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Article ; Online: An integrated omics approach highlights how epigenetic events can explain and predict response to neoadjuvant chemotherapy and bevacizumab in breast cancer.

Fleischer, Thomas / Haugen, Mads Haugland / Ankill, Jørgen / Silwal-Pandit, Laxmi / Børresen-Dale, Anne-Lise / Hedenfalk, Ingrid / Hatschek, Thomas / Tost, Jörg / Engebraaten, Olav / Kristensen, Vessela N

Molecular oncology

2024

Abstract: Treatment with the anti-angiogenic drug bevacizumab in addition to chemotherapy has shown efficacy for breast cancer in some clinical trials, but better biomarkers are needed to optimally select patients for treatment. Here, we present an omics approach ... ...

Abstract	Treatment with the anti-angiogenic drug bevacizumab in addition to chemotherapy has shown efficacy for breast cancer in some clinical trials, but better biomarkers are needed to optimally select patients for treatment. Here, we present an omics approach where DNA methylation profiles are integrated with gene expression and results from proteomic data in breast cancer patients to predict response to therapy and pinpoint response-related epigenetic events. Fresh-frozen tumor biopsies taken before, during, and after treatment from human epidermal growth factor receptor 2 negative non-metastatic patients receiving neoadjuvant chemotherapy with or without bevacizumab were subjected to molecular profiling. Here, we report that DNA methylation at enhancer CpGs related to cell cycle regulation can predict response to chemotherapy and bevacizumab for the estrogen receptor positive subset of patients (AUC = 0.874), and we validated this observation in an independent patient cohort with a similar treatment regimen (AUC = 0.762). Combining the DNA methylation scores with the scores from a previously published protein signature resulted in a slight increase in the prediction performance (AUC = 0.784). We also show that tumors receiving the combination treatment underwent more extensive epigenetic alterations. Finally, we performed an integrative expression-methylation quantitative trait loci analysis on alterations in DNA methylation and gene expression levels, showing that the epigenetic alterations that occur during treatment are different between responders and non-responders and that these differences may be explained by the proliferation-epithelial-to-mesenchymal transition axis through the activity of grainyhead like transcription factor 2. Using tumor purity computed from copy number data, we developed a method for estimating cancer cell-specific methylation to confirm that the association to response reflects DNA methylation in cancer cells. Taken together, these results support the potential for clinical benefit of the addition of bevacizumab to chemotherapy when administered to the correct patients.
Language	English
Publishing date	2024-04-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2415106-3
ISSN	1878-0261 ; 1574-7891
ISSN (online)	1878-0261
ISSN	1574-7891
DOI	10.1002/1878-0261.13656
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Article ; Online: A

Nygaard, Vigdis / Ree, Anne Hansen / Dagenborg, Vegar Johansen / Børresen-Dale, Anne-Lise / Edwin, Bjørn / Fretland, Åsmund Avdem / Grzyb, Krzysztof / Haugen, Mads H / Mælandsmo, Gunhild M / Flatmark, Kjersti

Cancer research communications

2023 Volume 3, Issue 2, Page(s) 235–244

Abstract: Disease recurrence and drug resistance are major challenges in the clinical management of patients with colorectal cancer liver metastases (CLM), and because tumors are generally microsatellite stable (MSS), responses to immune therapies are poor. The ... ...

Abstract	Disease recurrence and drug resistance are major challenges in the clinical management of patients with colorectal cancer liver metastases (CLM), and because tumors are generally microsatellite stable (MSS), responses to immune therapies are poor. The mesenchymal phenotype is overrepresented in treatment-resistant cancers and is associated with an immunosuppressed microenvironment. The aim of this work was to molecularly identify and characterize a mesenchymal subgroup of MSS CLM to identify novel therapeutic approaches. We here generated a mesenchymal gene expression signature by analysis of resection specimens from 38 patients with CLM using ranked expression level of the epithelial-to-mesenchymal transition-related transcription factor Significance: CLM is an important cause of colorectal cancer mortality where the majority of patients have yet to benefit from immunotherapies. In this study of gene expression profiling analyses, we uncovered novel immune checkpoint targets in a subgroup of patients with MSS CLMs harboring a mesenchymal phenotype.
MeSH term(s)	Humans ; B7-H1 Antigen/genetics ; Hepatitis A Virus Cellular Receptor 2/genetics ; Programmed Cell Death 1 Receptor/genetics ; Neoplasm Recurrence, Local/genetics ; Colorectal Neoplasms/genetics ; Liver Neoplasms/genetics ; Microsatellite Repeats ; Tumor Microenvironment/genetics ; Homeodomain Proteins/genetics
Chemical Substances	B7-H1 Antigen ; Hepatitis A Virus Cellular Receptor 2 ; Programmed Cell Death 1 Receptor ; PRRX1 protein, human ; Homeodomain Proteins
Language	English
Publishing date	2023-02-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2767-9764
ISSN (online)	2767-9764
DOI	10.1158/2767-9764.CRC-22-0295
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Article ; Online: TP53 Mutations in Breast and Ovarian Cancer.

Silwal-Pandit, Laxmi / Langerød, Anita / Børresen-Dale, Anne-Lise

Cold Spring Harbor perspectives in medicine

2017 Volume 7, Issue 1

Abstract: Breast and ovarian cancers are the second and fifth leading causes of cancer deaths among women. Both breast and ovarian cancers are highly heterogeneous and are presented with diverse morphology, natural history, and response to therapy. In recent years, ...

Abstract	Breast and ovarian cancers are the second and fifth leading causes of cancer deaths among women. Both breast and ovarian cancers are highly heterogeneous and are presented with diverse morphology, natural history, and response to therapy. In recent years, international efforts have led to extensive molecular characterization of both breast and ovarian tumors and identified biologically and clinically relevant subtypes of the diseases based on these molecular features. The role of TP53 in tumor initiation and progression is context dependent, and abrogation of the TP53 pathway seems to be essential for the development of basal-like breast cancers and high-grade serous ovarian cancers. These subtypes of breast and ovarian cancer show several genomic similarities including high frequency of TP53 mutation, which seems to be an early, initiating, and driving alteration in these cancer subtypes.
MeSH term(s)	Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Mutation ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; Tumor Suppressor Protein p53/genetics
Chemical Substances	TP53 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2017-01-03
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2157-1422
ISSN (online)	2157-1422
DOI	10.1101/cshperspect.a026252
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Article ; Online: Cis-regulatory mutations associate with transcriptional and post-transcriptional deregulation of gene regulatory programs in cancers.

Castro-Mondragon, Jaime A / Aure, Miriam Ragle / Lingjærde, Ole Christian / Langerød, Anita / Martens, John W M / Børresen-Dale, Anne-Lise / Kristensen, Vessela N / Mathelier, Anthony

Nucleic acids research

2022 Volume 50, Issue 21, Page(s) 12131–12148

Abstract: Most cancer alterations occur in the noncoding portion of the human genome, where regulatory regions control gene expression. The discovery of noncoding mutations altering the cells' regulatory programs has been limited to few examples with high ... ...

Abstract	Most cancer alterations occur in the noncoding portion of the human genome, where regulatory regions control gene expression. The discovery of noncoding mutations altering the cells' regulatory programs has been limited to few examples with high recurrence or high functional impact. Here, we show that transcription factor binding sites (TFBSs) have similar mutation loads to those in protein-coding exons. By combining cancer somatic mutations in TFBSs and expression data for protein-coding and miRNA genes, we evaluate the combined effects of transcriptional and post-transcriptional alterations on the regulatory programs in cancers. The analysis of seven TCGA cohorts culminates with the identification of protein-coding and miRNA genes linked to mutations at TFBSs that are associated with a cascading trans-effect deregulation on the cells' regulatory programs. Our analyses of cis-regulatory mutations associated with miRNAs recurrently predict 12 mature miRNAs (derived from 7 precursors) associated with the deregulation of their target gene networks. The predictions are enriched for cancer-associated protein-coding and miRNA genes and highlight cis-regulatory mutations associated with the dysregulation of key pathways associated with carcinogenesis. By combining transcriptional and post-transcriptional regulation of gene expression, our method predicts cis-regulatory mutations related to the dysregulation of key gene regulatory networks in cancer patients.
MeSH term(s)	Humans ; Gene Expression Regulation ; Neoplasms/genetics ; Mutation ; MicroRNAs/physiology ; Gene Regulatory Networks
Chemical Substances	MicroRNAs
Language	English
Publishing date	2022-12-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkac1143
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Article ; Online: Personalized Cancer Care: Risk Prediction, Early Diagnosis, Progression, and Therapy.

Zänker, Kurt S / Borresen-Dale, Anne-Lise / Huber, Hans-Peter

Biomedicine hub

2016 Volume 1, Issue 3, Page(s) 1–9

Abstract: At the annual prestigious International Symposium of the Fritz-Bender Foundation, Munich, 18-20 May, 2016, researchers, clinicians, and students discussed the state of the art and future perspectives of genomic medicine in cancer. Genomic medicine (also ... ...

Abstract	At the annual prestigious International Symposium of the Fritz-Bender Foundation, Munich, 18-20 May, 2016, researchers, clinicians, and students discussed the state of the art and future perspectives of genomic medicine in cancer. Genomic medicine (also known as precision medicine/oncology) should help clinicians to provide a more precise diagnosis and therapy in oncology for individual patients. The meeting focused on next-generation sequencing methods, analytical computational analysis of big data, and data mining on the way to translational and evidence-based medicine. The meeting covered the social and ethical impact of genomic medicine as well as news and views on antibody targeting of intracellular proteins, on the architecture of intracellular proteins and their impact on carcinogenesis, and on the adaptation of tumor therapy in due consideration of tumor evolution. Subheadings like "Genetic Profiling of Patients and Risk Prediction," "Molecular Profiling of Tumors and Metastases," "Tumor-Host Microenvironment Interaction and Metabolism," and "Targeted Therapy" were subsumed under the main heading of "Personalized Cancer Care."
Language	English
Publishing date	2016-12-13
Publishing country	Switzerland
Document type	Journal Article
ISSN	2296-6870
ISSN (online)	2296-6870
DOI	10.1159/000453253
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Article ; Online: Breast Cancer Molecular Stratification: From Intrinsic Subtypes to Integrative Clusters.

Russnes, Hege G / Lingjærde, Ole Christian / Børresen-Dale, Anne-Lise / Caldas, Carlos

The American journal of pathology

2017 Volume 187, Issue 10, Page(s) 2152–2162

Abstract: Breast carcinomas can be stratified into different entities based on clinical behavior, histologic features, and/or by biological properties. A classification of breast cancer should be based on underlying biology, which we know must be determined by the ...

Abstract	Breast carcinomas can be stratified into different entities based on clinical behavior, histologic features, and/or by biological properties. A classification of breast cancer should be based on underlying biology, which we know must be determined by the somatic genomic landscape of mutations. Moreover, because the latest generations of anticancer agents are founded on biological mechanisms, a detailed molecular stratification is a requirement for appropriate clinical management. Such stratification, based on genomic drivers, will be important for selecting patients for clinical trials. It will also facilitate the discovery of novel drivers, the study of tumor evolution, and the identification of mechanisms of treatment resistance. Assays for risk stratification have focused mainly on response prediction to existing treatment regimens. Molecular stratification based on gene expression profiling revealed that breast cancers could be classified in so-called intrinsic subtypes (luminal A and B, HER2-enriched, basal-like, and normal-like), which mostly corresponded to hormone receptor and HER2 status, and further stratified luminal tumors based on proliferation. The realization that a significant proportion of the gene expression landscape is determined by the somatic copy number alterations that drive expression in cis led to the newer classification of breast cancers into integrative clusters. This stratification of breast cancers into integrative clusters reveals prototypical patterns of single-nucleotide variants and is associated with distinct clinical courses and response to therapy.
MeSH term(s)	Breast Neoplasms/classification ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; DNA Copy Number Variations/genetics ; Female ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; Humans ; Multilevel Analysis ; Mutation/genetics
Language	English
Publishing date	2017-07-19
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2017.04.022
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Article ; Online: PathTracer: High-sensitivity detection of differential pathway activity in tumours.

Nygård, Ståle / Lingjærde, Ole Christian / Caldas, Carlos / Hovig, Eivind / Børresen-Dale, Anne-Lise / Helland, Åslaug / Haakensen, Vilde D

Scientific reports

2019 Volume 9, Issue 1, Page(s) 16332

Abstract: Gene expression profiling of tumours is an important source of information for cancer patient stratification. Detecting subtle alterations of gene expression remains a challenge, however. Here, we propose a novel tool for high-sensitivity detection of ... ...

Abstract	Gene expression profiling of tumours is an important source of information for cancer patient stratification. Detecting subtle alterations of gene expression remains a challenge, however. Here, we propose a novel tool for high-sensitivity detection of differential pathway activity in tumours. For a pathway defined by a collection of genes, the samples are projected onto a low-dimensional manifold in the subspace spanned by those genes. For each sample, a score is next found by calculating the distance between each projected sample and the projection of a subgroup of reference samples. Depending on the aim of the analysis and the available data, the reference samples may represent e.g. normal tissue or tumour samples with a particular genotype or phenotype. The proposed tool, PathTracer, is demonstrated on gene expression data from 1952 invasive breast cancer samples, 10 DCIS, 9 benign samples and 144 tumour adjacent normal breast tissue samples. PathTracer scores are shown to predict survival, clinical subtypes, cellular proliferation and genomic instability. Furthermore, predictions are shown to outperform those obtained with other comparable methods.
MeSH term(s)	Breast Neoplasms/genetics ; Computational Biology/methods ; Gene Expression Profiling ; Mutation ; Oligonucleotide Array Sequence Analysis ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2019-11-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-52529-3
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Article ; Online: Protein Signature Predicts Response to Neoadjuvant Treatment With Chemotherapy and Bevacizumab in HER2-Negative Breast Cancers.

Haugen, Mads H / Lingjærde, Ole Christian / Hedenfalk, Ingrid / Garred, Øystein / Borgen, Elin / Loman, Niklas / Hatschek, Thomas / Børresen-Dale, Anne-Lise / Naume, Bjørn / Mills, Gordon B / Mælandsmo, Gunhild M / Engebraaten, Olav

JCO precision oncology

2021 Volume 5

Abstract: Purpose: Antiangiogenic therapy using bevacizumab has proven effective for a number of cancers; however, in breast cancer (BC), there is an unmet need to identify patients who benefit from such treatment.: Patients and methods: In the NeoAva phase II ...

Abstract	Purpose: Antiangiogenic therapy using bevacizumab has proven effective for a number of cancers; however, in breast cancer (BC), there is an unmet need to identify patients who benefit from such treatment. Patients and methods: In the NeoAva phase II clinical trial, patients (N = 132) with large (≥ 25 mm) human epidermal growth factor receptor 2 (HER2)-negative primary tumors were randomly assigned 1:1 to treatment with neoadjuvant chemotherapy (CTx) alone or in combination with bevacizumab (Bev plus CTx). The ratio of the tumor size after relative to before treatment was calculated into a continuous response scale. Tumor biopsies taken prior to neoadjuvant treatment were analyzed by reverse-phase protein arrays (RPPA) for expression levels of 210 BC-relevant (phospho-) proteins. Lasso regression was used to derive a predictor of tumor shrinkage from the expression of selected proteins prior to treatment. Results: We identified a nine-protein signature score named vascular endothelial growth factor inhibition response predictor (ViRP) for use in the Bev plus CTx treatment arm able to predict with accuracy pathologic complete response (pCR) (area under the curve [AUC] = 0.85; 95% CI, 0.74 to 0.97) and low residual cancer burden (RCB 0/I) (AUC = 0.80; 95% CI, 0.68 to 0.93). The ViRP score was significantly lower in patients with pCR ( Conclusion: Our ViRP score, integrating the expression of nine proteins and validated on mRNA data both internally and in an independent clinical trial, may be used to increase the likelihood of benefit from treatment with bevacizumab combined with chemotherapy in patients with HER2-negative BC.
MeSH term(s)	Antineoplastic Agents, Immunological/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Bevacizumab/therapeutic use ; Breast Neoplasms/chemistry ; Breast Neoplasms/drug therapy ; Female ; Humans ; Neoadjuvant Therapy ; Neoplasm Proteins ; Predictive Value of Tests ; Receptor, ErbB-2/analysis ; Treatment Outcome
Chemical Substances	Antineoplastic Agents, Immunological ; Neoplasm Proteins ; Bevacizumab (2S9ZZM9Q9V) ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1)
Language	English
Publishing date	2021-01-28
Publishing country	United States
Document type	Clinical Trial, Phase II ; Journal Article ; Randomized Controlled Trial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2473-4284
ISSN (online)	2473-4284
DOI	10.1200/PO.20.00086
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Article ; Online: Crosstalk between microRNA expression and DNA methylation drives the hormone-dependent phenotype of breast cancer.

Aure, Miriam Ragle / Fleischer, Thomas / Bjørklund, Sunniva / Ankill, Jørgen / Castro-Mondragon, Jaime A / Børresen-Dale, Anne-Lise / Tost, Jörg / Sahlberg, Kristine K / Mathelier, Anthony / Tekpli, Xavier / Kristensen, Vessela N

Genome medicine

2021 Volume 13, Issue 1, Page(s) 72

Abstract: Background: Abnormal DNA methylation is observed as an early event in breast carcinogenesis. However, how such alterations arise is still poorly understood. microRNAs (miRNAs) regulate gene expression at the post-transcriptional level and play key roles ...

Abstract	Background: Abnormal DNA methylation is observed as an early event in breast carcinogenesis. However, how such alterations arise is still poorly understood. microRNAs (miRNAs) regulate gene expression at the post-transcriptional level and play key roles in various biological processes. Here, we integrate miRNA expression and DNA methylation at CpGs to study how miRNAs may affect the breast cancer methylome and how DNA methylation may regulate miRNA expression. Methods: miRNA expression and DNA methylation data from two breast cancer cohorts, Oslo2 (n = 297) and The Cancer Genome Atlas (n = 439), were integrated through a correlation approach that we term miRNA-methylation Quantitative Trait Loci (mimQTL) analysis. Hierarchical clustering was used to identify clusters of miRNAs and CpGs that were further characterized through analysis of mRNA/protein expression, clinicopathological features, in silico deconvolution, chromatin state and accessibility, transcription factor binding, and long-range interaction data. Results: Clustering of the significant mimQTLs identified distinct groups of miRNAs and CpGs that reflect important biological processes associated with breast cancer pathogenesis. Notably, two major miRNA clusters were related to immune or fibroblast infiltration, hence identifying miRNAs associated with cells of the tumor microenvironment, while another large cluster was related to estrogen receptor (ER) signaling. Studying the chromatin landscape surrounding CpGs associated with the estrogen signaling cluster, we found that miRNAs from this cluster are likely to be regulated through DNA methylation of enhancers bound by FOXA1, GATA2, and ER-alpha. Further, at the hub of the estrogen cluster, we identified hsa-miR-29c-5p as negatively correlated with the mRNA and protein expression of DNA methyltransferase DNMT3A, a key enzyme regulating DNA methylation. We found deregulation of hsa-miR-29c-5p already present in pre-invasive breast lesions and postulate that hsa-miR-29c-5p may trigger early event abnormal DNA methylation in ER-positive breast cancer. Conclusions: We describe how miRNA expression and DNA methylation interact and associate with distinct breast cancer phenotypes.
MeSH term(s)	Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Chromatin/metabolism ; CpG Islands/genetics ; DNA Methylation/genetics ; DNA Methyltransferase 3A/metabolism ; Enhancer Elements, Genetic/genetics ; Female ; Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks ; Hormones/pharmacology ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Molecular Sequence Annotation ; Multigene Family ; Phenotype ; Quantitative Trait Loci/genetics
Chemical Substances	Chromatin ; Hormones ; MicroRNAs ; DNA Methyltransferase 3A (EC 2.1.1.37)
Language	English
Publishing date	2021-04-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2484394-5
ISSN	1756-994X ; 1756-994X
ISSN (online)	1756-994X
ISSN	1756-994X
DOI	10.1186/s13073-021-00880-4
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Article ; Online: TP53 and breast cancer.

Børresen-Dale, Anne-Lise

Human mutation

2003 Volume 21, Issue 3, Page(s) 292–300

Abstract: The TP53 gene (p53) is found altered in breast carcinomas in approximately 20-40% of all cases depending on tumor size and stage of the disease. It seems to be an early event in breast tumorigenesis. Several polymorphisms in the TP53 gene have been ... ...

Abstract	The TP53 gene (p53) is found altered in breast carcinomas in approximately 20-40% of all cases depending on tumor size and stage of the disease. It seems to be an early event in breast tumorigenesis. Several polymorphisms in the TP53 gene have been detected and their possible roles in breast cancer risk and association to type of cancer developed are discussed. The different mutation spectra seen in geographical and ethnic populations may be used to identify environmental exposure contributing to breast cancer development. The role of TP53 mutation as a prognostic marker is reviewed as well as its role as a predictor for therapy response. All data available on TP53 mutation analyses of human breast carcinomas, as well data from transgenic animal studies and experimental cell studies, support an important role for TP53 in mammary carcinogenesis.
MeSH term(s)	Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Female ; Humans ; Mutation ; Prognosis ; Risk Factors ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2003-03
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1126646-6
ISSN	1098-1004 ; 1059-7794
ISSN (online)	1098-1004
ISSN	1059-7794
DOI	10.1002/humu.10174
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