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Accueil Nota Bene Cancer V2 Numéro 131 du 11 Avril 2012 Biologie

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Nota Bene Cancer Numéro 131 du 11 Avril 2012 RSS

Biologie

Aberrations chromosomiques

Menée sur des échantillons prélevés sur 29 patientes atteintes d'un carcinome canalaire in situ (CCIS), 26 patientes atteintes d'un carcinome canalaire invasif (CCI) et 23 patientes atteintes de CCIS et CCI synchrones, cette étude analyse la fréquence des mutations de la région D310 de l'ADN mitochondrial

  • Mitochondrial D310 mutations in the early development of breast cancer
    British Journal of Cancer, sous presse, 2012 (résumé)
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    Menée sur des échantillons prélevés sur 29 patientes atteintes d'un carcinome canalaire in situ (CCIS), 26 patientes atteintes d'un carcinome canalaire invasif (CCI) et 23 patientes atteintes de CCIS et CCI synchrones, cette étude analyse la fréquence des mutations de la région D310 de l'ADN mitochondrial

    “Mitochondrial D310 mutations in the early development of breast cancer”

    • Xu, C.;Tran-Thanh, D.;Ma, C.;May, K.;Jung, J.;Vecchiarelli, J.;Done, S. J.

    Background: The role of mitochondrial DNA (mtDNA) mutations in the development of breast cancer is largely unknown. In this study, we investigated the frequency and pattern of mutations in the D310 region, the most commonly mutated region in mtDNA, in a series of breast lesions. Methods: Using capillary electrophoresis, we genotyped the D310 sequence of neoplastic epithelial cells from 23 patients with synchronous ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC), 26 patients with IDC only and 29 patients with DCIS only. Results: A majority of DCIS (68.4%) and IDC (71.4%) lesions harbour different D310 sequences compared with their matched normal control. Specific D310 sequences were more frequently identified in tumour samples (77.1% of DCIS and 75.5% of IDC) compared with normal tissues (35.3% of normal; P<0.0001). No difference was identified between DCIS lesions with synchronous IDC and those from pure DCIS cases. In five cases, histologically normal tissue ...


Mots clés : Sein; Biologie (Aberrations chromosomiques)

Menée sur 104 échantillons tumoraux prélevés sur des patientes atteintes d'un cancer primitif du sein triplement négatif, cette étude met en évidence un large spectre d'évolution génomique dans ces tumeurs

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    Menée sur 104 échantillons tumoraux prélevés sur des patientes atteintes d'un cancer primitif du sein triplement négatif, cette étude met en évidence un large spectre d'évolution génomique dans ces tumeurs

    “The clonal and mutational evolution spectrum of primary triple-negative breast cancers”

    • Shah, Sohrab P.;Roth, Andrew;Goya, Rodrigo;Oloumi, Arusha;Ha, Gavin;Zhao, Yongjun;Turashvili, Gulisa;Ding, Jiarui;Tse, Kane;Haffari, Gholamreza;Bashashati, Ali;Prentice, Leah M.;Khattra, Jaswinder;Burleigh, Angela;Yap, Damian;Bernard, Virginie;McPherson, Andrew;Shumansky, Karey;Crisan, Anamaria;Giuliany, Ryan;Heravi-Moussavi, Alireza;Rosner, Jamie;Lai, Daniel;Birol, Inanc;Varhol, Richard;Tam, Angela;Dhalla, Noreen;Zeng, Thomas;Ma, Kevin;Chan, Simon K.;Griffith, Malachi;Moradian, Annie;Cheng, S. W. Grace;Morin, Gregg B.;Watson, Peter;Gelmon, Karen;Chia, Stephen;Chin, Suet-Feung;Curtis, Christina;Rueda, Oscar M.;Pharoah, Paul D.;Damaraju, Sambasivarao;Mackey, John;Hoon, Kelly;Harkins, Timothy;Tadigotla, Vasisht;Sigaroudinia, Mahvash;Gascard, Philippe;Tlsty, Thea;Costello, Joseph F.;Meyer, Irmtraud M.;Eaves, Connie J.;Wasserman, Wyeth W.;Jones, Steven;Huntsman, David;Hirst, Martin;Caldas, Carlos;Marra, Marco A.;Aparicio, Samuel

    Primary triple-negative breast cancers (TNBCs), a tumour type defined by lack of oestrogen receptor, progesterone receptor and ERBB2 gene amplification, represent approximately 16% of all breast cancers. Here we show in 104 TNBC cases that at the time of diagnosis these cancers exhibit a wide and continuous spectrum of genomic evolution, with some having only a handful of coding somatic aberrations in a few pathways, whereas others contain hundreds of coding somatic mutations. High-throughput RNA sequencing (RNA-seq) revealed that only approximately 36% of mutations are expressed. Using deep re-sequencing measurements of allelic abundance for 2,414 somatic mutations, we determine for the first time—to our knowledge—in an epithelial tumour subtype, the relative abundance of clonal frequencies among cases representative of the population. We show that TNBCs vary widely in their clonal frequencies at the time of diagnosis, with the basal subtype of TNBC2, 3 showing more variation ...


Mots clés : Sein; Biologie (Aberrations chromosomiques)

Menée sur des échantillons tumoraux prélevés sur 15 patients atteints d'un adénocarcinome gastrique, cette étude de séquençage des exons met en évidence des mutations somatiques de gènes impliqués dans le remodelage de la chromatine et l'adhérence cellulaire

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    Menée sur des échantillons tumoraux prélevés sur 15 patients atteints d'un adénocarcinome gastrique, cette étude de séquençage des exons met en évidence des mutations somatiques de gènes impliqués dans le remodelage de la chromatine et l'adhérence cellulaire

    “Exome sequencing of gastric adenocarcinoma identifies recurrent somatic mutations in cell adhesion and chromatin remodeling genes”

    • Zang, Zhi Jiang;Cutcutache, Ioana;Poon, Song Ling;Zhang, Shen Li;McPherson, John R.;Tao, Jiong;Rajasegaran, Vikneswari;Heng, Hong Lee;Deng, Niantao;Gan, Anna;Lim, Kiat Hon;Ong, Choon Kiat;Huang, DaChuan;Chin, Sze Yung;Tan, Iain Beehuat;Ng, Cedric Chuan Young;Yu, Willie;Wu, Yingting;Lee, Minghui;Wu, Jeanie;Poh, Dianne;Wan, Wei Keat;Rha, Sun Young;So, Jimmy;Salto-Tellez, Manuel;Yeoh, Khay Guan;Wong, Wai Keong;Zhu, Yi-Jun;Futreal, P. Andrew;Pang, Brendan;Ruan, Yijun;Hillmer, Axel M.;Bertrand, Denis;Nagarajan, Niranjan;Rozen, Steve;Teh, Bin Tean;Tan, Patrick

    Gastric cancer is a major cause of global cancer mortality. We surveyed the spectrum of somatic alterations in gastric cancer by sequencing the exomes of 15 gastric adenocarcinomas and their matched normal DNAs. Frequently mutated genes in the adenocarcinomas included TP53 (11/15 tumors), PIK3CA (3/15) and ARID1A (3/15). Cell adhesion was the most enriched biological pathway among the frequently mutated genes. A prevalence screening confirmed mutations in FAT4, a cadherin family gene, in 5% of gastric cancers (6/110) and FAT4 genomic deletions in 4% (3/83) of gastric tumors. Frequent mutations in chromatin remodeling genes (ARID1A, MLL3 and MLL) also occurred in 47% of the gastric cancers. We detected ARID1A mutations in 8% of tumors (9/110), which were associated with concurrent PIK3CA mutations and microsatellite instability. In functional assays, we observed both FAT4 and ARID1A to exert tumor-suppressor activity. Somatic inactivation of FAT4 and ARID1A may thus be key tumorigenic ...


Mots clés : Estomac; Biologie (Aberrations chromosomiques)

Oncogènes et suppresseurs de tumeurs

Menée sur un modèle murin, cette étude met en évidence un mécanisme de régulation d'une tumorigenèse de la prostate impliquant un gène suppresseur de tumeurs, Nkx3.1, et un oncogène, Myc

  • Nkx3.1 and Myc crossregulate shared target genes in mouse and human prostate tumorigenesis
    The Journal of Clinical Investigation, sous presse, 2012 (article en libre accès)
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    Menée sur un modèle murin, cette étude met en évidence un mécanisme de régulation d'une tumorigenèse de la prostate impliquant un gène suppresseur de tumeurs, Nkx3.1, et un oncogène, Myc

    “Nkx3.1 and Myc crossregulate shared target genes in mouse and human prostate tumorigenesis”

    • Anderson, Philip D.;McKissic, Sydika A.;Logan, Monica;Roh, Meejeon;Franco, Omar E.;Wang, Jie;Doubinskaia, Irina;Meer, Riet van der;Hayward, Simon W.;Eischen, Christine M.;Eltoum, Isam-Eldin;Abdulkadir, Sarki A.

    Cooperativity between oncogenic mutations is recognized as a fundamental feature of malignant transformation, and it may be mediated by synergistic regulation of the expression of pro- and antitumorigenic target genes. However, the mechanisms by which oncogenes and tumor suppressors coregulate downstream targets and pathways remain largely unknown. Here, we used ChIP coupled to massively parallel sequencing (ChIP-seq) and gene expression profiling in mouse prostates to identify direct targets of the tumor suppressor Nkx3.1. Further analysis indicated that a substantial fraction of Nkx3.1 target genes are also direct targets of the oncoprotein Myc. We also showed that Nkx3.1 and Myc bound to and crossregulated shared target genes in mouse and human prostate epithelial cells and that Nkx3.1 could oppose the transcriptional activity of Myc. Furthermore, loss of Nkx3.1 cooperated with concurrent overexpression of Myc to promote prostate cancer in transgenic mice. In human prostate cancer ...


Mots clés : Prostate; Biologie (Oncogènes et suppresseurs de tumeurs)

Menée in vitro et in vivo, cette étude montre que l'activité des facteurs de transcription de la famille Gli est nécessaire au développement d'une tumeur du pancréas lié à l'activation du gène Kras

  • The activity of Gli transcription factors is essential for Kras-induced pancreatic tumorigenesis
    Proceedings of the National Academy of Sciences, sous presse, 2012 (résumé)
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    Menée in vitro et in vivo, cette étude montre que l'activité des facteurs de transcription de la famille Gli est nécessaire au développement d'une tumeur du pancréas lié à l'activation du gène Kras

    “The activity of Gli transcription factors is essential for Kras-induced pancreatic tumorigenesis”

    • Rajurkar, Mihir;De Jesus-Monge, Wilfredo E.;Driscoll, David R.;Appleman, Victoria A.;Huang, He;Cotton, Jennifer L.;Klimstra, David S.;Zhu, Lihua J.;Simin, Karl;Xu, Lan;McMahon, Andrew P.;Lewis, Brian C.;Mao, Junhao

    Pancreatic ductal adenocarcinoma (PDAC), one of the most aggressive human malignancies, is thought to be initiated by KRAS activation. Here we find that transcriptional activation mediated by the Gli family of transcription factors, although dispensable for pancreatic development, is required for Kras-induced proliferation and survival in primary pancreatic epithelial cells in culture and for Kras-driven pancreatic intraepithelial neoplasia and PDAC formation in vivo. Further, ectopic Gli1 activation in the mouse pancreas accelerates Kras-driven tumor formation, underscoring the importance of Gli transcription factors in pancreatic tumorigenesis. Interestingly, we demonstrate Gli-regulated I-kappa-B kinase epsilon (IKBKE) and NF-κB activity in pancreatic cancer cells and show that this activity is a critical downstream mediator for Gli-dependent PDAC cell transformation and survival. Together, these studies demonstrate the requirement for Gli in Kras-dependent pancreatic epithelial ...


Mots clés : Pancréas; Biologie (Oncogènes et suppresseurs de tumeurs)

Menée sur des lignées cellulaires de cancer du pancréas, cette étude met en évidence un mécanisme par lequel la chimiokine CXCL12 active la co-expression des récepteurs CXCR4 et CXCR7

  • Chemokine CXCL12 activates dual CXCR4 and CXCR7-mediated signaling pathways in pancreatic cancer cells
    Journal of Translational Medicine, Vol. 10 (1), pp. 68, 2012 (article en libre accès)
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    Menée sur des lignées cellulaires de cancer du pancréas, cette étude met en évidence un mécanisme par lequel la chimiokine CXCL12 active la co-expression des récepteurs CXCR4 et CXCR7

    “Chemokine CXCL12 activates dual CXCR4 and CXCR7-mediated signaling pathways in pancreatic cancer cells”

    • Heinrich, Eileen;Lee, Wendy;Lu, Jianming;Lowy, Andrew;Kim, Joseph

    BACKGROUND:Previously assumed to be a select ligand for chemokine receptor CXCR4, chemokine CXCL12 is now known to activate both CXCR4 and CXCR7. However, very little is known about the co-expression of these receptors in cancer cells.METHODS:We used immunohistochemistry to determine the extent of co-expression in pancreatic cancer tissue samples and immunoblotting to verify expression in pancreatic cancer cell lines. In cell culture studies, siRNA was used to knock down expression of CXCR4, CXCR7, K-Ras and beta-arrestin 2 prior to stimulating the cells with CXCL12. Activation of the mitogen-activated protein kinase pathway (MAPK) was assessed using both a Raf-pull down assay and western blotting. The involvement of the receptors in CXCL12-mediated increases in cell proliferation was examined via an ATP-based proliferation assay.RESULTS:First, we discovered frequent CXCR4/CXCR7 co-expression in human pancreatic cancer tissues and cell lines. Next, we observed consistent increases in ...


Mots clés : Pancréas; Biologie (Oncogènes et suppresseurs de tumeurs)

Cette étude évalue un nouveau modèle murin où, à l'instar des tumeurs chez l'humain, la 15-lipoxygénase-1 est sous-exprimée dans les tissus tumoraux se développant dans le côlon

  • Effects of Gut-Targeted 15-LOX-1 Transgene Expression on Colonic Tumorigenesis in Mice
    Journal of the National Cancer Institute, sous presse, 2012 (résumé)
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    Cette étude évalue un nouveau modèle murin où, à l'instar des tumeurs chez l'humain, la 15-lipoxygénase-1 est sous-exprimée dans les tissus tumoraux se développant dans le côlon

    “Effects of Gut-Targeted 15-LOX-1 Transgene Expression on Colonic Tumorigenesis in Mice”

    • Zuo, Xiangsheng;Peng, Zhanglong;Wu, Yuanqing;Moussalli, Micheline J.;Yang, Xiu L.;Wang, Yan;Parker-Thornburg, Jan;Morris, Jeffrey S.;Broaddus, Russell R.;Fischer, Susan M.;Shureiqi, Imad

    Expression of 15-lipoxygenase-1 (15-LOX-1) is decreased in many human cancers; however, the mechanistic significance of its decreased expression has been difficult to determine because its mouse homolog 12/15-LOX has opposing functions. We generated a mouse model in which expression of a human 15-LOX-1 transgene was targeted to the intestinal epithelium via the villin promoter. Targeted expression was confirmed by real-time reverse transcription–polymerase chain reaction and immunoblotting. When the 15-LOX-1 transgene was expressed in colonic epithelial cells of two independent mouse lines (B6 and FVB), azoxymethane-inducible colonic tumorigenesis was suppressed (mean number of tumors: wild type [WT] = 8.2, 15-LOX-1+/− = 4.91, 15-LOX-1+/+ = 3.57; WT vs 15-LOX-1+/− two-sided P = .003, WT vs 15-LOX-1+/+ two-sided P < .001; n = 10–14 mice per group). 15-LOX-1 transgene expression was always decreased in the tumors that did develop. In the presence of expression of the 15-LOX-1 ...


  • Is 15-LOX-1 a Tumor Suppressor?
    Journal of the National Cancer Institute, sous presse, 2012 (éditorial en libre accès)
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    Cette étude évalue un nouveau modèle murin où, à l'instar des tumeurs chez l'humain, la 15-lipoxygénase-1 est sous-exprimée dans les tissus tumoraux se développant dans le côlon

    “Is 15-LOX-1 a Tumor Suppressor?”

    • Umar, Asad


Mots clés : Colon-rectum; Biologie (Oncogènes et suppresseurs de tumeurs)

Cet article passe en revue les travaux récents sur le rôle des micro-ARNs dans la biologie des cancers

  • microRNA involvement in human cancer
    Carcinogenesis, sous presse, 2012 (résumé)
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    Cet article passe en revue les travaux récents sur le rôle des micro-ARNs dans la biologie des cancers

    “microRNA involvement in human cancer”

    • Iorio, Marilena V.;Croce, Carlo M.

    When, approximately 20 years ago, investigators first determined that components of the genome considered nonfunctional had, in fact, gene regulatory capacity, they probably had no idea of their potential in controlling cell fate, and were forced to revise and somehow reorganize their view of the molecular biology.Indeed, it is currently well documented how a class of small non coding RNAs, microRNAs, are conserved among the species, expressed in different tissues and cell types, and involved in almost every biological process, including cell cycle, growth, apoptosis, differentiation, and stress response, exerting a finely tuned regulation of gene expression by targeting multiple molecules.As a consequence of the widespread range of processes they are able to influence, it is not surprising that miRNA deregulation is a hallmark of several pathological conditions, including cancer. Indeed, the aberrant expression of these tiny molecules in human tumors is not just a casual association, ...


Mots clés : Cancer (général); Biologie (Oncogènes et suppresseurs de tumeurs)

Progression et métastases

Menée à l'aide d'un modèle murin, cette étude met en évidence un mécanisme par lequel le facteur de transcription SIX1 favorise la dissémination lymphatique des cellules de cancer du sein

  • SIX1 induces lymphangiogenesis and metastasis via upregulation of VEGF-C in mouse models of breast cancer
    The Journal of Clinical Investigation, sous presse, 2012 (article en libre accès)
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    Menée à l'aide d'un modèle murin, cette étude met en évidence un mécanisme par lequel le facteur de transcription SIX1 favorise la dissémination lymphatique des cellules de cancer du sein

    “SIX1 induces lymphangiogenesis and metastasis via upregulation of VEGF-C in mouse models of breast cancer”

    • Wang, Chu-An;Jedlicka, Paul;Patrick, Aaron N.;Micalizzi, Douglas S.;Lemmer, Kimberly C.;Deitsch, Erin;Casás-Selves, Matias;Harrell, J. Chuck;Ford, Heide L.

    An association between lymph node metastasis and poor prognosis in breast cancer was observed decades ago. However, the mechanisms by which tumor cells infiltrate the lymphatic system are not completely understood. Recently, it has been proposed that the lymphatic system has an active role in metastatic dissemination and that tumor-secreted growth factors stimulate lymphangiogenesis. We therefore investigated whether SIX1, a homeodomain-containing transcription factor previously associated in breast cancer with lymph node positivity, was involved in lymphangiogenesis and lymphatic metastasis. In a model in which human breast cancer cells were injected into immune-compromised mice, we found that SIX1 expression promoted peritumoral and intratumoral lymphangiogenesis, lymphatic invasion, and distant metastasis of breast cancer cells. SIX1 induced transcription of the prolymphangiogenic factor VEGF-C, and this was required for lymphangiogenesis and lymphatic metastasis. Using a mouse ...


Mots clés : Sein; Biologie (Progression et métastases)

Menée in vitro et à l'aide de xénogreffes, cette étude met en évidence un mécanisme de régulation des cellules souches de cancer du sein par la chimiokine CCL2

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    Menée in vitro et à l'aide de xénogreffes, cette étude met en évidence un mécanisme de régulation des cellules souches de cancer du sein par la chimiokine CCL2

    “CCL2 mediates crosstalk between cancer cells and stromal fibroblasts that regulates breast cancer stem cells”

    • Tsuyada, Akihiro;Chow, Amy;Wu, Jun;Somlo, George;Chu, Peiguo;Loera, Sofia;Luu, Thehang;Li, Xuejun;Wu, Xiwei;Ye, Wei;Chen, Shiuan;Zhou, Weiying;Yu, Yang;Wang, Yuan-Zhong;Ren, Xiubao;Li, Hui;Scherle, Peggy;Kuroki, Yukio;Wang, Shizhen Emily

    Cancer stem cells (CSCs) play critical roles in cancer initiation, progression, and therapeutic refractoriness. Although many studies have focused on the genes and pathways involved in stemness, characterization of the factors in the tumor microenvironment that regulate CSCs is lacking. In this study, we investigated the effects of stromal fibroblasts on breast cancer (BC) stem cells. We found that compared to normal fibroblasts, primary cancer-associated fibroblasts (CAFs) and fibroblasts activated by co-cultured BC cells produce higher levels of chemokine (C-C motif) ligand 2 (CCL2), which stimulates the stem cell-specific, sphere-forming phenotype in BC cells and CSC self-renewal. Increased CCL2 expression in activated fibroblasts required STAT3 activation by diverse BC-secreted cytokines, and in turn, induced NOTCH1 expression and the CSC features in BC cells, constituting a "cancer-stroma-cancer" signaling circuit. In a xenograft model of paired fibroblasts and BC tumor cells, ...


Mots clés : Sein; Biologie (Progression et métastases)

Cet article passe en revue les travaux récents mettant en évidence le rôle de la réponse immunitaire face aux cellules sénescentes dans la progression d'un cancer

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    Cet article passe en revue les travaux récents mettant en évidence le rôle de la réponse immunitaire face aux cellules sénescentes dans la progression d'un cancer

    “Immune surveillance of senescent cells - biological significance in cancer- and non-cancer pathologies”

    • Hoenicke, Lisa;Zender, Lars

    Cellular senescence, a state of stable growth arrest, can occur in response to various stress stimuli such as telomere shortening, treatment with chemotherapeutic drugs or the aberrant activation of oncogenes. Senescent cells communicate with their environment by secreting various cytokines and growth factors, and it has become clear that this ‘secretory phenotype’ can have pro- as well as anti-tumorigenic effects. Recent work from our laboratory showed that premalignant, senescent hepatocytes are recognized and cleared through an antigen specific immune response and that this immune response, designated as “senescence surveillance” is crucial for tumor suppression in the liver (1). It is an emerging concept that immune responses against senescent cells have a broader biological significance in cancer- as well as non-cancer pathologies and current data suggest that distinct immune responses are engaged to clear senescent cells in different disease settings. In this review ...


Mots clés : Cancer (général); Biologie (Progression et métastases)

Ressources et infrastructures (Biologie)

Cet article passe en revue les méthodes permettant de mener des études sur des voies de signalisation fonctionnelles à partir de données génomiques

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    Cet article passe en revue les méthodes permettant de mener des études sur des voies de signalisation fonctionnelles à partir de données génomiques

    “Pathway analysis of genomic data: concepts, methods and prospects for future development”

    • Ramanan, Vijay K.;Shen, Li;Moore, Jason H.;Saykin, Andrew J.

    Genome-wide data sets are increasingly being used to identify biological pathways and networks underlying complex diseases. In particular, analyzing genomic data through sets defined by functional pathways offers the potential of greater power for discovery and natural connections to biological mechanisms. With the burgeoning availability of next-generation sequencing, this is an opportune moment to revisit strategies for pathway-based analysis of genomic data. Here, we synthesize relevant concepts and extant methodologies to guide investigators in study design and execution. We also highlight ongoing challenges and proposed solutions. As relevant analytical strategies mature, pathways and networks will be ideally placed to integrate data from diverse -omics sources to harness the extensive, rich information related to disease and treatment mechanisms.


Mots clés : Cancer (général); Biologie (Ressources et infrastructures (Biologie))

A l'aide d'un modèle statistique, cette étude montre qu'il est relativement aisé d'identifier une personne à partir de données issues d'études d'association sur le génome entier

  • On Sharing Quantitative Trait GWAS Results in an Era of Multiple-omics Data and the Limits of Genomic Privacy
    American journal of human genetics, Vol. 90 (4), pp. 591-598, 2012 (résumé)
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    A l'aide d'un modèle statistique, cette étude montre qu'il est relativement aisé d'identifier une personne à partir de données issues d'études d'association sur le génome entier

    “On Sharing Quantitative Trait GWAS Results in an Era of Multiple-omics Data and the Limits of Genomic Privacy”

    • Im, Hae Kyung;Gamazon, Eric R;Nicolae, Dan L;Cox, Nancy J

    Recent advances in genome-scale, system-level measurements of quantitative phenotypes (transcriptome, metabolome, and proteome) promise to yield unprecedented biological insights. In this environment, broad dissemination of results from genome-wide association studies (GWASs) or deep-sequencing efforts is highly desirable. However, summary results from case-control studies (allele frequencies) have been withdrawn from public access because it has been shown that they can be used for inferring participation in a study if the individual's genotype is available. A natural question that follows is how much private information is contained in summary results from quantitative trait GWAS such as regression coefficients or p values. We show that regression coefficients for many SNPs can reveal the person's participation and for participants his or her phenotype with high accuracy. Our power calculations show that regression coefficients contain as much information on individuals as allele ...


Mots clés : Cancer (général); Biologie (Ressources et infrastructures (Biologie))

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