scispace - formally typeset
Search or ask a question
Institution

University of Massachusetts Medical School

EducationWorcester, Massachusetts, United States
About: University of Massachusetts Medical School is a education organization based out in Worcester, Massachusetts, United States. It is known for research contribution in the topics: Population & Health care. The organization has 16161 authors who have published 31822 publications receiving 1909739 citations. The organization is also known as: UMass Medical School.


Papers
More filters
Journal ArticleDOI
TL;DR: It is suggested that interactions with RISC dictate siRNA localization even when siRNA is conjugated to TAT(47-57) peptide, which was distinctly different from nonconjugated free TAT peptide nucleolar localization.

412 citations

Journal ArticleDOI
TL;DR: A growing body of evidence indicates that centrosomes might not be essential for spindle assembly, whereas recent data indicate that they might be important for initiating S phase and completing cytokinesis.
Abstract: Over the past 100 years, the centrosome has risen in status from an enigmatic organelle, located at the focus of microtubules, to a key player in cell-cycle progression and cellular control. A growing body of evidence indicates that centrosomes might not be essential for spindle assembly, whereas recent data indicate that they might be important for initiating S phase and completing cytokinesis. Molecules that regulate centrosome duplication have been identified, and the expanding list of intriguing centrosome-anchored activities, the functions of which have yet to be determined, promises continued discovery.

412 citations

Journal ArticleDOI
TL;DR: The goals of these experiments are to obtain a clearer behavioral profile of genetically/phenotypically distant mouse strains after UCMS treatment and to evaluate the limitations and strengths of the UCMS model in mice.

411 citations

Journal ArticleDOI
22 Dec 2016-Nature
TL;DR: This work identifies a mechanism for early dissemination in which Her2 aberrantly activates a program similar to mammary ductal branching that generates eDCCs that are capable of forming metastasis after a dormancy phase.
Abstract: Metastasis is the leading cause of cancer-related deaths; metastatic lesions develop from disseminated cancer cells (DCCs) that can remain dormant. Metastasis-initiating cells are thought to originate from a subpopulation present in progressed, invasive tumours. However, DCCs detected in patients before the manifestation of breast-cancer metastasis contain fewer genetic abnormalities than primary tumours or than DCCs from patients with metastases. These findings, and those in pancreatic cancer and melanoma models, indicate that dissemination might occur during the early stages of tumour evolution. However, the mechanisms that might allow early disseminated cancer cells (eDCCs) to complete all steps of metastasis are unknown. Here we show that, in early lesions in mice and before any apparent primary tumour masses are detected, there is a sub-population of Her2+p-p38lop-Atf2loTwist1hiE-cadlo early cancer cells that is invasive and can spread to target organs. Intra-vital imaging and organoid studies of early lesions showed that Her2+ eDCC precursors invaded locally, intravasated and lodged in target organs. Her2+ eDCCs activated a Wnt-dependent epithelial-mesenchymal transition (EMT)-like dissemination program but without complete loss of the epithelial phenotype, which was reversed by Her2 or Wnt inhibition. Notably, although the majority of eDCCs were Twist1hiE-cadlo and dormant, they eventually initiated metastasis. Our work identifies a mechanism for early dissemination in which Her2 aberrantly activates a program similar to mammary ductal branching that generates eDCCs that are capable of forming metastasis after a dormancy phase.

411 citations

Journal ArticleDOI
TL;DR: The need to better understand the mechanisms linking visceral adiposity with liver fat accumulation, the mechanisms by which ectopic fat accumulation cause insulin resistance, and the size of adipose tissue depots is determined is underscored.
Abstract: Purpose of review The association between obesity and insulin resistance is an area of much interest and enormous public health impact, with hundreds of articles being published in the last year focused on the possible mechanisms that underlie this association. The purpose to this review is to highlight some of the key recent literature with emphasis on emerging concepts.

411 citations


Authors

Showing all 16331 results

NameH-indexPapersCitations
Michael Karin236704226485
Richard A. Flavell2311328205119
Robert M. Califf1961561167961
Eric J. Topol1931373151025
Joan Massagué189408149951
Stuart H. Orkin186715112182
Ramachandran S. Vasan1721100138108
Mark Gerstein168751149578
David R. Jacobs1651262113892
Bruce L. Miller1631153115975
Yuh Nung Jan16246074818
Christopher J. O'Donnell159869126278
David W. Bates1591239116698
Adi F. Gazdar157776104116
John E. Morley154137797021
Network Information
Related Institutions (5)
National Institutes of Health
297.8K papers, 21.3M citations

97% related

University of California, San Francisco
186.2K papers, 12M citations

97% related

Brigham and Women's Hospital
110.5K papers, 6.8M citations

96% related

Emory University
122.4K papers, 6M citations

96% related

Yale University
220.6K papers, 12.8M citations

95% related

Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202341
2022241
20212,038
20201,960
20191,734
20181,653