about
Tumor-extracellular matrix interactions: Identification of tools associated with breast cancer progressionRole of HER2/neu in tumor progression and therapyTumor suppressor genes are frequently methylated in lymph node metastases of breast cancersReplacement of Fhit in cancer cells suppresses tumorigenicityPathobiological implications of the d16HER2 splice variant for stemness and aggressiveness of HER2-positive breast cancer.The human splice variant Δ16HER2 induces rapid tumor onset in a reporter transgenic mouse.Increased sensitivity to chemotherapy induced by CpG-ODN treatment is mediated by microRNA modulation.Identification of relevant conformational epitopes on the HER2 oncoprotein by using Large Fragment Phage Display (LFPD).New insights into the role of extracellular matrix during tumor onset and progression.FHIT-proteasome degradation caused by mitogenic stimulation of the EGF receptor family in cancer cells.Molecular portrait of breast cancer in China reveals comprehensive transcriptomic likeness to Caucasian breast cancer and low prevalence of luminal A subtype.Poly(I:C) and CpG-ODN combined aerosolization to treat lung metastases and counter the immunosuppressive microenvironment.HER-2: a biomarker at the crossroads of breast cancer immunotherapy and molecular medicine.Surveillance of spontaneous breast cancer metastasis by TRAIL-expressing CD34⁺ cells in a xenograft modelWhole-transcriptome analysis links trastuzumab sensitivity of breast tumors to both HER2 dependence and immune cell infiltrationDiadenosines as FHIT-ness instructors.CpG-oligodeoxynucleotides exert remarkable antitumor activity against diffuse malignant peritoneal mesothelioma orthotopic xenografts.Neoplastic and stromal cells contribute to an extracellular matrix gene expression profile defining a breast cancer subtype likely to progress.Taxanes enhance trastuzumab-mediated ADCC on tumor cells through NKG2D-mediated NK cell recognition.miR-302b enhances breast cancer cell sensitivity to cisplatin by regulating E2F1 and the cellular DNA damage response.Oncosuppressive role of p53-induced miR-205 in triple negative breast cancer.Effect of adjuvant trastuzumab treatment in conventional clinical setting: an observational retrospective multicenter Italian study.MicroRNA profiling as a tool to understand prognosis, therapy response and resistance in breast cancer.Sodium glucose cotransporter 1 ligand BLF501 as a novel tool for management of gastrointestinal mucositis.HER2 as a target for breast cancer therapy.Triple-negative breast cancer: present challenges and new perspectives.Activity and resistance of trastuzumab according to different clinical settings.Breast cancer and microRNAs: therapeutic impact.International expert consensus on primary systemic therapy in the management of early breast cancer: highlights of the Fourth Symposium on Primary Systemic Therapy in the Management of Operable Breast Cancer, Cremona, Italy (2010).FOXP3 expression in tumor cells and implications for cancer progression.Association of adiposity, dysmetabolisms, and inflammation with aggressive breast cancer subtypes: a cross-sectional study.Prognostic significance of laminin production in relation with its receptor expression in human breast carcinomas.Prognostic significance of the 67-kilodalton laminin receptor expression in human breast carcinomas.Expression and prognostic significance of the autoimmune regulator gene in breast cancer cells.Breast cancer-secreted miR-939 downregulates VE-cadherin and destroys the barrier function of endothelial monolayers.Predictive biomarkers in the treatment of HER2-positive breast cancer: an ongoing challenge.Fhit Nuclear Import Following EGF Stimulation Sustains Proliferation of Breast Cancer Cells.Activated d16HER2 homodimers and SRC kinase mediate optimal efficacy for trastuzumab.PDGFRβ and FGFR2 mediate endothelial cell differentiation capability of triple negative breast carcinoma cells.Maspin influences response to doxorubicin by changing the tumor microenvironment organization.
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P108
P1053
B-9377-2017
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