Genomic Analysis of the Clonal Origins of Relapsed Acute Lymphoblastic Leukemia
By C. Mullighan, Letha A A Phillips, X. Su, Jing Ma, C. Miller, S. Shurtleff, J. Downing. Science, 2008
869 citations recorded by the source corpus.
Subfields: Hematology, Public Health, Environmental and Occupational Health
View Paper: https://www.semanticscholar.org/paper/ff4e0d98f74ed00602d0f1f558ef5347755ccf1c
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Citations in the corpus
- Rearrangement of CRLF2 in B-progenitor– and Down syndrome–associated acute lymphoblastic leukemia (2009, neutral): “Other-SNP-#33 Yes None Yes Pos Pos NA 47,XX,del(9)(p22),+21c[8]/47,XX,add(9)(p23),+21c[5]/47,XX,+ 21c[7] Down-SNP-#09 Yes IR682RG Yes Pos Pos Neg 48,XY,+X,+21c[20] Down-SNP-#10 Yes None No Neg Neg Neg 46,XX,-7,i(9)(q10),+21c[9]/46,idem,3,der(12)t(3;12)(p13;p13),+mar[4] Down-SNP-#11 Yes None No Neg N”
- Clonal evolution in relapsed acute myeloid leukemia revealed by whole genome sequencing (2012, positive): “This study extends the findings of previous studie”
- Evolution of the cancer stem cell model. (2014, background): “Genome-wide CNA profiling of paired diagnostic and relapse samples of ALL has been informative (Inaba et al., 2013; Mullighan et al., 2008).”
- Tumor heterogeneity: causes and consequences (2009, background): “However, the approach is still useful given that it allows for establishing evolutionary relationships between primary disease and relapses [55–58] and permits tracing the evolutionary history of leukemias.”
- Evolution and impact of subclonal mutations in chronic lymphocytic leukemia (2013, neutral): “Recent genomic studies have revealed that individual cancer samples are genetically heterogeneous and contain subclonal populations (Carter et al., 2012; Ding et al., 2012; Gerlinger et al., 2012; Mullighan et al., 2008; Navin et al., 2011; Nik-Zainal et al., 2012; Shah et al., 2012).”
- Cancer epigenetics: Tumor Heterogeneity, Plasticity of Stem-like States, and Drug Resistance (2014, background): “In this concept, independent subclones arise in bursts of subclonal expansion (Navin et al., 2011) that may well arise in response to pressures fromDarwinian selection—including those imposed on cancers from therapeutic intervention (Mullighan et al., 2008).”
- Biological and therapeutic impact of intratumor heterogeneity in cancer evolution. (2015, background): “Modes of Tumor Evolution and Cooperation between Tumor Subclones Longitudinal (Johnson et al., 2014; Mullighan et al., 2008; Shah et al., 2009), spatial (Aerts et al.”