0000000000336158

AUTHOR

Sonja Thaler

showing 4 related works from this author

The proteasome inhibitor Bortezomib (Velcade) as potential inhibitor of estrogen receptor-positive breast cancer

2015

Around 70% of breast cancers express the estrogen receptor α (ERα) and depend on estrogen for growth, survival and disease progression. The presence of hormone sensitivity is usually associated with a favorable prognosis. Use of adjuvant anti-endocrine therapy has significantly decreased breast cancer mortality in patients with early-stage disease, and anti-endocrine therapy also plays a central role in the treatment of advanced stages. However a subset of hormone receptor-positive breast cancers do not benefit from anti-endocrine therapy, and nearly all hormone receptor-positive metastatic breast cancers ultimately develop resistance to anti-hormonal therapies. Despite new insights into me…

OncologyCancer Researchmedicine.medical_specialtyKinasebusiness.industryBortezomibmedicine.drug_classEstrogen receptormedicine.diseaseBreast cancerOncologyEstrogenInternal medicineProteasome inhibitormedicineskin and connective tissue diseasesbusinessProtein kinase BPI3K/AKT/mTOR pathwaymedicine.drugInternational Journal of Cancer
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RASSF1A inhibits estrogen receptor alpha expression and estrogen-independent signalling: implications for breast cancer development

2012

The Ras association domain family 1 isoform A (RASSF1A) is a tumor suppressor whose inactivation is implicated in the development of many human cancers, including breast carcinomas. Little is known about the tumor-suppressive function of RASSF1A in breast tissue and whether its inactivation is mechanistically involved in the initiation and progression of breast tumors. Here, we show that RASSF1A inhibits breast cancer growth in vivo, and suppresses estrogen receptor (ERα) expression and function. Reconstitution of RASSF1A in MCF7 cells led to decreased ERα levels and reduced sensitivity to estrogen (E2). Concomitantly, we observed decreased expression of Id1 as well as the E2-responsive gen…

endocrine systemCancer Researchmedicine.medical_specialtyCell SurvivalGene ExpressionEstrogen receptorApoptosisBreast NeoplasmsCell Cycle ProteinsMice SCIDBiologyMiceBreast cancerDownregulation and upregulationMice Inbred NODInternal medicineGeneticsmedicineAnimalsHumansFulvestrantMolecular BiologyCellular SenescenceCell ProliferationRegulation of gene expressionEstradiolFulvestrantTumor Suppressor ProteinsEstrogen AntagonistsEstrogen Receptor alphaCancerEstrogensCell Cycle Checkpointsmedicine.diseaseGene Expression Regulation NeoplasticEndocrinologyProteolysisMCF-7 CellsCancer researchFemaleEctopic expressionEstrogen receptor alphaNeoplasm TransplantationSignal Transductionmedicine.drugOncogene
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An immune escape screen reveals Cdc42 as regulator of cancer susceptibility to lymphocyte-mediated tumor suppression.

2007

Abstract Adoptive cellular immunotherapy inducing a graft-versus-tumor (GVT) effect is the therapeutic mainstay of allogeneic hematopoietic stem cell transplantation (ASCT) for high-risk leukemias. Autologous immunotherapies using vaccines or adoptive transfer of ex vivo–manipulated lymphocytes are clinically explored in patients with various cancer entities. Main reason for failure of ASCT and cancer immunotherapy is progression of the underlying malignancy, which is more prevalent in patients with advanced disease. Elucidating the molecular mechanisms contributing to immune escape will help to develop strategies for the improvement of immunologic cancer treatment. To this end, we have und…

MAPK/ERK pathwayCytotoxicity ImmunologicAdoptive cell transferTranscription GeneticMAP Kinase Signaling Systemmedicine.medical_treatmentImmunologyMolecular Sequence DataApoptosisBiologyBiochemistryMiceImmune systemCancer immunotherapyNeoplasmsmedicineCytotoxic T cellAnimalsHumansLymphocytescdc42 GTP-Binding ProteinCells CulturedBase SequenceCancerCell BiologyHematologymedicine.diseaseGene Expression Regulation NeoplasticMice Inbred C57BLCdc42 GTP-Binding ProteinProto-Oncogene Proteins c-bcl-2ImmunologyCancer cellCancer researchDisease SusceptibilityNeoplasm TransplantationBlood
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Functional characterization of circulating tumor cells (CTCs) from metastatic ER+/HER2− breast cancer reveals dependence on HER2 and FOXM1 for endocr…

2021

Simple Summary Acquired endocrine resistance and late recurrence in patients with ER+/HER2− breast cancer are complex and not fully understood. Here, we evaluated mechanisms of acquired resistance in circulating tumor cells (CTCs) from an ER+/HER2− breast cancer patient who initially responded but later progressed under endocrine treatment. We found a switch from ERα-dependent to HER2-dependent and ERα-independent expression of FOXM1, which may enable disseminated ER+/HER2− cells to re-initiate tumor cell growth and metastasis formation in the presence of endocrine treatment. We found that NFkB signaling sustains HER2 and FOXM1 expression in CTCs in the presence of ERα inhibitors suggesting…

0301 basic medicineDrugLife sciences; biologyCancer Researchmedia_common.quotation_subjectTumor cellslcsh:RC254-282Article03 medical and health sciencesTherapeutic approach0302 clinical medicineCirculating tumor cellBreast cancerHER2-dependent FOXM1 expressionddc:570ER+/HER2− circulating tumor cellsMedicineEndocrine systemskin and connective tissue diseasesmedia_commonER+/HER2��� circulating tumor cellsbusiness.industryendocrine therapy resistancelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease030104 developmental biologyOncologyApoptosis030220 oncology & carcinogenesisFOXM1Cancer researchbusiness
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