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  • Kimbung, SikerLund University,Lunds universitet,Create Health,Annan verksamhet, LTH,Lunds Tekniska Högskola,Bröstcancer - prevention & intervention,Forskargrupper vid Lunds universitet,Other operations, LTH,Faculty of Engineering, LTH,Breast cancer prevention & intervention,Lund University Research Groups,Skåne University Hospital (author)

Assessment of early response biomarkers in relation to long-term survival in patients with HER2-negative breast cancer receiving neoadjuvant chemotherapy plus bevacizumab : Results from the Phase II PROMIX trial

  • Article/chapterEnglish2018

Publisher, publication year, extent ...

  • 2017-10-13
  • Wiley,2018

Numbers

  • LIBRIS-ID:oai:lup.lub.lu.se:7c1fed99-8fba-4fec-848f-3c46b9d72c5b
  • https://lup.lub.lu.se/record/7c1fed99-8fba-4fec-848f-3c46b9d72c5bURI
  • https://doi.org/10.1002/ijc.31070DOI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:137267453URI

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  • Language:English
  • Summary in:English

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  • Subject category:art swepub-publicationtype
  • Subject category:ref swepub-contenttype

Notes

  • Pathologic complete response (pCR) is a predictor for favorable outcome after neoadjuvant treatment in early breast cancer. Modulation of gene expression may also provide early readouts of biological activity and prognosis, offering the possibility for timely response-guided treatment adjustment. The role of early transcriptional changes in predicting response to neoadjuvant chemotherapy plus bevacizumab was investigated. One-hundred-and-fifty patients with large, operable and locally advanced HER2-negative breast cancer received epirubicin and docetaxel, with the addition of bevacizumab. Patients underwent tumor biopsies at baseline, after Cycle 2 and at the time of surgery. The primary end point, pCR, and its relation with the secondary endpoints event-free survival (EFS), overall survival (OS) and gene expression profiles, are reported. The pCR rate was 13% (95% CI 8.6-20.2), with significantly more pCRs among triple-negative [28% (95% CI 14.8-45.4)] than among hormone receptor positive (HR+) tumors [9% (95% CI 4.6-16.3); (OR=3.9 [CI=1.5-10.3])]. pCR rates were not associated with EFS or OS. PAM50 subtypes significantly changed after Cycle 2 (p=0.03) and an index of absolute changes in PAM50 correlations between these time-points was associated with EFS [HR=0.62 (CI=0.3-1.1)]. In univariable analyses, signatures for angiogenesis, proliferation, estrogen receptor signaling, invasion and metastasis, and immune response, measured after Cycle 2, were associated with pCR in HR+ tumors. Evaluation of changes in molecular subtypes and other signatures early in the course of neoadjuvant treatment may be predictive of pCR and EFS. These factors may help guide further treatment and should be considered when designing neoadjuvant trials.

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  • Markholm, IdaSkåne University Hospital,Lund University (author)
  • Bjöhle, JudithKarolinska University Hospital (author)
  • Lekberg, TobiasKarolinska University Hospital (author)
  • Wachenfeldt, von AnnaKarolinska University Hospital (author)
  • Azavedo, EdwardKarolinska University Hospital (author)
  • Saracco, ArielKarolinska University Hospital (author)
  • Hellström, MatsKarolinska University Hospital (author)
  • Veerla, SrinivasLund University,Lunds universitet,Bröstcancer-genetik,Sektion I,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Breastcancer-genetics,Section I,Department of Clinical Sciences, Lund,Faculty of Medicine,Skåne University Hospital(Swepub:lu)klin-sve (author)
  • Paquet, EricSwiss Federal Institute of Technology (author)
  • Bendahl, Pär OlaLund University,Lunds universitet,Bröstcancer-genetik,Sektion I,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Individuell Bröstcancerbehandling,Forskargrupper vid Lunds universitet,Breastcancer-genetics,Section I,Department of Clinical Sciences, Lund,Faculty of Medicine,Personalized Breast Cancer Treatment,Lund University Research Groups,Skåne University Hospital(Swepub:lu)onk-pbe (author)
  • Fernö, MårtenLund University,Lunds universitet,Bröstcancer-genetik,Sektion I,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Individuell Bröstcancerbehandling,Forskargrupper vid Lunds universitet,Breastcancer-genetics,Section I,Department of Clinical Sciences, Lund,Faculty of Medicine,Personalized Breast Cancer Treatment,Lund University Research Groups,Skåne University Hospital(Swepub:lu)onk-mfe (author)
  • Bergh, JonasKarolinska Institutet,Karolinska University Hospital (author)
  • Loman, NiklasLund University,Lunds universitet,Tumörmikromiljö,Sektion I,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Bröstcancer-genetik,Institutionen för kliniska vetenskaper, Lund,Tumor microenvironment,Section I,Department of Clinical Sciences, Lund,Faculty of Medicine,Breastcancer-genetics,Department of Clinical Sciences, Lund,Skåne University Hospital(Swepub:lu)onk-nlo (author)
  • Hatschek, ThomasKarolinska Institutet,Karolinska University Hospital (author)
  • Hedenfalk, IngridLund University,Lunds universitet,Bröstcancer-genetik,Sektion I,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Bröst- och ovarialcancer,Forskargrupper vid Lunds universitet,Breastcancer-genetics,Section I,Department of Clinical Sciences, Lund,Faculty of Medicine,Breast and Ovarian Cancer Genomics,Lund University Research Groups,Skåne University Hospital(Swepub:lu)onk-ifa (author)
  • Create HealthAnnan verksamhet, LTH (creator_code:org_t)

Related titles

  • In:International Journal of Cancer: Wiley142:3, s. 618-6280020-71361097-0215

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