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

c-Ha-ras oncogene expression in immortalized human keratinocytes (HaCaT) alters growth potential in vivo but lacks correlation with malignancy.

Cancer research - 1 May 1990

Boukamp P, Stanbridge E J, Foo D Y, Cerutti P A, Fusenig N E

Abstract excerpt

Spontaneously immortalized human skin keratinocytes (HaCaT) were transfected with the c-Ha-ras (EJ) oncogene via a plasmid construct which also contained the selectable neomycin gene. Clones were selected on the basis of G418 resistance. Those clones that had stable integrants of Ha-ras fell into 3 classes with respect to tumorigenicity. Class I clones were nontumorigenic, i.e., formed nodules which rapidly...

Topics

Blotting, Northern
Cell Division
Cell Line
Cell Transformation, Neoplastic
Genes, ras
Humans
Keratinocytes
Neoplasm Transplantation
Phenotype
Proto-Oncogene Proteins
Proto-Oncogene Proteins p21(ras)

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Transfection

Source

Identifiers

PMID: 2183932

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-2183932-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

0

discussions

0

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

c-Ha-ras oncogene expression in immortalized human keratinocytes (HaCaT) alters growth potential in vivo but lacks correlation with malignancy.PMID 2183932Read ↗

Tumor progression of skin carcinoma cells in vivo promoted by clonal selection, mutagenesis, and autocrine growth regulation by granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor.Semantic proximity Read ↗

Epidermal morphogenesis and keratin expression in c-Ha-ras-transfected tumorigenic clones of the human HaCaT cell line.Semantic proximity Read ↗

Characterization of mutant HA-ras gene expression in transformed murine keratinocyte lines grown under in vitro and in vivo conditions.Semantic proximity Read ↗

Multiple stages and genetic alterations in immortalization, malignant transformation, and tumor progression of human skin keratinocytes.Semantic proximity Read ↗

Characterisation of the novel spontaneously immortalized and invasively growing human skin keratinocyte line HaSKpwSemantic proximity Read ↗

Malignant Transformation of Immortalized HaCaT Keratinocytes through Deregulated Nuclear Factor κB SignalingSemantic proximity Read ↗

Progression of human papillomavirus type 18-immortalized human keratinocytes to a malignant phenotype.Semantic proximity Read ↗

Different immortalized keratinocyte cell lines display distinct capabilities to differentiate and reconstitute an epidermis in vitroSemantic proximity Read ↗

Transforming and oncogenic potential of activated c-Ha-ras in three immortalized human breast epithelial cell lines.Semantic proximity Read ↗

E-cadherin loss promotes the initiation of squamous cell carcinoma invasion through modulation of integrin-mediated adhesionSemantic proximity Read ↗

Noncorrelative c-myc and ras oncogene expression in squamous cell carcinoma cells with tumorigenic potential.Semantic proximity Read ↗

Human epithelial cells immortalized by human papilloma viruses.Semantic proximity Read ↗

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