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30 results on '"Sackmann Sala, Lucila"'

1. Ponatinib evaluation and safety in real-life chronic myelogenous leukemia patients failing more than two tyrosine kinase inhibitors: the PEARL observational study

Author

Heiblig, Maël, Rea, Delphine, Chrétien, Marie-Lorraine, Charbonnier, Aude, Rousselot, Philippe, Coiteux, Valérie, Escoffre-Barbe, Martine, Dubruille, Viviane, Huguet, Françoise, Cayssials, Emilie, Hermet, Eric, Guerci-Bresler, Agnès, Amé, Shanti, Sackmann-Sala, Lucila, Roy, Lydia, Sobh, Mohamad, Morisset, Stéphane, Etienne, Gabriel, and Nicolini, Franck E.

Published
2018
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2. Prolactin-Induced Prostate Tumorigenesis

Author

Sackmann-Sala, Lucila, Goffin, Vincent, Cohen, Irun R., Series editor, Lajtha, N.S. Abel, Series editor, Paoletti, Rodolfo, Series editor, Lambris, John D., Series editor, and Diakonova, PhD, Maria, editor

Published
2015
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5. A rare castration‐resistant progenitor cell population is highly enriched in Pten‐null prostate tumours

Author

Sackmann Sala, Lucila, Boutillon, Florence, Menara, Giulia, De Goyon‐Pélard, Andréa, Leprévost, Mylène, Codzamanian, Julie, Lister, Natalie, Pencik, Jan, Clark, Ashlee, Cagnard, Nicolas, Bole‐Feysot, Christine, Moriggl, Richard, Risbridger, Gail P, Taylor, Renea A, Kenner, Lukas, Guidotti, Jacques‐Emmanuel, and Goffin, Vincent

Published
2017
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29. STAT5a/b Deficiency Delays, but does not Prevent, Prolactin-Driven Prostate Tumorigenesis in Mice.

Author

Boutillon, Florence, Pigat, Natascha, Sackmann Sala, Lucila, Reyes-Gomez, Edouard, Moriggl, Richard, Guidotti, Jacques-Emmanuel, and Goffin, Vincent

Subjects
CARCINOGENESIS, ANIMAL experimentation, CARRIER proteins, CELLULAR signal transduction, EPITHELIAL cells, GENE expression, GENETIC polymorphisms, MICE, PROLACTIN, PHENOTYPES, DISEASE progression, PROSTATE tumors, TUMOR risk factors, PREVENTION
Abstract

The canonical prolactin (PRL) Signal Transducer and Activator of Transcription (STAT) 5 pathway has been suggested to contribute to human prostate tumorigenesis via an autocrine/paracrine mechanism. The probasin (Pb)-PRL transgenic mouse models this mechanism by overexpressing PRL specifically in the prostate epithelium leading to strong STAT5 activation in luminal cells. These mice exhibit hypertrophic prostates harboring various pre-neoplastic lesions that aggravate with age and accumulation of castration-resistant stem/progenitor cells. As STAT5 signaling is largely predominant over other classical PRL-triggered pathways in Pb-PRL prostates, we reasoned that Pb-Cre recombinase-driven genetic deletion of a floxed Stat5a/b locus should prevent prostate tumorigenesis in so-called Pb-PRLΔSTAT5 mice. Anterior and dorsal prostate lobes displayed the highest Stat5a/b deletion efficiency with no overt compensatory activation of other PRLR signaling cascade at 6 months of age; hence the development of tumor hallmarks was markedly reduced. Stat5a/b deletion also reversed the accumulation of stem/progenitor cells, indicating that STAT5 signaling regulates prostate epithelial cell hierarchy. Interestingly, ERK1/2 and AKT, but not STAT3 and androgen signaling, emerged as escape mechanisms leading to delayed tumor development in aged Pb-PRLΔSTAT5 mice. Unexpectedly, we found that Pb-PRL prostates spontaneously exhibited age-dependent decline of STAT5 signaling, also to the benefit of AKT and ERK1/2 signaling. As a consequence, both Pb-PRL and Pb-PRLΔSTAT5 mice ultimately displayed similar pathological prostate phenotypes at 18 months of age. This preclinical study provides insight on STAT5-dependent mechanisms of PRL-induced prostate tumorigenesis and alternative pathways bypassing STAT5 signaling down-regulation upon prostate neoplasia progression. [ABSTRACT FROM AUTHOR]

Published
2019
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30. Depot-Specific Differences in White Adipose Tissue of Wild-Type and GHR-/- Mice of Different Ages

Author

Sackmann Sala, Lucila

Subjects
Molecular Biology, Adipose tissue depots, insulin sensitivity, obesity, proteomics, aging, growth hormone
Abstract

White adipose tissue (WAT) produces many hormones and cytokines with various functions, such as glucose homeostasis, inflammation, and hemostasis, among others. The contributions of individual WAT depots to these functions differ, such that intra-abdominal depots correlate more closely than subcutaneous depots with obesity-related disorders (insulin resistance, type 2 diabetes, cardiovascular disease, etc.). However, the molecular mechanisms behind these depot-specific differences and their relation to age are not well understood. Growth hormone receptor gene-disrupted (GHR-/-) mice are dwarf and display enhanced insulin sensitivity and prolonged longevity in spite of obesity. The accumulation of WAT in GHR-/- mice is mainly in subcutaneous depots; thus, these mice represent a useful tool to study depot-specific effects on insulin responsiveness and lifespan. To analyze depot- and age-related differences in protein expression in WAT depots of GHR-/- and wild-type mice, four WAT depots (inguinal, retroperitoneal, mesenteric, and epididymal) of 12 and 24-month-old male mice of each genotype were resolved by two-dimensional gel electrophoresis and subsequent mass spectrometry. Comparisons among wild-type WAT depots showed differences in the levels of many proteins, including metabolic enzymes and stress-resistant proteins that were higher in epididymal and mesenteric depots and lower in inguinal (subcutaneous) WAT. Also, several protein levels were consistent with higher vascularization in mesenteric WAT than in the other depots. On the other hand, age-related changes in WAT depots suggested higher aerobic glucose oxidation, lipolysis and oxidative damage at old age. Interestingly, depot- and age-related variations in protein levels were similar between wild-type and GHR-/- mice. However, genotype differences were found in the expression of proteins related to senescence and glucose uptake, among others. In conclusion, WAT depots display marked differences in their proteomes that are affected similarly with advancing age (e.g. increased insulin resistance and oxidative damage). In addition, altered senescence-related processes in WAT depots of GHR-/- mice may contribute to the favorable phenotype observed in these animals. Our results provide valuable information about WAT physiology in different depots and ages of wild-type and GHR-/- mice. Specific proteins shown to vary in this study may represent targets for treatment of age-associated insulin resistance, oxidative damage, and other WAT-related pathologies.

Published
2010

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