Ellinor Johnsson (Former)
1 – 13 of 13
- show: 20
- |
- sort: year (new to old)
Close
Embed this list
<iframe src=" "
width=" "
height=" "
allowtransparency="true"
frameborder="0">
</iframe>
- 2019
-
Mark
Essential genes shape cancer genomes through linear limitation of homozygous deletions
(
- Contribution to journal › Article
- 2018
-
Mark
The multiple myeloma risk allele at 5q15 lowers ELL2 expression and increases ribosomal gene expression
(
- Contribution to journal › Article
-
Mark
Identification of multiple risk loci and regulatory mechanisms influencing susceptibility to multiple myeloma
(
- Contribution to journal › Article
- 2017
-
Mark
Direct evidence for a polygenic etiology in familial multiple myeloma
(
- Contribution to journal › Article
-
Mark
Identification of sequence variants influencing immunoglobulin levels
(
- Contribution to journal › Article
- 2016
-
Mark
Genome-wide association study identifies multiple susceptibility loci for multiple myeloma
(
- Contribution to journal › Article
- 2015
-
Mark
Variants in ELL2 influencing immunoglobulin levels associate with multiple myeloma.
(
- Contribution to journal › Article
- 2014
-
Mark
Robust isolation of malignant plasma cells in multiple myeloma.
(
- Contribution to journal › Article
- 2012
-
Mark
The retinoblastoma gene undergoes rearrangements in BRCA1-deficient basal-like breast cancer.
(
- Contribution to journal › Article
- 2006
-
Mark
Neutrophil elastase sorting involves plasma membrane trafficking requiring the C-terminal propeptide.
(
- Contribution to journal › Article
- 1998
-
Mark
p53-dependent and -independent differentiation of leukemic U-937 cells : relationship to cell cycle control
(
- Contribution to journal › Article
- 1997
-
Mark
Altered expression of the retinoblastoma tumor-suppressor gene in leukemic cell lines inhibits induction of differentiation but not G1-accumulation
(
- Contribution to journal › Article
-
Mark
The tumor suppressor gene p53 can mediate transforming growth [corrected] factor beta1-induced differentiation of leukemic cells independently of activation of the retinoblastoma protein
(
- Contribution to journal › Article