"10.4103/jcar.JCar_11_20\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Context: </strong>Lung cancer is the leading cause of cancer-related deaths worldwide. The constitutive activation of multiple signaling pathways is the major cause of carcinogenesis.</p><p><strong>Aims: </strong>The study evaluates the frequency of Kirsten rat sarcoma virus (KRAS) protein overexpression and correlates with clinicopathological and histomorphological features in non-small cell lung carcinoma (NSCLC)-adenocarcinoma.</p><p><strong>Settings and design: </strong>Tertiary hospital-based retrospective and prospective case series included 100 cases of NSCLC-adenocarcinoma.</p><p><strong>Materials and methods: </strong>The basic panel of Immunohistochemistry including Napsin-A, thyroid transcription factor-1 (TTF-1), and markers for squamous differentiation, p-40 was used in formalin-fixed paraffin-embedded tissue blocks. The KRAS monoclonal antibody (9.13, Thermo Fisher Scientific, USA) was used.</p><p><strong>Statistical analysis used: </strong>The IBM-Statistical Package for the Social Sciences (SPSS) (SPSS, International Business Machines Corporation, New York, NY, USA) analysis software, version 16 was used for all statistical calculations.</p><p><strong>Results: </strong>KRAS protein expressed in 28.0% (28/100) cases. Cases were grouped as KRAS positive and negative. TTF-1 and Napsin-A were expressed in 89.25% (<i>n</i> = 25) and 92.86% (<i>n</i> = 26) cases, respectively. Stage IV clinical disease was identified in 55% of cases, and 36.84% of cases had a mean survival between 6 and 12 months. In KRAS positive group, the most common pattern of cellular arrangement was acinar/loose clusters pattern present in 64.29% (<i>n</i> = 21) and 75.0% (<i>n</i> = 18) cases followed by the solid pattern present in 42.86% of cases (<i>n</i> = 12), respectively. Necrosis was identified in 57.14% (<i>n</i> = 16) cases. Mucin pattern was present in 32.14% of cases (<i>n</i> = 9), which was significantly different when compared with the KRAS negative group (<i>P</i> = 0.036).</p><p><strong>Conclusions: </strong>This finding may imply that KRAS mutations may not be entirely triggered by alterations induced by carcinogens in smoke. KRAS gene is frequently mutated in pulmonary tumors. It should be tested in NSCLC owing to its predictive and prognostic effects.</p>\",\"PeriodicalId\":52464,\"journal\":{\"name\":\"Journal of Carcinogenesis\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-10-08\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7921778/pdf/\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Carcinogenesis\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4103/jcar.JCar_11_20\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2020/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q1\",\"JCRName\":\"Environmental Science\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Carcinogenesis","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4103/jcar.JCar_11_20","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2020/1/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"Environmental Science","Score":null,"Total":0}
引用次数: 2
摘要
背景:肺癌是全球癌症相关死亡的主要原因。多种信号通路的组成性激活是致癌的主要原因。目的:研究Kirsten大鼠肉瘤病毒(KRAS)蛋白在非小细胞肺癌(NSCLC)-腺癌中的过表达频率及其与临床病理和组织形态学特征的相关性。背景和设计:以三级医院为基础的回顾性和前瞻性病例系列包括100例非小细胞肺癌腺癌。材料和方法:采用免疫组化基本板Napsin-A、甲状腺转录因子-1 (TTF-1)和鳞状分化标志物p-40作为福尔马林固定石蜡包埋组织块。采用KRAS单克隆抗体(9.13,Thermo Fisher Scientific, USA)。统计分析使用IBM-Statistical Package for The Social Sciences (SPSS) (SPSS, International Business Machines Corporation, New York, NY, USA)分析软件，version 16进行所有统计计算。结果:KRAS蛋白表达率为28.0%(28/100)。病例分为KRAS阳性和阴性。TTF-1和Napsin-A分别在89.25% (n = 25)和92.86% (n = 26)的病例中表达。在55%的病例中发现了IV期临床疾病，36.84%的病例平均生存期为6至12个月。KRAS阳性组最常见的细胞排列模式为腺泡/松散簇状排列，分别占64.29% (n = 21)和75.0% (n = 18)，其次为实型排列，分别占42.86% (n = 12)。16例(57.14%)出现坏死。32.14% (n = 9)的病例出现粘蛋白型，与KRAS阴性组比较差异有统计学意义(P = 0.036)。结论:这一发现可能意味着KRAS突变可能不完全是由烟雾中的致癌物引起的改变引起的。KRAS基因在肺肿瘤中经常发生突变。由于其预测和预后作用，应在非小细胞肺癌中进行测试。
Kirsten rat sarcoma virus protein overexpression in adenocarcinoma lung: Association with clinicopathological and histomorphological features.
Context: Lung cancer is the leading cause of cancer-related deaths worldwide. The constitutive activation of multiple signaling pathways is the major cause of carcinogenesis.
Aims: The study evaluates the frequency of Kirsten rat sarcoma virus (KRAS) protein overexpression and correlates with clinicopathological and histomorphological features in non-small cell lung carcinoma (NSCLC)-adenocarcinoma.
Settings and design: Tertiary hospital-based retrospective and prospective case series included 100 cases of NSCLC-adenocarcinoma.
Materials and methods: The basic panel of Immunohistochemistry including Napsin-A, thyroid transcription factor-1 (TTF-1), and markers for squamous differentiation, p-40 was used in formalin-fixed paraffin-embedded tissue blocks. The KRAS monoclonal antibody (9.13, Thermo Fisher Scientific, USA) was used.
Statistical analysis used: The IBM-Statistical Package for the Social Sciences (SPSS) (SPSS, International Business Machines Corporation, New York, NY, USA) analysis software, version 16 was used for all statistical calculations.
Results: KRAS protein expressed in 28.0% (28/100) cases. Cases were grouped as KRAS positive and negative. TTF-1 and Napsin-A were expressed in 89.25% (n = 25) and 92.86% (n = 26) cases, respectively. Stage IV clinical disease was identified in 55% of cases, and 36.84% of cases had a mean survival between 6 and 12 months. In KRAS positive group, the most common pattern of cellular arrangement was acinar/loose clusters pattern present in 64.29% (n = 21) and 75.0% (n = 18) cases followed by the solid pattern present in 42.86% of cases (n = 12), respectively. Necrosis was identified in 57.14% (n = 16) cases. Mucin pattern was present in 32.14% of cases (n = 9), which was significantly different when compared with the KRAS negative group (P = 0.036).
Conclusions: This finding may imply that KRAS mutations may not be entirely triggered by alterations induced by carcinogens in smoke. KRAS gene is frequently mutated in pulmonary tumors. It should be tested in NSCLC owing to its predictive and prognostic effects.
期刊介绍：
Journal of Carcinogenesis considers manuscripts in many areas of carcinogenesis and Chemoprevention. Primary areas of interest to the journal include: physical and chemical carcinogenesis and mutagenesis; processes influencing or modulating carcinogenesis, such as DNA repair; genetics, nutrition, and metabolism of carcinogens; the mechanism of action of carcinogens and modulating agents; epidemiological studies; and, the formation, detection, identification, and quantification of environmental carcinogens. Manuscripts that contribute to the understanding of cancer prevention are especially encouraged for submission
京公网安备 11010802042870号
京ICP备2023020795号-1
分享
求助内容：
应助结果提醒方式：
扫码关注我们
