scispace - formally typeset
J

Jonathan M. Gerber

Researcher at University of Massachusetts Medical School

Publications -  56
Citations -  1931

Jonathan M. Gerber is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: Myeloid leukemia & Leukemia. The author has an hindex of 15, co-authored 48 publications receiving 1571 citations. Previous affiliations of Jonathan M. Gerber include Johns Hopkins University & Carolinas Healthcare System.

Papers
More filters
Journal ArticleDOI

Global 5-hydroxymethylcytosine content is significantly reduced in tissue stem/progenitor cell compartments and in human cancers

TL;DR: It is found that 5hmC was abundant in the majority of embryonic and adult tissues and closely tracked with the differentiation state of cells in hierarchically organized tissues, and5hmC levels were profoundly reduced in carcinoma of the prostate, breast and colon compared to normal tissues.
Journal ArticleDOI

A clinically relevant population of leukemic CD34(+)CD38(-) cells in acute myeloid leukemia.

TL;DR: Minimal residual disease detected during complete remission was enriched for the CD34(+)CD38(-)ALDH(int) leukemic cells, and the presence of these cells after therapy highly correlated with subsequent clinical relapse.
Journal ArticleDOI

Contributions of Pathway and Neuron to Preferential Motor Reinnervation

TL;DR: Stimulation of regenerative collateral sprouting increased preferential motor reinnervation, confirming the pruning hypothesis, but this effect was overshadowed by the dramatic specificity with which predegenerated grafts were reinnervated by fresh uncrushed proximal axons.
Journal ArticleDOI

Circulating clonotypic B cells in classic Hodgkin lymphoma.

TL;DR: It is found that both the L428 and KM-H2 HL cell lines contained rare B-cell subpopulations responsible for the generation and maintenance of the predominant HRS cell population.
Journal ArticleDOI

Regulation of human hematopoietic stem cell self-renewal by the microenvironment’s control of retinoic acid signaling

TL;DR: Primitive hematopoietic cells appear to be intrinsically programmed to undergo RA-mediated differentiation unless prevented from doing so by bone marrow niche CYP26, andModulation of RA signaling also holds promise for clinical HSC expansion, a prerequisite for the wide-scale use of these cells in regenerative medicine and gene therapy.