M
Matthew R. Ramsey
Researcher at Brigham and Women's Hospital
Publications - 31
Citations - 4805
Matthew R. Ramsey is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Stem cell & Transcription factor. The author has an hindex of 15, co-authored 26 publications receiving 4373 citations. Previous affiliations of Matthew R. Ramsey include University of North Carolina at Chapel Hill & Harvard University.
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Journal ArticleDOI
Ink4a/Arf expression is a biomarker of aging
Janakiraman Krishnamurthy,Chad Torrice,Matthew R. Ramsey,Grigoriy I. Kovalev,Khalid A. Al-Regaiey,Lishan Su,Norman E. Sharpless +6 more
TL;DR: In this article, the authors examined the links between senescence and aging in vivo, and showed that expression of p16INK4a and Arf markedly increases in almost all rodent tissues with advancing age, while there is little or no change in the expression of related cell cycle inhibitors.
Journal ArticleDOI
LKB1 modulates lung cancer differentiation and metastasis
Hongbin Ji,Matthew R. Ramsey,D. Neil Hayes,Cheng Fan,Kate McNamara,Piotr Kozlowski,Chad Torrice,Michael C. Wu,Takeshi Shimamura,Samanthi A. Perera,Mei-Chih Liang,Dongpo Cai,George N. Naumov,Lei Bao,Cristina Contreras,Danan Li,Liang Chen,Janakiraman Krishnamurthy,Jussi Koivunen,Lucian R. Chirieac,Robert F. Padera,Roderick T. Bronson,Neal I. Lindeman,David C. Christiani,Xihong Lin,Geoffrey I. Shapiro,Pasi A. Jänne,Bruce E. Johnson,Matthew Meyerson,David J. Kwiatkowski,Diego H. Castrillon,Nabeel Bardeesy,Norman E. Sharpless,Kwok-Kin Wong +33 more
TL;DR: LKB1 is established as a critical barrier to pulmonary tumorigenesis, controlling initiation, differentiation and metastasis in lung cancer, and expression profiling in human lung cancer cell lines and mouse lung tumours identified a variety of metastasis-promoting genes as targets of LKB1 repression.
Journal ArticleDOI
p16INK4a induces an age-dependent decline in islet regenerative potential.
Janakiraman Krishnamurthy,Matthew R. Ramsey,Keith L. Ligon,Chad Torrice,Angela Koh,Susan Bonner-Weir,Norman E. Sharpless +6 more
TL;DR: The genetic data support the view that an age-induced increase of p16INK4a expression limits the regenerative capacity of β-cells with ageing and constrains islet proliferation and regeneration in anAge-dependent manner.
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A two-stage, p16(INK4A)- and p53-dependent keratinocyte senescence mechanism that limits replicative potential independent of telomere status.
James G. Rheinwald,William C. Hahn,William C. Hahn,Matthew R. Ramsey,Jenny Y. Wu,Zongyou Guo,Hensin Tsao,Michele De Luca,Caterina Catricalà,Kathleen M. O'Toole +9 more
TL;DR: It is confirmed that keratinocytes undergo p16-related senescence during growth in culture, whether in the fibroblast feeder cell system or in the specialized K-sfm medium formulation, and that this mechanism can act as a barrier to immortalization following hTERT expression.
Journal ArticleDOI
The differential impact of p16INK4a or p19ARF deficiency on cell growth and tumorigenesis
Norman E. Sharpless,Matthew R. Ramsey,Periasamy Balasubramanian,Diego H. Castrillon,Diego H. Castrillon,Ronald A. DePinho +5 more
TL;DR: The cancer-prone conditions of mice singly deficient for either p16INK4a or p19ARF agree with data derived from human cancer genetics, and reinforce the view that both gene products play significant and nonredundant roles in suppressing malignant transformation in vivo.