Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Effect of wild-type and mutant E-cadherin on cell proliferation and responsiveness to the chemotherapeutic agents cisplatin, etoposide, and 5-fluorouracil.

Oncology - 1 Jan 2004

Fricke Elena, Hermannstädter Christine, Keller Gisela, Fuchs Margit, Brunner Ingrid, Busch Raymonde, Höfler Heinz, Becker Karl-Friedrich, Luber Birgit

Abstract excerpt

OBJECTIVES: The cell adhesion molecule E-cadherin acts as a tumor and invasion suppressor and regulates cell proliferation. The aim of the present study was to investigate the impact of wild-type (wt) E-cadherin and tumor-derived mutant E-cadherin variants on the proliferation rate of MDA-MB-435S mammary carcinoma cells and the sensitivity of the cells to the chemotherapeutic drugs cisplatin, etoposide and...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Antimetabolites, Antineoplastic
Share to Antineoplastic Agents, Phytogenic

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cadherins

Share to Cell Division

Share to Cisplatin

Share to Colony-Forming Units Assay

Share to Etoposide

Share to Fluorouracil

Source

Identifiers

PMID: 15138368
DOI: 10.1159/000077442

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Effect of wild-type and mutant E-cadherin on cell proliferation and responsiveness to the chemotherapeutic agents cisplatin, etoposide, and 5-fluorouracil.PMID 15138368Read ↗

Relevance of MET activation and genetic alterations of KRAS and E-cadherin for cetuximab sensitivity of gastric cancer cell lines.Semantic proximity Read ↗

Influence of tumor-associated E-cadherin mutations on tumorigenicity and metastasis.Semantic proximity Read ↗

E-cadherin mediated adhesion system in cancer cellsSemantic proximity Read ↗

Tumour-associated E-cadherin mutations alter cellular morphology, decrease cellular adhesion and increase cellular motility.Semantic proximity Read ↗

Sensitivity to epidermal growth factor receptor inhibitor requires E-cadherin expression in urothelial carcinoma cells.Semantic proximity Read ↗

Characterization and resistance mechanisms of a 5-fluorouracil- resistant hepatocellular carcinoma cell line.Semantic proximity Read ↗

The mutational status of p53 protein in gastric and esophageal adenocarcinoma cell lines predicts sensitivity to chemotherapeutic agentsSemantic proximity Read ↗

The E-cadherin-mediated cell-cell adhesion system in human cancers.Semantic proximity Read ↗

Transcriptional Repression of Epithelial Cell Adhesion Molecule Contributes to p53 Control of Breast Cancer InvasionSemantic proximity Read ↗

Deletion of exon 8 increases cisplatin-induced E-cadherin cleavage.Semantic proximity Read ↗

Cell proliferation and cell cycle alterations in oesophageal p53-mutated cancer cells treated with cisplatin in combination with photodynamic therapy.Semantic proximity Read ↗

Chemotherapy-induced apoptosis in melanoma cells is p53 dependent.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.