Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2090
Z. Yao, D. Yao, William W. Yu, A. Malki, Z. Sherif
{"title":"Abstract 2090: TP73 expression may be influenced by DNA methylation in human tumorigenesis","authors":"Z. Yao, D. Yao, William W. Yu, A. Malki, Z. Sherif","doi":"10.1158/1538-7445.AM2021-2090","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2090","url":null,"abstract":"","PeriodicalId":18754,"journal":{"name":"Molecular and Cellular Biology / Genetics","volume":"1121 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91444314","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}
Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2021
Vengatesh Ganapathy, Jimmy Manyanga, L. Queimado
Background The BioFire FilmArrary GI Panel Assay is a highly sensitive PCR-based diagnostic test capable of detecting 22 different gastrointestinal pathogens from stool specimens. The predominant pathogens associated with hospital-acquired gastroenteritis are Clostridioides difficile and Norovirus, both of which can be assayed individually with PCR-based tests performed at UCHealth. Previous studies favor a cost-saving ‘3-day rule,’ that restricts ordering culture-based stool testing on inpatient adults following the 3rd day of hospitalization. However, the previous studies performed a limited analysis of pathogens using predominantly culture-based assays. Furthermore certain patient groups may be at high risk for developing nosocomial diarrhea with less common organisms, which may go undetected if the 3-day rule were enforced for the GI panel assay. Thus there is a need to validate whether the 3-day rule is appropriate for restricting the use of the GI panel assay for the evaluation of nosocomial diarrhea.
BioFire FilmArrary GI Panel Assay是一种高度敏感的基于pcr的诊断试验，能够从粪便标本中检测出22种不同的胃肠道病原体。与医院获得性胃肠炎相关的主要病原体是艰难梭菌和诺如病毒，这两种病毒都可以在uhealth进行基于pcr的检测。先前的研究倾向于节省成本的“3天规则”，即限制住院成年人在住院3天后进行基于培养的粪便检测。然而，以前的研究主要使用基于培养的检测方法对病原体进行了有限的分析。此外，某些患者群体可能有发生院内腹泻的高风险，这些腹泻可能是由不常见的微生物引起的，如果强制执行3天规则进行胃肠道检测，则可能无法检测到。因此，有必要验证3天规则是否适用于限制使用GI panel assay来评估医院性腹泻。
{"title":"Abstract 2021: Differential expression of antioxidant and detoxifying enzymes induced by e-cigarette aerosol","authors":"Vengatesh Ganapathy, Jimmy Manyanga, L. Queimado","doi":"10.1158/1538-7445.AM2021-2021","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2021","url":null,"abstract":"Background The BioFire FilmArrary GI Panel Assay is a highly sensitive PCR-based diagnostic test capable of detecting 22 different gastrointestinal pathogens from stool specimens. The predominant pathogens associated with hospital-acquired gastroenteritis are Clostridioides difficile and Norovirus, both of which can be assayed individually with PCR-based tests performed at UCHealth. Previous studies favor a cost-saving ‘3-day rule,’ that restricts ordering culture-based stool testing on inpatient adults following the 3rd day of hospitalization. However, the previous studies performed a limited analysis of pathogens using predominantly culture-based assays. Furthermore certain patient groups may be at high risk for developing nosocomial diarrhea with less common organisms, which may go undetected if the 3-day rule were enforced for the GI panel assay. Thus there is a need to validate whether the 3-day rule is appropriate for restricting the use of the GI panel assay for the evaluation of nosocomial diarrhea.","PeriodicalId":18754,"journal":{"name":"Molecular and Cellular Biology / Genetics","volume":"11 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80765477","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}
Background: Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and devastating cancers without effective treatments. Amplified in breast cancer 1 (AIB1) is a member of the steroid receptor coactivator family that mediates the transcriptional activities of nuclear receptors. While AIB1 is associated with the initiation and progression of multiple cancers, the mechanism by which AIB1 contributes to PDAC progression remains largely unknown. In this study, we aimed to explore the role of AIB1 in the progression of PDAC and elucidate the underlying mechanisms. Methods: The clinical significance and mRNA level of AIB1 in PDAC were studied by database analysis. To demonstrate whether AIB1 mediates the malignant features of PDAC cells, namely, proliferation, migration, invasion, we performed real-time PCR and Western blot analysis, established xenograft models and used in vivo metastasis assay. With insights into the mechanism of AIB1, we performed RNA sequencing (Seq), ChIP-Seq, luciferase reporter assays and pull-down assays. Furthermore, we analyzed the relationship between AIB1 expression and its target expression in PDAC cells and patients and explored whether PDAC cells with high AIB1 levels are sensitive to inhibitors of its target. Results: We found that AIB1 was significantly upregulated in PDAC and associated with its malignancy. Silencing AIB1 impaired hedgehog (Hh) activation by reducing the expression of smoothened (SMO), leading to cell cycle arrest and the inhibition of PDAC cell proliferation. In addition, AIB1, via upregulation of integrin αv (ITGAV) expression, promoted extracellular matrix (ECM) signaling, which played an important role in PDAC progression. Further studies showed that AIB1 preferably bound to AP-1 related elements and served as a coactivator for enhancing the transcriptional activity of MafB, which promoted the expression of SMO and ITGAV. PDAC cells with high AIB1 levels were sensitive to Hh signaling inhibitors, suggesting that blocking Hh activation is an effective treatment against PDAC with high AIB1 expression. Conclusions: These findings reveal that AIB1 is a crucial oncogenic regulator associated with PDAC progression via Hh and ECM signaling and suggest potential therapeutic targets for PDAC treatment. Citation Format: Licen Li, Jiaolin Bao, Haitao Wang, Haipeng Lei, Peng Cheng, Jianming Zeng, Wenhui Hao, Xu Zhang, Xiaoling Xu, Chundong Yu, Chu-Xia Deng, Qiang Chen. Upregulation of amplified in breast cancer 1 contributes to pancreatic ductal adenocarcinoma progression and vulnerability to blockage of hedgehog activation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2416.
{"title":"Abstract 2416: Upregulation of amplified in breast cancer 1 contributes to pancreatic ductal adenocarcinoma progression and vulnerability to blockage of hedgehog activation","authors":"Licen Li, Jiaolin Bao, Haitao Wang, Haipeng Lei, P.-T. Cheng, Jianming Zeng, Wenhui Hao, Xu Zhang, Xiaoling Xu, Chundong Yu, C. Deng, Qiang Chen","doi":"10.1158/1538-7445.AM2021-2416","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2416","url":null,"abstract":"Background: Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and devastating cancers without effective treatments. Amplified in breast cancer 1 (AIB1) is a member of the steroid receptor coactivator family that mediates the transcriptional activities of nuclear receptors. While AIB1 is associated with the initiation and progression of multiple cancers, the mechanism by which AIB1 contributes to PDAC progression remains largely unknown. In this study, we aimed to explore the role of AIB1 in the progression of PDAC and elucidate the underlying mechanisms. Methods: The clinical significance and mRNA level of AIB1 in PDAC were studied by database analysis. To demonstrate whether AIB1 mediates the malignant features of PDAC cells, namely, proliferation, migration, invasion, we performed real-time PCR and Western blot analysis, established xenograft models and used in vivo metastasis assay. With insights into the mechanism of AIB1, we performed RNA sequencing (Seq), ChIP-Seq, luciferase reporter assays and pull-down assays. Furthermore, we analyzed the relationship between AIB1 expression and its target expression in PDAC cells and patients and explored whether PDAC cells with high AIB1 levels are sensitive to inhibitors of its target. Results: We found that AIB1 was significantly upregulated in PDAC and associated with its malignancy. Silencing AIB1 impaired hedgehog (Hh) activation by reducing the expression of smoothened (SMO), leading to cell cycle arrest and the inhibition of PDAC cell proliferation. In addition, AIB1, via upregulation of integrin αv (ITGAV) expression, promoted extracellular matrix (ECM) signaling, which played an important role in PDAC progression. Further studies showed that AIB1 preferably bound to AP-1 related elements and served as a coactivator for enhancing the transcriptional activity of MafB, which promoted the expression of SMO and ITGAV. PDAC cells with high AIB1 levels were sensitive to Hh signaling inhibitors, suggesting that blocking Hh activation is an effective treatment against PDAC with high AIB1 expression. Conclusions: These findings reveal that AIB1 is a crucial oncogenic regulator associated with PDAC progression via Hh and ECM signaling and suggest potential therapeutic targets for PDAC treatment. Citation Format: Licen Li, Jiaolin Bao, Haitao Wang, Haipeng Lei, Peng Cheng, Jianming Zeng, Wenhui Hao, Xu Zhang, Xiaoling Xu, Chundong Yu, Chu-Xia Deng, Qiang Chen. Upregulation of amplified in breast cancer 1 contributes to pancreatic ductal adenocarcinoma progression and vulnerability to blockage of hedgehog activation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2416.","PeriodicalId":18754,"journal":{"name":"Molecular and Cellular Biology / Genetics","volume":"43 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83758251","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}
Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2466
Sean M. Lenahan, Hailey M. Sarausky, D. Seward
{"title":"Abstract 2466: Stochastic loss of GLUL expression correlates with STK11-loss-dependent glutamine addiction and may impact anti-PD1 therapy resistance in NSCLC","authors":"Sean M. Lenahan, Hailey M. Sarausky, D. Seward","doi":"10.1158/1538-7445.AM2021-2466","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2466","url":null,"abstract":"","PeriodicalId":18754,"journal":{"name":"Molecular and Cellular Biology / Genetics","volume":"6 6 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81033588","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}
Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2377
B. Wilson, Rebekah Betar, Alexander Martin, Z. Niazi, Michael P. Boyer, Lori Winter, V. Babich, F. Sole, E. Ananieva
Lymphoma accounts for approximately 4% of cancers in the United States, with an estimated 20,910 number of deaths per year. The standard method of diagnosis and staging of lymphoma involves surgical biopsy of the tumor - a procedure that has many negative associated risks. Exosomes are extracellular vesicles secreted in biological fluids that can serve as “liquid biomarkers”. Identification of unique cancer-related biomarkers in urinary exosomes may provide a novel non-invasive and cost-effective tool for lymphoma diagnosis. Analyses of biomarkers obtained from urinary exosomes have been used to evaluate urological cancers, however, these methods have not yet been translated to non-urological pathologies, such as lymphomas. The objective for this study was to determine the profile of microRNAs (miRNAs) expressed in urinary exosomes of mice challenged with lymphoma and compare it to miRNAs identified in urinary exosomes of control mice. Male and female C57BL/6 mice, (tumor (+), n=12), were injected with either 2.5x105 mouse EL-4 lymphoma cells or phosphate-buffered saline (tumor (-), n=12). Tumor growth was monitored for 20 days. Urine was collected for 48 hours starting on day 17 and serum, tumor tissues, and organs were collected on day 20. Extraction of urinary exosomes was followed by total RNA isolation and RT-qPCR for which a set of PCR arrays consisting of 709 mouse-specific miRNA primers was used. Fold changes in miRNA expression were quantified using the ΔΔCt method. Mice developed tumors by day 13 with initial tumor appearance around day seven. There were no statistically significant differences between final tumor mass, body weight, or food and water intake in tumor (+) versus tumor (-) mice. RT-qPCR arrays of miRNAs extracted from urinary exosomes revealed 464 miRNAs that were differentially expressed between tumor (+) and tumor (-). 215 miRNAs were up-regulated, while 249 miRNAs were down-regulated in tumor (+) mice. These results will be compared to miRNAs from serum and tumor tissues to identify tumor-specific miRNAs that can be used for potential application in the clinical setting. Citation Format: Brittany Wilson, Rebekah Betar, Alexander Martin, Zackaria Niazi, Michael Boyer, Lori Winter, Victor Babich, Francesca Di Sole, Elitsa Ananieva. microRNA expression profile in urinary exosomes is dependent on non-invasive lymphoma induction in mice [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2377.
在美国，淋巴瘤约占癌症的4%，估计每年有20910人死亡。淋巴瘤诊断和分期的标准方法包括肿瘤的手术活检，这一过程有许多负面的相关风险。外泌体是生物体液中分泌的细胞外囊泡，可作为“液体生物标志物”。识别尿外泌体中独特的癌症相关生物标志物可能为淋巴瘤诊断提供一种新的非侵入性和经济有效的工具。从尿外泌体获得的生物标志物分析已被用于评估泌尿系统癌症，然而，这些方法尚未被转化为非泌尿系统疾病，如淋巴瘤。本研究的目的是确定淋巴瘤小鼠尿外泌体中表达的microRNAs (miRNAs)的谱，并将其与对照小鼠尿外泌体中鉴定的miRNAs进行比较。将雄性和雌性C57BL/6小鼠(肿瘤(+)，n=12)分别注射2.5 × 105小鼠EL-4淋巴瘤细胞或磷酸盐缓冲盐水(肿瘤(-)，n=12)。监测肿瘤生长20 d。从第17天开始收集尿液48小时，第20天收集血清、肿瘤组织和器官。提取尿外泌体后进行总RNA分离和RT-qPCR，其中使用了一组由709个小鼠特异性miRNA引物组成的PCR阵列。使用ΔΔCt方法定量miRNA表达的折叠变化。小鼠在第13天出现肿瘤，第7天左右出现肿瘤。肿瘤(+)和肿瘤(-)小鼠的最终肿瘤质量、体重、食物和水的摄入量没有统计学上的显著差异。从尿外泌体中提取的mirna的RT-qPCR阵列显示464个mirna在肿瘤(+)和肿瘤(-)之间差异表达。在肿瘤(+)小鼠中，215个mirna上调，249个mirna下调。这些结果将与来自血清和肿瘤组织的mirna进行比较，以确定可用于临床环境潜在应用的肿瘤特异性mirna。引文格式:Brittany Wilson, Rebekah Betar, Alexander Martin, Zackaria Niazi, Michael Boyer, Lori Winter, Victor Babich, Francesca Di Sole, Elitsa Ananieva。小鼠尿外泌体中的microRNA表达谱依赖于非侵袭性淋巴瘤诱导[摘要]。见:美国癌症研究协会2021年年会论文集;2021年4月10日至15日和5月17日至21日。费城(PA): AACR;癌症杂志，2021;81(13 -增刊):摘要nr 2377。
{"title":"Abstract 2377: microRNA expression profile in urinary exosomes is dependent on non-invasive lymphoma induction in mice","authors":"B. Wilson, Rebekah Betar, Alexander Martin, Z. Niazi, Michael P. Boyer, Lori Winter, V. Babich, F. Sole, E. Ananieva","doi":"10.1158/1538-7445.AM2021-2377","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2377","url":null,"abstract":"Lymphoma accounts for approximately 4% of cancers in the United States, with an estimated 20,910 number of deaths per year. The standard method of diagnosis and staging of lymphoma involves surgical biopsy of the tumor - a procedure that has many negative associated risks. Exosomes are extracellular vesicles secreted in biological fluids that can serve as “liquid biomarkers”. Identification of unique cancer-related biomarkers in urinary exosomes may provide a novel non-invasive and cost-effective tool for lymphoma diagnosis. Analyses of biomarkers obtained from urinary exosomes have been used to evaluate urological cancers, however, these methods have not yet been translated to non-urological pathologies, such as lymphomas. The objective for this study was to determine the profile of microRNAs (miRNAs) expressed in urinary exosomes of mice challenged with lymphoma and compare it to miRNAs identified in urinary exosomes of control mice. Male and female C57BL/6 mice, (tumor (+), n=12), were injected with either 2.5x105 mouse EL-4 lymphoma cells or phosphate-buffered saline (tumor (-), n=12). Tumor growth was monitored for 20 days. Urine was collected for 48 hours starting on day 17 and serum, tumor tissues, and organs were collected on day 20. Extraction of urinary exosomes was followed by total RNA isolation and RT-qPCR for which a set of PCR arrays consisting of 709 mouse-specific miRNA primers was used. Fold changes in miRNA expression were quantified using the ΔΔCt method. Mice developed tumors by day 13 with initial tumor appearance around day seven. There were no statistically significant differences between final tumor mass, body weight, or food and water intake in tumor (+) versus tumor (-) mice. RT-qPCR arrays of miRNAs extracted from urinary exosomes revealed 464 miRNAs that were differentially expressed between tumor (+) and tumor (-). 215 miRNAs were up-regulated, while 249 miRNAs were down-regulated in tumor (+) mice. These results will be compared to miRNAs from serum and tumor tissues to identify tumor-specific miRNAs that can be used for potential application in the clinical setting. Citation Format: Brittany Wilson, Rebekah Betar, Alexander Martin, Zackaria Niazi, Michael Boyer, Lori Winter, Victor Babich, Francesca Di Sole, Elitsa Ananieva. microRNA expression profile in urinary exosomes is dependent on non-invasive lymphoma induction in mice [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2377.","PeriodicalId":18754,"journal":{"name":"Molecular and Cellular Biology / Genetics","volume":"18 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89366780","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}
Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2400
Brandon Chen, S. Devenport, C. Lyssiotis, Y. Shah
{"title":"Abstract 2400: PINK1 is a novel regulator of mitochondria and iron metabolism in colon cancer","authors":"Brandon Chen, S. Devenport, C. Lyssiotis, Y. Shah","doi":"10.1158/1538-7445.AM2021-2400","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2400","url":null,"abstract":"","PeriodicalId":18754,"journal":{"name":"Molecular and Cellular Biology / Genetics","volume":"27 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87232155","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}
Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2046
Anne Olazabal-Herrero, Allison M. Green, Xiaoyong Chen, P. Sung, Pillai M. Manoj, G. Kupfer
{"title":"Abstract 2046: Binding of FANCD2 to SRSF1 splicing factor prevents genomic instability through R-loop regulation","authors":"Anne Olazabal-Herrero, Allison M. Green, Xiaoyong Chen, P. Sung, Pillai M. Manoj, G. Kupfer","doi":"10.1158/1538-7445.AM2021-2046","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2046","url":null,"abstract":"","PeriodicalId":18754,"journal":{"name":"Molecular and Cellular Biology / Genetics","volume":"74 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90601714","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}
Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2244
N. Siemers, Jasmine Chen, P. Mankoo, S. Ilyas
{"title":"Abstract 2244: Evaluation of large antibody panels in single-cell genomic immunophenotyping of fresh and preserved human leukocytes","authors":"N. Siemers, Jasmine Chen, P. Mankoo, S. Ilyas","doi":"10.1158/1538-7445.AM2021-2244","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2244","url":null,"abstract":"","PeriodicalId":18754,"journal":{"name":"Molecular and Cellular Biology / Genetics","volume":"19 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86953525","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}
Pub Date : 2021-07-01DOI: 10.1158/1538-7445.AM2021-2233
S. Sivakumar, E. Sokol, G. Frampton, P. Hegde, D. Fabrizio
{"title":"Abstract 2233: Landscape of driver mutations in MAPK/PI3K/AKT signaling pathways reveals insights into therapeutic targeting strategies","authors":"S. Sivakumar, E. Sokol, G. Frampton, P. Hegde, D. Fabrizio","doi":"10.1158/1538-7445.AM2021-2233","DOIUrl":"https://doi.org/10.1158/1538-7445.AM2021-2233","url":null,"abstract":"","PeriodicalId":18754,"journal":{"name":"Molecular and Cellular Biology / Genetics","volume":"346 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79667395","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}
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