Europe: recommendations The authors of “Towards a cancer mission in Horizon Europe: recommendations” (Mol. Oncol. 2020 Aug; 14(8): 1589-1615. PMID: 32749074) [1], have decided to update Fig. 4 and the related legend, to clarify that it visualizes information about the distribution and numbers of ERN PaedCan network, using as vector image a product of artwork, and not a political map. This change does not affect any discussion, or conclusions made in the article.
{"title":"Corrigendum to: Towards a cancer mission in Horizon Europe: recommendations","authors":"","doi":"10.1002/1878-0261.12801","DOIUrl":"https://doi.org/10.1002/1878-0261.12801","url":null,"abstract":"Europe: recommendations The authors of “Towards a cancer mission in Horizon Europe: recommendations” (Mol. Oncol. 2020 Aug; 14(8): 1589-1615. PMID: 32749074) [1], have decided to update Fig. 4 and the related legend, to clarify that it visualizes information about the distribution and numbers of ERN PaedCan network, using as vector image a product of artwork, and not a political map. This change does not affect any discussion, or conclusions made in the article.","PeriodicalId":51134,"journal":{"name":"Molecular Oncology","volume":"14 1","pages":"2697 - 2697"},"PeriodicalIF":6.6,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/1878-0261.12801","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48097476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Total RNAs of breast cancer cells and mouse embryonic fibroblasts MEF BRCA1 and MEF BRCA1 were extracted with TRIzol reagent (Invitrogen, Carlsbad, CA, USA). The cDNA was synthesized with the PrimeScript RT reagent Kit (Promega, Madison, WI, USA). Real-time PCR was carried out using an ABI 7500 real-time PCR system (Applied Biosystems, Foster City, CA, USA). The mRNA expression level of GOT2 and ASS1 was normalized to the endogenous expression of GAPDH. Primers were provided by Invitrogen as described below:
用TRIzol试剂(Invitrogen, Carlsbad, CA, USA)提取乳腺癌细胞和小鼠胚胎成纤维细胞MEF BRCA1和MEF BRCA1的总rna。cDNA用PrimeScript RT reagent Kit (Promega, Madison, WI, USA)合成。实时PCR采用ABI 7500实时PCR系统(Applied Biosystems, Foster City, CA, USA)。将GOT2和ASS1 mRNA表达水平归一化为内源性GAPDH的表达。引物由Invitrogen公司提供，如下所述:
{"title":"Corrigendum to: Preventing BRCA1/ZBRK1 repressor complex binding to the GOT2 promoter results in accelerated aspartate biosynthesis and promotion of cell proliferation","authors":"","doi":"10.1002/1878-0261.12784","DOIUrl":"https://doi.org/10.1002/1878-0261.12784","url":null,"abstract":"Total RNAs of breast cancer cells and mouse embryonic fibroblasts MEF BRCA1 and MEF BRCA1 were extracted with TRIzol reagent (Invitrogen, Carlsbad, CA, USA). The cDNA was synthesized with the PrimeScript RT reagent Kit (Promega, Madison, WI, USA). Real-time PCR was carried out using an ABI 7500 real-time PCR system (Applied Biosystems, Foster City, CA, USA). The mRNA expression level of GOT2 and ASS1 was normalized to the endogenous expression of GAPDH. Primers were provided by Invitrogen as described below:","PeriodicalId":51134,"journal":{"name":"Molecular Oncology","volume":"14 1","pages":"2696 - 2696"},"PeriodicalIF":6.6,"publicationDate":"2020-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/1878-0261.12784","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46995340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-05-02DOI: 10.1101/2020.04.30.070037
Gal Benor, G. Fuks, S. Chin, O. Rueda, Saptaparna Mukherjee, Sharathchandra Arandkar, Yael Aylon, C. Caldas, E. Domany, M. Oren
TP53 gene mutations are very common in human cancer. While such mutations abrogate the tumor suppressive activities of the wild type (wt) p53 protein, some of them also endow the mutant protein with oncogenic gain-of-function (GOF), facilitating cancer progression. Yet, p53 may acquire altered functionality even without being mutated; in particular, experiments with cultured cells revealed that wt p53 can be rewired to adopt mutant-like features in response to growth factors or cancer-mimicking genetic manipulations. To assess whether such rewiring also occurs in human tumors, we interrogated gene expression profiles and pathway deregulation patterns in the METABRIC breast cancer (BC) dataset as a function of TP53 gene mutation status. Harnessing the power of machine learning, we optimized a gene expression classifier for ER+Her2- patients that distinguishes tumors carrying TP53 mutations from those retaining wt TP53. Interestingly, a small subset of wt TP53 tumors displayed gene expression and pathway deregulation patterns markedly similar to those of TP53-mutated tumors. Moreover, similar to TP53 mutated tumors, these “pseudomutant” cases displayed a signature for enhanced proliferation and had worse prognosis than typical wt p53 tumors. Notably, these tumors revealed upregulation of genes which, in BC cell lines, were reported to be positively regulated by p53 GOF mutants. Thus, such tumors may benefit from mutant p53-associated activities without having to accrue TP53 mutations.
{"title":"Transcriptional profiling reveals a subset of human breast tumors that retain wt TP53 but display mutant p53‐associated features","authors":"Gal Benor, G. Fuks, S. Chin, O. Rueda, Saptaparna Mukherjee, Sharathchandra Arandkar, Yael Aylon, C. Caldas, E. Domany, M. Oren","doi":"10.1101/2020.04.30.070037","DOIUrl":"https://doi.org/10.1101/2020.04.30.070037","url":null,"abstract":"TP53 gene mutations are very common in human cancer. While such mutations abrogate the tumor suppressive activities of the wild type (wt) p53 protein, some of them also endow the mutant protein with oncogenic gain-of-function (GOF), facilitating cancer progression. Yet, p53 may acquire altered functionality even without being mutated; in particular, experiments with cultured cells revealed that wt p53 can be rewired to adopt mutant-like features in response to growth factors or cancer-mimicking genetic manipulations. To assess whether such rewiring also occurs in human tumors, we interrogated gene expression profiles and pathway deregulation patterns in the METABRIC breast cancer (BC) dataset as a function of TP53 gene mutation status. Harnessing the power of machine learning, we optimized a gene expression classifier for ER+Her2- patients that distinguishes tumors carrying TP53 mutations from those retaining wt TP53. Interestingly, a small subset of wt TP53 tumors displayed gene expression and pathway deregulation patterns markedly similar to those of TP53-mutated tumors. Moreover, similar to TP53 mutated tumors, these “pseudomutant” cases displayed a signature for enhanced proliferation and had worse prognosis than typical wt p53 tumors. Notably, these tumors revealed upregulation of genes which, in BC cell lines, were reported to be positively regulated by p53 GOF mutants. Thus, such tumors may benefit from mutant p53-associated activities without having to accrue TP53 mutations.","PeriodicalId":51134,"journal":{"name":"Molecular Oncology","volume":"132 1","pages":"1640 - 1652"},"PeriodicalIF":6.6,"publicationDate":"2020-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76176650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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