دورية أكاديمية
أعرض في EDS

Notch promotes recurrence of dormant tumor cells following HER2/neu-targeted therapy.

التفاصيل البيبلوغرافية
العنوان: Notch promotes recurrence of dormant tumor cells following HER2/neu-targeted therapy.
المؤلفون: Abravanel DL, Belka GK, Pan TC, Pant DK, Collins MA, Sterner CJ, Chodosh LA
المصدر: The Journal of clinical investigation [J Clin Invest] 2015 Jun; Vol. 125 (6), pp. 2484-96. Date of Electronic Publication: 2015 May 11.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
اللغة: English
بيانات الدورية: Publisher: American Society for Clinical Investigation Country of Publication: United States NLM ID: 7802877 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1558-8238 (Electronic) Linking ISSN: 00219738 NLM ISO Abbreviation: J Clin Invest Subsets: MEDLINE
أسماء مطبوعة: Publication: 1999- : Ann Arbor, MI : American Society for Clinical Investigation
Original Publication: New Haven [etc.] American Society for Clinical Investigation.
مواضيع طبية MeSH: Gene Expression Regulation, Neoplastic* , Receptor, ErbB-2* , Signal Transduction*, Breast Neoplasms/*metabolism , Neoplasm Recurrence, Local/*metabolism , Receptors, Notch/*metabolism, Aged ; Animals ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Databases, Genetic ; Female ; Gene Expression Profiling ; Heterografts ; Humans ; Meta-Analysis as Topic ; Mice ; Mice, Nude ; Mice, Transgenic ; Middle Aged ; Neoplasm Recurrence, Local/genetics ; Neoplasm Recurrence, Local/pathology ; Neoplasm Transplantation ; Oligonucleotide Array Sequence Analysis ; Receptors, Notch/genetics ; Tumor Cells, Cultured
مستخلص: Breast cancer mortality is principally due to recurrent tumors that arise from a reservoir of residual tumor cells that survive therapy. Remarkably, breast cancers can recur after extended periods of clinical remission, implying that at least some residual tumor cells pass through a dormant phase prior to relapse. Nevertheless, the mechanisms that contribute to breast cancer recurrence are poorly understood. Using a mouse model of recurrent mammary tumorigenesis in combination with bioinformatics analyses of breast cancer patients, we have identified a role for Notch signaling in mammary tumor dormancy and recurrence. Specifically, we found that Notch signaling is acutely upregulated in tumor cells following HER2/neu pathway inhibition, that Notch signaling remains activated in a subset of dormant residual tumor cells that persist following HER2/neu downregulation, that activation of Notch signaling accelerates tumor recurrence, and that inhibition of Notch signaling by either genetic or pharmacological approaches impairs recurrence in mice. Consistent with these findings, meta-analysis of microarray data from over 4,000 breast cancer patients revealed that elevated Notch pathway activity is independently associated with an increased rate of recurrence. Together, these results implicate Notch signaling in tumor recurrence from dormant residual tumor cells and provide evidence that dormancy is a targetable stage of breast cancer progression.
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معلومات مُعتمدة: T32 HD007505 United States HD NICHD NIH HHS
المشرفين على المادة: 0 (Receptors, Notch)
EC 2.7.10.1 (ERBB2 protein, human)
EC 2.7.10.1 (Receptor, ErbB-2)
تواريخ الأحداث: Date Created: 20150512 Date Completed: 20150812 Latest Revision: 20181113
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC4497740
DOI: 10.1172/JCI74883
PMID: 25961456
قاعدة البيانات: MEDLINE
الوصف
تدمد:1558-8238
DOI:10.1172/JCI74883