LIVIVO - Search results -

Search results

Result 1 - 10 of total 10

Search options

Article ; Online: Mutant p53 gains oncogenic functions through a chromosomal instability-induced cytosolic DNA response

Nature Communications, Vol 15, Iss 1, Pp 1-

2024 Volume 18

Abstract: Abstract Inactivating TP53 mutations leads to a loss of function of p53, but can also often result in oncogenic gain-of-function (GOF) of mutant p53 (mutp53) proteins which promotes tumor development and progression. The GOF activities of TP53 mutations ... ...

Abstract	Abstract Inactivating TP53 mutations leads to a loss of function of p53, but can also often result in oncogenic gain-of-function (GOF) of mutant p53 (mutp53) proteins which promotes tumor development and progression. The GOF activities of TP53 mutations are well documented, but the mechanisms involved remain poorly understood. Here, we study the mutp53 interactome and find that by targeting minichromosome maintenance complex components (MCMs), GOF mutp53 predisposes cells to replication stress and chromosomal instability (CIN), leading to a tumor cell-autonomous and cyclic GMP–AMP synthase (cGAS)-stimulator of interferon genes (STING)-dependent cytosolic DNA response that activates downstream non-canonical nuclear factor kappa light chain enhancer of activated B cell (NC-NF-κB) signaling. Consequently, GOF mutp53-MCMs-CIN-cytosolic DNA-cGAS-STING-NC-NF-κB signaling promotes tumor cell metastasis and an immunosuppressive tumor microenvironment through antagonizing interferon signaling and regulating genes associated with pro-tumorigenic inflammation. Our findings have important implications for understanding not only the GOF activities of TP53 mutations but also the genome-guardian role of p53 and its inactivation during tumor development and progression.
Keywords	Science ; Q
Subject code	572
Language	English
Publishing date	2024-01-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Gene promoter hypermethylation in leukoplakia of the oral mucosa

Mingli Liu / Lei Feng / Ximing Tang

Pathology and Laboratory Medicine International, Vol 2010, Iss default, Pp 71-

2010 Volume 77

Abstract: Mingli Liu1, Lei Feng2, Ximing Tang3, Shanchun Guo41Department of Physics, Tufts University School of Medicine, Boston, Massachussetts; 2Department of Thoracic/Head and Neck Medical Oncology, 3Biostatistics, The University of Texas MD Anderson Cancer ... ...

Abstract	Mingli Liu1, Lei Feng2, Ximing Tang3, Shanchun Guo41Department of Physics, Tufts University School of Medicine, Boston, Massachussetts; 2Department of Thoracic/Head and Neck Medical Oncology, 3Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, Texas; 4Sylvester Cancer Center, University of Miami School of Medicine, Florida, USAAbstract: To examine whether aberrant DNA methylation in the promoter region might occur earlier in tumorigenesis, particularly in premalignant lesions, we examined biopsies from 111 participants in a chemoprevention trial aimed at reversal of oral leukoplakia, using methylation-specific polymerase chain reaction for the promoter regions of the tumor suppressor gene CDKN2A (p16), the putative metastasis suppressor gene for death-associated protein kinase (DAP-K), the DNA repair gene O6-methyguanine-DNA-methyltransferase (MGMT), and the detoxification gene glutathione S-transferase p1(GSTP1). p16 promoter hypermethylation was detected in 21 of 82 (25.6%), DAP-K hypermethylation in 28 of 87 (32.2%), and MGMT hypermethylation in 32 of 106 (30.2%) oral leukoplakia lesions analyzed. No aberrant methylation was found at the GSTP1 gene in 110 lesions examined. Among 68 biopsies analyzed for all three genes (p16, DAP-K, MGMT), 17 biopsies were detected with an abnormal methylation pattern at only one gene, 15 at two genes, and 8 at all three genes. Among clinical characteristics and their correlation with methylation, only alcohol consumption was correlated with DAP-K methylation (P = 0.027), while MGMT methylation was more frequent in females (P = 0.003) and nonsmokers (P = 0.0005). A significant correlation was found between p16 and DAP-K hypermethylation; p16 promoter was methylated in 14 (56%) of 25 lesions with DAP-K methylation, and only 5 (11.1%) of 45 DAP-K methylation-negative lesions (P = 0.0001). DAP-K aberrant methylation was also significantly correlated with MGMT methylation (16 of 31 in MGMT methylation-positive lesions versus 12 of 52 MGMT methylation-negative lesions, P = 0.0016). Our results suggest that epigenetic mechanisms of inactivation, such as aberrant methylation of p16, DAP-K, and MGMT genes, occur early in head and neck tumorigenesis, and might play a role in the progression of these lesions.Keywords: p16, DAP-K, MGMT, GSTP1 genes, methylation, leukoplakia
Keywords	Medicine (General) ; R5-920 ; Medicine ; R ; DOAJ:Medicine (General) ; DOAJ:Health Sciences ; Pathology ; RB1-214 ; DOAJ:Pathology
Subject code	570
Language	English
Publishing date	2010-07-01T00:00:00Z
Publisher	Dove Medical Press
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Transcriptome Deconvolution of Heterogeneous Tumor Samples with Immune Infiltration

Zeya Wang / Shaolong Cao / Jeffrey S. Morris / Jaeil Ahn / Rongjie Liu / Svitlana Tyekucheva / Fan Gao / Bo Li / Wei Lu / Ximing Tang / Ignacio I. Wistuba / Michaela Bowden / Lorelei Mucci / Massimo Loda / Giovanni Parmigiani / Chris C. Holmes / Wenyi Wang

iScience, Vol 9, Iss , Pp 451-

2018 Volume 460

Abstract: Summary: Transcriptome deconvolution in cancer and other heterogeneous tissues remains challenging. Available methods lack the ability to estimate both component-specific proportions and expression profiles for individual samples. We present DeMixT, a ... ...

Abstract	Summary: Transcriptome deconvolution in cancer and other heterogeneous tissues remains challenging. Available methods lack the ability to estimate both component-specific proportions and expression profiles for individual samples. We present DeMixT, a new tool to deconvolve high-dimensional data from mixtures of more than two components. DeMixT implements an iterated conditional mode algorithm and a novel gene-set-based component merging approach to improve accuracy. In a series of experimental validation studies and application to TCGA data, DeMixT showed high accuracy. Improved deconvolution is an important step toward linking tumor transcriptomic data with clinical outcomes. An R package, scripts, and data are available: https://github.com/wwylab/DeMixTallmaterials. : Computational Bioinformatics; Cancer; Transcriptomics Subject Areas: Computational Bioinformatics, Cancer, Transcriptomics
Keywords	Science ; Q
Language	English
Publishing date	2018-11-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: PIAS1-FAK Interaction Promotes the Survival and Progression of Non-Small Cell Lung Cancer

Jerfiz D. Constanzo / Ke-jing Tang / Smita Rindhe / Margherita Melegari / Hui Liu / Ximing Tang / Jaime Rodriguez-Canales / Ignacio Wistuba / Pier Paolo Scaglioni

Neoplasia : An International Journal for Oncology Research, Vol 18, Iss 5, Pp 282-

2016 Volume 293

Abstract: The sequence of genomic alterations acquired by cancer cells during tumor progression and metastasis is poorly understood. Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that integrates cytoskeleton remodeling, mitogenic signaling and cell ...

Abstract	The sequence of genomic alterations acquired by cancer cells during tumor progression and metastasis is poorly understood. Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that integrates cytoskeleton remodeling, mitogenic signaling and cell survival. FAK has previously been reported to undergo nuclear localization during cell migration, cell differentiation and apoptosis. However, the mechanism behind FAK nuclear accumulation and its contribution to tumor progression has remained elusive. We report that amplification of FAK and the SUMO E3 ligase PIAS1 gene loci frequently co-occur in non-small cell lung cancer (NSCLC) cells, and that both gene products are enriched in a subset of primary NSCLCs. We demonstrate that endogenous FAK and PIAS1 proteins interact in the cytoplasm and the cell nucleus of NSCLC cells. Ectopic expression of PIAS1 promotes proteolytic cleavage of the FAK C-terminus, focal adhesion maturation and FAK nuclear localization. Silencing of PIAS1 deregulates focal adhesion turnover, increases susceptibility to apoptosis in vitro and impairs tumor xenograft formation in vivo. Nuclear FAK in turn stimulates gene transcription favoring DNA repair, cell metabolism and cytoskeleton regulation. Consistently, ablation of FAK by CRISPR/Cas9 editing, results in basal DNA damage, susceptibility to ionizing radiation and impaired oxidative phosphorylation. Our findings provide insight into a mechanism regulating FAK cytoplasm-nuclear distribution and demonstrate that FAK activity in the nucleus promotes NSCLC survival and progression by increasing cell-ECM interaction and DNA repair regulation.
Keywords	Medicine ; R ; Internal medicine ; RC31-1245 ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282
Subject code	570
Publishing date	2016-05-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Corrigendum to “PIAS1-FAK Interaction Promotes the Survival and Progression of Non–Small Cell Lung Cancer” [Neoplasia 18 (2016) 282-293].

Jerfiz D. Constanzo / Ke-jing Tang / Smita Rindhe / Margherita Melegari / Hui Liu / Ximing Tang / Jaime Rodriguez-Canales / Ignacio Wistuba / Pier Paolo Scaglioni

Neoplasia: An International Journal for Oncology Research, Vol 18, Iss 7, p

2016 Volume 457

Keywords	Medicine ; R ; Internal medicine ; RC31-1245 ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282
Language	English
Publishing date	2016-07-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: ErbB2 Pathway Activation upon Smad4 Loss Promotes Lung Tumor Growth and Metastasis

Jian Liu / Sung-Nam Cho / Bindu Akkanti / Nili Jin / Jianqiang Mao / Weiwen Long / Tenghui Chen / Yiqun Zhang / Ximing Tang / Ignacio I. Wistub / Chad J. Creighton / Farrah Kheradmand / Francesco J. DeMayo

Cell Reports, Vol 10, Iss 9, Pp 1599-

2015 Volume 1613

Abstract: Lung cancer remains the leading cause of cancer death. Genome sequencing of lung tumors from patients with squamous cell carcinoma has identified SMAD4 to be frequently mutated. Here, we use a mouse model to determine the molecular mechanisms by which ... ...

Abstract	Lung cancer remains the leading cause of cancer death. Genome sequencing of lung tumors from patients with squamous cell carcinoma has identified SMAD4 to be frequently mutated. Here, we use a mouse model to determine the molecular mechanisms by which Smad4 loss leads to lung cancer progression. Mice with ablation of Pten and Smad4 in airway epithelium develop metastatic adenosquamous tumors. Comparative transcriptomic and in vivo cistromic analyses determine that loss of PTEN and SMAD4 results in ELF3 and ErbB2 pathway activation due to decreased expression of ERRFI1, a negative regulator of ERBB2 in mouse and human cells. The combinatorial inhibition of ErbB2 and Akt signaling attenuate tumor progression and cell invasion, respectively. Expression profile analysis of human lung tumors substantiated the importance of the ErbB2/Akt/ELF3 signaling pathway as both a prognostic biomarker and a therapeutic drug target for treating lung cancer.
Keywords	Biology (General) ; QH301-705.5
Language	English
Publishing date	2015-03-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Fatty Acid Oxidation Mediated by Acyl-CoA Synthetase Long Chain 3 Is Required for Mutant KRAS Lung Tumorigenesis

Mahesh S. Padanad / Georgia Konstantinidou / Niranjan Venkateswaran / Margherita Melegari / Smita Rindhe / Matthew Mitsche / Chendong Yang / Kimberly Batten / Kenneth E. Huffman / Jingwen Liu / Ximing Tang / Jaime Rodriguez-Canales / Neda Kalhor / Jerry W. Shay / John D. Minna / Jeffrey McDonald / Ignacio I. Wistuba / Ralph J. DeBerardinis / Pier Paolo Scaglioni

Cell Reports, Vol 16, Iss 6, Pp 1614-

2016 Volume 1628

Abstract: KRAS is one of the most commonly mutated oncogenes in human cancer. Mutant KRAS aberrantly regulates metabolic networks. However, the contribution of cellular metabolism to mutant KRAS tumorigenesis is not completely understood. We report that mutant ... ...

Abstract	KRAS is one of the most commonly mutated oncogenes in human cancer. Mutant KRAS aberrantly regulates metabolic networks. However, the contribution of cellular metabolism to mutant KRAS tumorigenesis is not completely understood. We report that mutant KRAS regulates intracellular fatty acid metabolism through Acyl-coenzyme A (CoA) synthetase long-chain family member 3 (ACSL3), which converts fatty acids into fatty Acyl-CoA esters, the substrates for lipid synthesis and β-oxidation. ACSL3 suppression is associated with depletion of cellular ATP and causes the death of lung cancer cells. Furthermore, mutant KRAS promotes the cellular uptake, retention, accumulation, and β-oxidation of fatty acids in lung cancer cells in an ACSL3-dependent manner. Finally, ACSL3 is essential for mutant KRAS lung cancer tumorigenesis in vivo and is highly expressed in human lung cancer. Our data demonstrate that mutant KRAS reprograms lipid homeostasis, establishing a metabolic requirement that could be exploited for therapeutic gain.
Keywords	ACSL3 ; mutant KRAS ; lung cancer ; cancer metabolism ; fatty acid oxidation ; lipid metabolism ; mouse cancer models ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2016-08-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Multiomics profiling of primary lung cancers and distant metastases reveals immunosuppression as a common characteristic of tumor cells with metastatic plasticity

Won-Chul Lee / Alexandre Reuben / Xin Hu / Nicholas McGranahan / Runzhe Chen / Ali Jalali / Marcelo V. Negrao / Shawna M. Hubert / Chad Tang / Chia-Chin Wu / Anthony San Lucas / Whijae Roh / Kenichi Suda / Jihye Kim / Aik-Choon Tan / David H. Peng / Wei Lu / Ximing Tang / Chi-Wan Chow /

Junya Fujimoto / Carmen Behrens / Neda Kalhor / Kazutaka Fukumura / Marcus Coyle / Rebecca Thornton / Curtis Gumbs / Jun Li / Chang-Jiun Wu / Latasha Little / Emily Roarty / Xingzhi Song / J. Jack Lee / Erik P. Sulman / Ganesh Rao / Stephen Swisher / Lixia Diao / Jing Wang / John V. Heymach / Jason T. Huse / Paul Scheet / Ignacio I. Wistuba / Don L. Gibbons / P. Andrew Futreal / Jianhua Zhang / Daniel Gomez / Jianjun Zhang

Genome Biology, Vol 21, Iss 1, Pp 1-

2020 Volume 21

Abstract: Abstract Background Metastasis is the primary cause of cancer mortality accounting for 90% of cancer deaths. Our understanding of the molecular mechanisms driving metastasis is rudimentary. Results We perform whole exome sequencing (WES), RNA sequencing, ...

Abstract	Abstract Background Metastasis is the primary cause of cancer mortality accounting for 90% of cancer deaths. Our understanding of the molecular mechanisms driving metastasis is rudimentary. Results We perform whole exome sequencing (WES), RNA sequencing, methylation microarray, and immunohistochemistry (IHC) on 8 pairs of non-small cell lung cancer (NSCLC) primary tumors and matched distant metastases. Furthermore, we analyze published WES data from 35 primary NSCLC and metastasis pairs, and transcriptomic data from 4 autopsy cases with metastatic NSCLC and one metastatic lung cancer mouse model. The majority of somatic mutations are shared between primary tumors and paired distant metastases although mutational signatures suggest different mutagenesis processes in play before and after metastatic spread. Subclonal analysis reveals evidence of monoclonal seeding in 41 of 42 patients. Pathway analysis of transcriptomic data reveals that downregulated pathways in metastases are mainly immune-related. Further deconvolution analysis reveals significantly lower infiltration of various immune cell types in metastases with the exception of CD4+ T cells and M2 macrophages. These results are in line with lower densities of immune cells and higher CD4/CD8 ratios in metastases shown by IHC. Analysis of transcriptomic data from autopsy cases and animal models confirms that immunosuppression is also present in extracranial metastases. Significantly higher somatic copy number aberration and allelic imbalance burdens are identified in metastases. Conclusions Metastasis is a molecularly late event, and immunosuppression driven by different molecular events, including somatic copy number aberration, may be a common characteristic of tumors with metastatic plasticity.
Keywords	Lung cancer ; Metastasis ; Multiomics ; Immune profiling ; Genomics ; DNA methylation ; Biology (General) ; QH301-705.5 ; Genetics ; QH426-470
Subject code	570
Language	English
Publishing date	2020-11-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Sex determining region Y-Box 2 (SOX2) is a potential cell-lineage gene highly expressed in the pathogenesis of squamous cell carcinomas of the lung.

Ping Yuan / Humam Kadara / Carmen Behrens / Ximing Tang / Denise Woods / Luisa M Solis / Jiaoti Huang / Monica Spinola / Wenli Dong / Guosheng Yin / Junya Fujimoto / Edward Kim / Yang Xie / Luc Girard / Cesar Moran / Waun Ki Hong / John D Minna / Ignacio I Wistuba

PLoS ONE, Vol 5, Iss 2, p e

2010 Volume 9112

Abstract: Non-small cell lung cancer (NSCLC) represents the majority (85%) of lung cancers and is comprised mainly of adenocarcinomas and squamous cell carcinomas (SCCs). The sequential pathogenesis of lung adenocarcinomas and SCCs occurs through dissimilar phases ...

Abstract	Non-small cell lung cancer (NSCLC) represents the majority (85%) of lung cancers and is comprised mainly of adenocarcinomas and squamous cell carcinomas (SCCs). The sequential pathogenesis of lung adenocarcinomas and SCCs occurs through dissimilar phases as the former tumors typically arise in the lung periphery whereas the latter normally arise near the central airway.We assessed the expression of SOX2, an embryonic stem cell transcriptional factor that also plays important roles in the proliferation of basal tracheal cells and whose expression is restricted to the main and central airways and bronchioles of the developing and adult mouse lung, in NSCLC by various methodologies. Here, we found that SOX2 mRNA levels, from various published datasets, were significantly elevated in lung SCCs compared to adenocarcinomas (all p<0.001). Moreover, a previously characterized OCT4/SOX2/NANOG signature effectively separated lung SCCs from adenocarcinomas in two independent publicly available datasets which correlated with increased SOX2 mRNA in SCCs. Immunohistochemical analysis of various histological lung tissue specimens demonstrated marked nuclear SOX2 protein expression in all normal bronchial epithelia, alveolar bronchiolization structures and premalignant lesions in SCC development (hyperplasia, dysplasia and carcinoma in situ) and absence of expression in all normal alveoli and atypical adenomatous hyperplasias. Moreover, SOX2 protein expression was greatly higher in lung SCCs compared to adenocarcinomas following analyses in two independent large TMA sets (TMA set I, n = 287; TMA set II, n = 511 both p<0.001). Furthermore, amplification of SOX2 DNA was detected in 20% of lung SCCs tested (n = 40) and in none of the adenocarcinomas (n = 17).Our findings highlight a cell-lineage gene expression pattern for the stem cell transcriptional factor SOX2 in the pathogenesis of lung SCCs and suggest a differential activation of stem cell-related pathways between squamous cell carcinomas and adenocarcinomas of the ...
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2010-02-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Oncogene mutations, copy number gains and mutant allele specific imbalance (MASI) frequently occur together in tumor cells.

Junichi Soh / Naoki Okumura / William W Lockwood / Hiromasa Yamamoto / Hisayuki Shigematsu / Wei Zhang / Raj Chari / David S Shames / Ximing Tang / Calum MacAulay / Marileila Varella-Garcia / Tõnu Vooder / Ignacio I Wistuba / Stephen Lam / Rolf Brekken / Shinichi Toyooka / John D Minna / Wan L Lam / Adi F Gazdar

PLoS ONE, Vol 4, Iss 10, p e

2009 Volume 7464

Abstract: Activating mutations in one allele of an oncogene (heterozygous mutations) are widely believed to be sufficient for tumorigenesis. However, mutant allele specific imbalance (MASI) has been observed in tumors and cell lines harboring mutations of ... ...

Abstract	Activating mutations in one allele of an oncogene (heterozygous mutations) are widely believed to be sufficient for tumorigenesis. However, mutant allele specific imbalance (MASI) has been observed in tumors and cell lines harboring mutations of oncogenes.We determined 1) mutational status, 2) copy number gains (CNGs) and 3) relative ratio between mutant and wild type alleles of KRAS, BRAF, PIK3CA and EGFR genes by direct sequencing and quantitative PCR assay in over 400 human tumors, cell lines, and xenografts of lung, colorectal, and pancreatic cancers. Examination of a public database indicated that homozygous mutations of five oncogenes were frequent (20%) in 833 cell lines of 12 tumor types. Our data indicated two major forms of MASI: 1) MASI with CNG, either complete or partial; and 2) MASI without CNG (uniparental disomy; UPD), due to complete loss of wild type allele. MASI was a frequent event in mutant EGFR (75%) and was due mainly to CNGs, while MASI, also frequent in mutant KRAS (58%), was mainly due to UPD. Mutant: wild type allelic ratios at the genomic level were precisely maintained after transcription. KRAS mutations or CNGs were significantly associated with increased ras GTPase activity, as measured by ELISA, and the two molecular changes were synergistic. Of 237 lung adenocarcinoma tumors, the small number with both KRAS mutation and CNG were associated with shortened survival.MASI is frequently present in mutant EGFR and KRAS tumor cells, and is associated with increased mutant allele transcription and gene activity. The frequent finding of mutations, CNGs and MASI occurring together in tumor cells indicates that these three genetic alterations, acting together, may have a greater role in the development or maintenance of the malignant phenotype than any individual alteration.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2009-10-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

To top

Full text online

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Inter-library loan at ZB MED