Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomics analysis of novel serum protein biomarkers for the diagnosis of trastuzumab-resistant breast cancer

ABSTRACT: we executed a study of serum proteome differences between trastuzumab-resistance and trastuzumab-response HER2-positive breast cancer patients using an isobaric TMT label-based multiplexed quantitative proteomic method in combination with a comprehensive functional bioinformatics analysis. An LC-MS/MS-based multiple/selective reaction monitoring (MRM/SRM) quantification method was applied to validate several candidate biomarkers.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Serum

SUBMITTER: Ting Yang

LAB HEAD: Ting Yang

PROVIDER: PXD016655 | Pride | 2022-04-01

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	180612-01-pro-pep.xlsx	Xlsx
	180612-01_1.raw	Raw
	180612-01_10.raw	Raw
	180612-01_2.raw	Raw
	180612-01_3.raw	Raw

Items per page:

1 - 5 of 11

Publications

Circulating Proteins Associated with Response and Resistance to Neoadjuvant Chemotherapy in HER2-Positive Breast Cancer.

Chantada-Vázquez María Del Pilar MDP Conde-Amboage Mercedes M Graña-López Lucía L Vázquez-Estévez Sergio S Bravo Susana B SB Núñez Cristina C

Cancers 20220221 4

Despite the increasing use of neoadjuvant chemotherapy (NAC) in HER2-positive breast cancer (BC) patients, the clinical problem of predicting individual treatment response remains unanswered. Furthermore, the use of ineffective chemotherapeutic regimens should be avoided. Serum biomarker levels are being studied more and more for their ability to predict therapy response and aid in the development of personalized treatment regimens. This study aims to identify effective protein networks and biom ...[more]

PMID: 35205837

Similar Datasets

mRNA profiling reveals determinants of trastuzumab efficiency in HER2-positive breast cancer

Project description:The intention was to detect genes that are determining trastuzumab efficiency in HER2-positive breast cancer cell lines with different resistance phenotypes. While BT474 should be sensitive to the drug treatment, HCC1954 is expected to be resistant due to a PI3K mutation. The cell line BTR50 has been derived from BT474 and was cultured to be resistant as well. Based on RNA-Seq data, we performed differential expression analyses on these breast cancer cell lines with and without trastuzumab treatment. In detail, five separate tests were performed, namely resistant cells vs. wild type, i.e. HCC1954 and BTR50 vs. BT474, respectively, and untreated vs. drug treated cells. The significant genes of the first two tests should contribute to resistance. The significant genes of the test BT474 vs. its drug treated version should contribute to the trastuzumab effect. To exclude false positives from the combined gene set (#64), we removed ten genes that were also significant in the test BTR50 vs. its drug treated version. This way we ended up with 54 genes that are very likely to determine trastuzumab efficiency in HER2-positive breast cancer cell lines. mRNA profiles of human breast cancer cell lines were generated by deep sequencing using Illumina HiSeq 2000. The cell lines BT474 and HCC1954 were analyzed with and without trastuzumab treatment. HCC1954 is known to be trastuzumab resistant. Additionally, the cell line BTR50 was generated as resistant version of BT474, and was analyzed with and without trastuzumab as well.

2015-04-21 | E-GEOD-55005 | biostudies-arrayexpress

Human HER2-breast cancer cell line, trastuzumab-resistant, LC-MSMS

Project description:We established an acquired trastuzumab-resistant model in vitro from a trastuzumab-sensitive, HER2-amplified breast-cancer cell line. A multi-omic strategy was implemented to obtain gene, proteome, and phosphoproteome signatures associated with acquired resistance to trastuzumab in HER2-positive breast cancer, followed by validation in human clinical samples.

2020-06-01 | PXD010574 | Pride

RNA sequencing of BT474 cells treated with trastuzumab or trastuzumab + pertuzumab and BT474-derived cells resistant to trastuzumab or trastuzumab + pertuzumab

Project description:We sequenced untreated BT474 cells, BT474 cells treated for three days with trastuzumab or trastuzumab + pertuzumab, as well as two BT474-derived trastuzumab-resistant pools and two BT474-derived trastuzumab + pertuzumab resistant pools. Resistant pools were generated by culturing BT474 cells in gradually increasing doses of trastuzumab and trastuzumab + pertuzumab over the course of several months and continually maintained in drug.

2020-01-26 | GSE121105 | GEO

Human breast cancer SKBr-3 cells: trastuzumab-resistant vs. parental

Project description:Human breast cancer SKBr-3 cells selected with trastuzumab for 6 month compared with parental SKBr-3 cells; Goal was to screen for microRNAs involved in development of trastuzumab resistance. Human breast cancer SKBr-3 cells were continuously cultured in the presence ofM-BM- 5M-BM-5g/ml trastuzumab for 6 months, and the resulting alive cells were regarded as trastuzumab-resistant. Total RNAs were prepared from these cells and cells cultured in parallel in control media, and were subjected to hybridization on the miRCURY LNA Array (Exiqon, version 11.0).

2013-05-25 | E-GEOD-47011 | biostudies-arrayexpress

Trastuzumab produces therapeutic actions by upregulating miR-26a and miR-30b in breast cancer cells

Project description:Objective: Trastuzumab has been used for the treatment of HER2-positive breast cancer (BC). However, a subset of BC patients exhibited resistance to trastuzumab therapy. Thus, clarifying the molecular mechanism of trastuzumab treatment will be beneficial to improve the treatment of HER2-positive BC patients. In this study, we identified trastuzumab-responsive microRNAs that are involved in the therapeutic effects of trastuzumab. Methods and results: RNA samples were obtained from HER2-positive (SKBR3 and BT474) and HER2-negetive (MCF7 and MDA-MB-231) cells with and without trastuzumab treatment for 6 days. Next, we conducted a microRNA profiling analysis using these samples to screen those microRNAs that were up- or downregulated only in HER2-positive cells. This analysis identified miR-26a and miR-30b as trastuzumab-inducible microRNAs. Transfecting miR-26a and miR-30b induced cell growth suppression in the BC cells by 40% and 32%, respectively. A cell cycle analysis showed that these microRNAs induced G1 arrest in HER2-positive BC cells as trastuzumab did. An Annexin-V assay revealed that miR-26a but not miR-30b induced apoptosis in HER2-positive BC cells. Using the prediction algorithms for microRNA targets, we identified cyclin E2 (CCNE2) as a target gene of miR-30b. A luciferase-based reporter assay demonstrated that miR-30b post-transcriptionally reduced 27% (p=0.005) of the gene expression by interacting with two binding sites in the 3’-UTR of CCNE2. Conclusion: In BC cells, trastuzumab modulated the expression of a subset of microRNAs, including miR-26a and miR-30b. The upregulation of miR-30b by trastuzumab may play a biological role in trastuzumab-induced cell growth inhibition by targeting CCNE2. We obtained microRNA expression profiles of breast cancer cell lines, MCF7, MDA-MB-231, SKBR3, and BT474, with or without trastuzumab (4microgram/mL) treatment.

2012-06-02 | E-GEOD-38415 | biostudies-arrayexpress

RNA sequencing of BT474 cells treated with trastuzumab or trastuzumab + pertuzumab and BT474-derived cells resistant to trastuzumab or trastuzumab + pertuzumab

Project description:RNA sequencing of BT474 cells treated with trastuzumab or trastuzumab + pertuzumab and BT474-derived cells resistant to trastuzumab or trastuzumab + pertuzumab

| PRJNA495653 | ENA

Gene expression data from trastuzumab-hypersensitive clones

Project description:Genes involved in trastuzumab response were identified using transcriptomic data from cells hypersensitive to trastuzumab derived from BT474.

2021-09-24 | GSE184655 | GEO

Modulation of microRNA-194 and Cell Migration by HER2-targeting Trastuzumab in Breast Cancer

Project description:We found that trastuzumab (herceptin) treatment significantly decreased five miRNAs and increased three others in SKBr3 cells, whereas in BT474 cells it significantly decreased two miRNAs and increased nine. The only miRNA that shared the same change in both cell lines was miRNA-194 (miR-194), which was upregulated following trastuzumab treatment.

2013-01-31 | E-MTAB-965 | biostudies-arrayexpress

Mass spectroscopy-based proteomics and metabolomics analysis of BT- 474 breast cancer cells treated with Tamoxifen and/or Trastuzumab

Project description:`Triple positive` BT-474 breast cancer cells were treated with anti-cancer compounds, Tamoxifen and Trastuzumab, and the metabolome and proteome analysed by LC-MS/MS using a timsTOF.

2023-01-17 | PXD033145 | Pride

ErbB2 Site-Specific α2,6-Sialylation Regulates Gastric Cancer Cell Sensitivity to Trastuzumab

Project description:The clinical performance of trastuzumab in the treatment of ErbB2-positive gastric cancer is severely hampered by the emergence of molecular resistance. The glycosylation landscape of ErbB2’s extracellular domain, and the molecular mechanisms through which it tunes gastric cell malignancy, including the acquisition of trastuzumab resistance, remain elusive. We show that the expression of ErbB2 sialylated glycoforms holds clinical utility in the prediction of clinical outcome and stratification of gastric cancer patients. In-depth glycoproteomic and glycomic analysis of ErbB2 extracellular region disclosed a site-specific profile in gastric cancer cells. We further demonstrate that ST6Gal1 sialyltransferase specifically targets ErbB2 N-glycosylation sites within the trastuzumab binding domain. Moreover, the abrogation of ST6Gal1-mediated α2,6-sialylation reshapes ErbB2 glycome and sensitizes gastric cancer cells to trastuzumab-induced cytotoxicity through receptor membrane stabilization and a downregulation of ErbB2 activation. Overall, this data demonstrates that aberrant sialylation tunes the molecular resistance of ErbB2-driven gastric cancer cells to trastuzumab.

2021-05-11 | PXD017609 | Pride