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Christina Curtis
Stanford University
86Publications
26H-index
8,491Citations
Publications 86
Newest
#1Jennifer L. Caswell-Jin (Stanford University)H-Index: 5
#2Katherine McNamara (Stanford University)H-Index: 2
Last.Christina Curtis (Stanford University)H-Index: 26
view all 20 authors...
The original version of this Article omitted from the Author Contributions statement that ‘R.S. and J.G.R contributed equally to this work.’ This has been corrected in both the PDF and HTML versions of the Article.
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#1Michael P. Menden (AstraZeneca)H-Index: 8
#2Dennis Wang (University of Sheffield)H-Index: 13
Last.Manuela ZucknickH-Index: 1
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The effectiveness of most cancer targeted therapies is short-lived. Tumors often develop resistance that might be overcome with drug combinations. However, the number of possible combinations is vast, necessitating data-driven approaches to find optimal patient-specific treatments. Here we report AstraZeneca’s large drug combination dataset, consisting of 11,576 experiments from 910 combinations across 85 molecularly characterized cancer cell lines, and results of a DREAM Challenge to evaluate c...
13 CitationsSource
#1Jennifer L. Caswell-Jin (Stanford University)H-Index: 5
#2Katherine McNamara (Stanford University)H-Index: 2
Last.Christina Curtis (Stanford University)H-Index: 26
view all 20 authors...
Genomic changes observed across treatment may result from either clonal evolution or geographically disparate sampling of heterogeneous tumors. Here we use computational modeling based on analysis of fifteen primary breast tumors and find that apparent clonal change between two tumor samples can frequently be explained by pre-treatment heterogeneity, such that at least two regions are necessary to detect treatment-induced clonal shifts. To assess for clonal replacement, we devise a summary stati...
4 CitationsSource
#1Zheng Hu (Stanford University)H-Index: 15
#2Zan Li (SU: Southern University and A&M College)
Last.Christina Curtis (Stanford University)H-Index: 26
view all 4 authors...
Metastasis is the primary cause of cancer-related deaths, but the natural history, clonal evolution and patterns of systemic spread are poorly understood. We analyzed exome sequencing data from 458 paired primary tumors (P) or metastasis (M) samples from 136 breast, colorectal and lung cancer patients, including both untreated (n=98) and treated (n=101) metastases. We find that treated metastases often harbored private driver gene mutations whereas untreated metastases did not, suggesting that t...
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#1Susanne Tilk (Stanford University)H-Index: 3
#2Christina Curtis (Stanford University)H-Index: 26
Last.Christopher D. McFarland (Stanford University)H-Index: 9
view all 4 authors...
Cancer genomes exhibit surprisingly weak signatures of negative selection1,2. This may be because tumors evolve either under very weak selective pressures (weak selection) or under conditions that prevent the elimination of many deleterious passenger mutations (poor efficacy of selection). The weak selection model argues that the majority of genes are only important for multicellular function. The poor efficacy of selection model argues, in contrast, that genome-wide linkage in cancer prevents m...
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#1Kathryn E. Yost (Stanford University)H-Index: 4
#2Ansu Satpathy (Stanford University)H-Index: 25
Last.Howard Y. ChangH-Index: 137
view all 16 authors...
Immunotherapies that block inhibitory checkpoint receptors on T cells have transformed the clinical care of patients with cancer1. However, whether the T cell response to checkpoint blockade relies on reinvigoration of pre-existing tumor-infiltrating lymphocytes or on recruitment of novel T cells remains unclear2–4. Here we performed paired single-cell RNA and T cell receptor sequencing on 79,046 cells from site-matched tumors from patients with basal or squamous cell carcinoma before and after ...
14 CitationsSource
#1Zheng Hu (Stanford University)H-Index: 15
#2Jie DingH-Index: 7
Last.Christina Curtis (Stanford University)H-Index: 26
view all 15 authors...
Both the timing and molecular determinants of metastasis are unknown, hindering treatment and prevention efforts. Here we characterize the evolutionary dynamics of this lethal process by analyzing exome-sequencing data from 118 biopsies from 23 patients with colorectal cancer with metastases to the liver or brain. The data show that the genomic divergence between the primary tumor and metastasis is low and that canonical driver genes were acquired early. Analysis within a spatial tumor growth mo...
4 CitationsSource
#1Jose A. Seoane (Stanford University)H-Index: 14
#2Jacob G. Kirkland (Stanford University)H-Index: 12
Last.Christina Curtis (Stanford University)H-Index: 26
view all 5 authors...
The aim of this study is to determine the effect of chromatin regulators on anthracycline response in breast cancer. Anthracyclines are a highly effective component of curative breast cancer chemotherapy, but can be associated with substantial side effects. Because anthracyclines work in part via inhibition of topoisomerase II (TOP2) on accessible DNA, we hypothesized that expression levels of chromatin regulatory proteins that mediate DNA accessibility might predict anthracycline response. We u...
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#1Michael F. Press (SC: University of Southern California)H-Index: 73
#2Jose A. Seoane (Stanford University)H-Index: 14
Last.Dennis J. Slamon (UCLA: University of California, Los Angeles)H-Index: 98
view all 17 authors...
Importance The 2013/2014 American Society of Clinical Oncology and College of American Pathologists (ASCO-CAP) guidelines forHER2testing by fluorescence in situ hybridization (FISH) designated an “equivocal” category (averageHER2copies per tumor cell ≥4-6 withHER2/CEP17 ratio Objective To evaluate the following hypotheses: (1) genetic loci used as alternative controls are heterozygously deleted in a substantial proportion of breast cancers; (2) use of these loci for assessment ofHER2by FISH lead...
3 CitationsSource
#1Oscar M. Rueda (University of Cambridge)H-Index: 26
#2Stephen John Sammut (University of Cambridge)H-Index: 10
Last.Christina Curtis (Stanford University)H-Index: 26
view all 24 authors...
The rates and routes of lethal systemic spread in breast cancer are poorly understood owing to a lack of molecularly characterized patient cohorts with long-term, detailed follow-up data. Long-term follow-up is especially important for those with oestrogen-receptor (ER)-positive breast cancers, which can recur up to two decades after initial diagnosis1–6. It is therefore essential to identify patients who have a high risk of late relapse7–9. Here we present a statistical framework that models di...
13 CitationsSource
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