scholarly journals Epigenetic reprogramming by naïve conditions establishes an irreversible state of partial X chromosome reactivation in female stem cells

Oncotarget ◽  
2018 ◽  
Vol 9 (38) ◽  
pp. 25136-25147 ◽  
Author(s):  
Alexandra V. Panova ◽  
Alexandra N. Bogomazova ◽  
Maria A. Lagarkova ◽  
Sergey L. Kiselev
2011 ◽  
Vol 22 (4) ◽  
pp. 336-342 ◽  
Author(s):  
Daniel H. Kim ◽  
Yesu Jeon ◽  
Montserrat C. Anguera ◽  
Jeannie T. Lee

2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Antonia A. Dominguez ◽  
H. Rosaria Chiang ◽  
Meena Sukhwani ◽  
Kyle E. Orwig ◽  
Renee A. Reijo Pera

Development ◽  
2016 ◽  
Vol 143 (16) ◽  
pp. 2958-2964 ◽  
Author(s):  
Shin Kobayashi ◽  
Yusuke Hosoi ◽  
Hirosuke Shiura ◽  
Kazuo Yamagata ◽  
Saori Takahashi ◽  
...  

2020 ◽  
Vol 14 (5) ◽  
pp. 745-754 ◽  
Author(s):  
Susmita Mandal ◽  
Deepshikha Chandel ◽  
Harman Kaur ◽  
Sudeshna Majumdar ◽  
Maniteja Arava ◽  
...  

2017 ◽  
Vol 4 (7) ◽  
pp. 54-54 ◽  
Author(s):  
Shafqat A. Khan ◽  
Pauline N. C. B. Audergon ◽  
Bernhard Payer

2014 ◽  
Vol 10 (4) ◽  
pp. 472-479 ◽  
Author(s):  
Juliana Andrea de Oliveira Georges ◽  
Naja Vergani ◽  
Simone Aparecida Siqueira Fonseca ◽  
Ana Maria Fraga ◽  
Joana Carvalho Moreira de Mello ◽  
...  

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 4058-4058
Author(s):  
Andres C Garcia-Montero ◽  
Maria Jara-Acevedo ◽  
Ivan Alvarez-Twose ◽  
Cristina Teodosio ◽  
Laura Sanchez-Muñoz ◽  
...  

Abstract PURPOSE: Multilineageinvolvement of bone marrow (BM) hematopoiesis by the somatic KIT D816V mutation is present in a subset of adult indolent systemic mastocytosis (ISM) patients in association with a poorer prognosis. Here we investigated the potential involvement of BM mesenchymal stem cells (MSC) from ISM patients by the KIT D816V mutation and its potential impact on disease progression and outcome. METHODS: The KIT D816V mutation was investigated in highly-purified BM MSC and other BM cell populations from 83 ISM patients followed for a median of 116 months. MC clonality was further evaluated in female patients by the pattern of inactivation of the X chromosome (XCIP). RESULTS: KIT D816V-mutated MSC were detected in 22/83 (27%) ISM patients. All MSC-mutated patients had multilineage KIT mutation (100% vs. 30%, p=0.0001) and they more frequently showed involvement of lymphoid plus myeloid BM cells (59% vs 22%; P =.03) and a polyclonal XCIP of the KIT- mutated BM MC (64% vs 0%; P =0.01) vs other multilineage ISM cases. Moreover, presence of KIT D816V-mutated MSC was associated with more advanced disease features of ISM, a greater rate of disease progression (50% vs 17%; P =.04) and a shorter progression-free survival at 10, 20 and 30 years (P ≤.003). CONCLUSION: Overall, these results support the notion that ISM patients with mutated MSC may have acquired the KIT mutation in a common pluripotent progenitor cell, prior to differentiation into MSC and hematopoietic precursor cells, before the X-chromosome inactivation process occurs. From a clinical point of view, acquisition of the KIT mutation in an earlier BM precursor cell confers a significantly greater risk for disease progression and a poorer outcome. Disclosures No relevant conflicts of interest to declare.


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