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Proto-Oncogene Transcription after Activation of Th-1 and Th-2 Cells (1991)

MOREL, PENELOPE A. ; WALKER, JEFFREY A. ; LIVINGSTONE, ALEXANDRA M. ; [et al.]

Oxford, UK : Blackwell Publishing Ltd

Annals of the New York Academy of Sciences 636 (1991), S. 0

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ISSN: 1749-6632

Source: Blackwell Publishing Journal Backfiles 1879-2005

Topics: Natural Sciences in General

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1111/j.1749-6632.1991.tb33474.x

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Tumor-derived Growth Factors That Support Proliferation and Differentiation of Normal and Leukemic Hemopoietic Cells (1987)

TWEARDY, DAVID J. ; CARACCIOLO, DANIELE ; VALTIERI, MAURO ; [et al.]

Oxford, UK : Blackwell Publishing Ltd

Annals of the New York Academy of Sciences 511 (1987), S. 0

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ISSN: 1749-6632

Source: Blackwell Publishing Journal Backfiles 1879-2005

Topics: Natural Sciences in General

Notes: The conditioned media of 34 human tumor cell lines were screened for the ability to induce granulocyte-macrophage colonies in vitro in bone marrow cultures, to stimulate proliferation of a murine IL-3 dependent hemopoietic cell line (32D clone 3) and to stimulate thymidine incorporation in suspension cultures of acute myelogenous leukemia cells. Twelve tumor cell lines produced factors that were active in these assays. The conditioned medium of the glioblastoma cell line U87 MG was characterized in detail and found to contain G-CSF and GM-CSF. Cloning and sequencing of the U87 MG G-CSF indicated that it was derived from G-CSF b mRNA, which encodes a protein with a deletion of 3 amino acids at residues 36–38. The gene for G-CSF was mapped to human chromosome 17 band q21, a region involved in translocations frequently found in acute promyelocytic leukemia. G-CSF (U87MG) was able to induce granulocytic differentiation of the total population of a murine IL-3 dependent cell line, 32D clone 3; this effect was antagonized by IL-3. GM-CSF (U87-MG) supported the proliferation without inducing differentiation of two growth factor-dependent leukemic cell lines, TALL 101 and AML-193.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1111/j.1749-6632.1987.tb36235.x

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TGF-α and EGFR in head and neck cancer (1993)

Grandis, Jennifer R. ; Tweardy, David J.

New York, N.Y. : Wiley-Blackwell

Journal of Cellular Biochemistry 53 (1993), S. 188-191

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ISSN: 0730-2312

Keywords: Transforming growth factor alpha ; epidermal growth factor receptor ; squamous cell carcinoma of the head and neck ; Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Chemistry and Pharmacology , Medicine

Notes: The upper aerodigestive tract mucosa of patients who develop squamous cell carcinoma of the head and neck (SCCHN) is predisposed to abnormally regulated growth, evidenced by the high incidence of synchronous and metachronous malignancies. We conducted a series of experiments to show that aberrant regulation of the epithelial growth factor, transforming growth factor alpha (TGF-α) and its cell surface receptor, the epidermal growth factor receptor (EGFR), contribute to this predisposition. Using molecular biological techniques, we compared the incidence and mechanism of TGF-α and EGFR over-production in fresh tumors and histologically normal mucosal specimens from patients with SCCHN and normal, control patients without cancer. In patients with SCCHN, TGF-α and EGFR mRNA levels were significantly elevated in both tumor and normal mucosal specimens as compared to levels in control mucosa from non-cancer patients. Neither an enhancement of message stability nor an increase in gene copy number alone accounted for the elevation of EGFR mRNA. Increased production of TGF-α and EGFR mRNAs in the histologically “normal” mucosa of patients at risk for a primary or secondary head and neck cancer may serve both as a marker for malignant transformation and as a target for chemoprevention.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1002/jcb.240531027

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