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Melanie J. McConnell

Researcher at Victoria University of Wellington

Publications -  47
Citations -  6220

Melanie J. McConnell is an academic researcher from Victoria University of Wellington. The author has contributed to research in topics: Glioma & Repressor. The author has an hindex of 23, co-authored 45 publications receiving 5155 citations. Previous affiliations of Melanie J. McConnell include Vanderbilt University & Mount Sinai Hospital.

Papers
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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Early epigenetic changes and DNA damage do not predict clinical response in an overlapping schedule of 5-azacytidine and entinostat in patients with myeloid malignancies

Tamer E. Fandy, +22 more
- 24 Sep 2009 - 
TL;DR: Methylation reversal of candidate TSGs during cycle 1 of therapy was not predictive of clinical response to combination "epigenetic" therapy.
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Aberrant eukaryotic translation initiation factor 4E-dependent mRNA transport impedes hematopoietic differentiation and contributes to leukemogenesis.

Ivan Topisirovic, +7 more
- 15 Dec 2003 - 
TL;DR: It is demonstrated that elevated eIF4E impedes granulocytic and monocytic differentiation and can contribute to leukemogenesis by promoting growth and by impeding differentiation.
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Growth suppression by acute promyelocytic leukemia-associated protein PLZF is mediated by repression of c-myc expression.

Melanie J. McConnell, +6 more
- 15 Dec 2003 - 
TL;DR: The data suggest that PLZF expression maintains a cell in a quiescent state by repressing c-myc expression and preventing cell cycle progression, which would have serious consequences for cell growth control.
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Side population is not necessary or sufficient for a cancer stem cell phenotype in glioblastoma multiforme.

Kate W.R. Broadley, +9 more
- 01 Mar 2011 - 
TL;DR: It is demonstrated that the GBM SP does not necessarily contribute to self‐renewal or tumor initiation, key properties of a CSC, and it is advised against using SP to enumerate or isolate CSC.