Scientific Literature

Jan 8, 2013

Automated Quantitative RNA in Situ Hybridization for Resolution of Equivocal and Heterogeneous ERBB2 (HER2) Status in Invasive Breast Carcinoma

Z. Wang, B. P. Portier, A. M. Gruver, S. Bui, H. Wang, N. Su, H.-T. Vo, X.-J. Ma, Y. Luo, G. T. Budd, R. R. Tubbs , The Journal of Molecular Diagnostics , DOI: 10.1016/j.jmoldx.2012.10.003
Patient management based on HER2 status in breast carcinoma is an archetypical example of personalized medicine but remains hampered by equivocal testing and intratumoral heterogeneity. We developed a fully automated, quantitative, bright-field in situ hybridization technique (RNAscope), applied it to quantify single-cell HER2 mRNA levels in 132 invasive breast carcinomas,...
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Jan 3, 2013

Acidity generated by the tumor microenvironment drives local invasion

Estrella V, Chen T, Lloyd M, Wojtkowiak J, Cornnell HH, Ibrahim-Hashim A, Bailey K, Balagurunathan Y, Rothberg JM, Sloane BF, Johnson J, Gatenby RA, Gillies RJ , Cancer Res , DOI: 10.1158/0008-5472.CAN-12-2796
The pH of solid tumors is acidic due to increased fermentative metabolism and poor perfusion. It has been hypothesized that acid pH promotes local invasive growth and metastasis. The hypothesis that acid mediates invasion proposes that H+ diffuses from the proximal tumor microenvironment into adjacent normal tissues where it causes...
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Jan 1, 2013

Protein tyrosine phosphatase 1B restrains mammary alveologenesis and secretory differentiation

Milani ES, Brinkhaus H, Dueggeli R, Klebba I, Mueller U, Stadler M, Kohler H, Smalley MJ, Bentires-Alj M , Development , Volume 140, pp. 117-125
Tyrosine phosphorylation plays a fundamental role in mammary gland development. However, the role of specific tyrosine phosphatases in controlling mammary cell fate remains ill defined. We have identified protein tyrosine phosphatase 1B (PTP1B) as an essential regulator of alveologenesis and lactogenesis. PTP1B depletion increased the number of luminal mammary progenitors...
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Dec 31, 2012

The central role and mechanisms of β-cell dysfunction and death in Friedreich's ataxia-associated diabetes

M. Cnop MD PhD, M. Igoillo-Esteve PhD, M. Rai PhD, A. Begu MD, Y. Serroukh MD, C. Depondt MD PhD, A. E. Musuaya, I. Marhfour PhD, L. Ladrière PhD, X. Moles Lopez, D. Lefkaditis PhD, F. Moore PhD, J.-P. Brion MD PhD, J M. Cooper MD PhD, A. H. V. Schapira MD PhD, A. Clark PhD, A. H. Koeppen MD, P. Marchetti MD PhD, M. Pandolfo MD PhD, D. L Eizirik MD PhD, F. Féry MD PhD , Annals of neurology , DOI: 10.1002/ana.23698
Objective: Friedreich ataxia (FRDA) is an autosomal recessive neurodegenerative disease caused in almost all cases by homozygosity for a GAA trinucleotide repeat expansion in the frataxin gene. Frataxin is a mitochondrial protein involved in iron homeostasis. FRDA patients have a high prevalence of diabetes, the pathogenesis of which is not...
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Dec 7, 2012

p27Kip1 Directly Represses Sox2 during Embryonic Stem Cell Differentiation

H. Li, M. Collado, A. Villasante, A. Matheu, C. J. Lynch, M. Cañamero, K. Rizzoti, C. Carneiro, G. Martínez, A. Vidal, R. Lovell-Badge, M. Serrano , Cell Stem Cell , DOI: 10.1016/j.stem.2012.09.01
The mechanisms responsible for the transcriptional silencing of pluripotency genes in differentiated cells are poorly understood. We have observed that cells lacking the tumor suppressor p27 can be reprogrammed into induced pluripotent stem cells (iPSCs) in the absence of ectopic Sox2. Interestingly, cells and tissues from p27 null mice, including...
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