GLORIA — GEOMAR Library Ocean Research Information Access

Hits per page

hits 1 - 2 | 2 hits

Sorting

Electronic Resource

Transforming growth factor-alpha (TGF α)-producing gastric carcinoma with acanthosis nigricans: An endocrine effect of TGF α in the pathogenesis of cutaneous paraneoplastic syndrome and epithelial hyperplasia of the esophagus (1997)

Koyama, Shohei ; Ikeda, Kazuho ; Sato, Mikio ; [et al.]

Springer

Journal of gastroenterology 32 (1997), S. 71-77

add to mindlist on the mindlist

Details

ISSN: 1435-5922

Keywords: acanthosis nigricans ; transforming growth factor-alpha (TGF α) ; epidermal growth factor (EGF) receptor ; gastric carcinoma

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Abstract A case of well-differentiated adenocarcinoma (Borrmann type 3) of the stomach in a 76-year-old man associated with the typical skin manifestations of acanthosis nigricans and with multiple protruding lesions showing epithelial hyperplasia of the esophagus is reported. The advanced tumor was located in the cardiac region of the stomach, and measured approximately 8cm in diameter, with partial invasion to the esophagus. The associated cutaneous lesions were characterized by hyperpigmentation and by protruding verrucous papules on the torso, head, face, neck, upper extremities, perineum, and inguinal region. Histologically, the protruding skin lesions showed keratinocytes proliferation throughout the epidermis, resulting in diffhyperkeratosis, papillomatosis, and acanthosis of the skin. Immunohistological analysis showed coexpression of transforming growth factor alpha (TGF-a) and epidermal growth factor (EGF) receptors in the tumor from the stomach. It is reasonable to conclude from this evidence that gastric carcinoma cells secrete TGF α in an autocrine for auto-stimulation. EGF receptor expression was also noted on the papillomatous hyperplasia of the cutaneous lesion. Serum level of TGF α, determined by an enzyme-linked immunosorbent assay, was high (144pg/ml; normal, 22.0 ±16pg/ml (Mean±SD)). Serum TGF α abruptly decreased to 49pg/ml on day 7 after the total gastrectomy, and then gradually increased to 77pg/ml within 28 days. Amelioration of the cutaneous lesions and the protruding lesions in the esophagus was observed after surgical resection of the gastric carcinoma. This suggests that the TGF α stimulates the proliferation of keratinocytes involved with EGF receptor. Large amounts of circulating TGF α in the blood over a long period released by the primary tumor seem to act as an endocrine-like mechanism causing epidermal and esophageal epithelial cells to proliferate. There is a possible link in the pathogenesis of the acanthosis nigricans as a cutaneous paraneoplastic syndrome, and epithelial hyperplasia of the esophagus.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF01213299

Permalink

	Location	Call Number	Limitation	Availability

Others were also interested in ...

Paper (German National Licenses)

Fulltext

Electronic Resource

Clonal variation of adenylyl cyclase activity in a rat tumor cell line caused by change in G protein-catalytic unit interaction (1990)

Kawabata, Masahiro ; Yoshikura, Hiroshi ; Horio, Keizo ; [et al.]

New York, NY [u.a.] : Wiley-Blackwell

Journal of Cellular Physiology 144 (1990), S. 448-456

add to mindlist on the mindlist

Details

ISSN: 0021-9541

Keywords: Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Medicine

Notes: Two subclones of the rat XC cell line characterized by different morphology exhibited quite different adenylyl cyclase responses upon various stimulations. Upon treatment with cholera toxin, clone RK1 accumulated a high level of intracellular cAMP thereby changing its polygonal morphology to an elongated morphology, while the other clone, LK1, with a fibroblastic morphology, failed to increase the intracellular cAMP and remained morphologically unchanged. When membrane fractions derived from these two clones were stimulated with 10 μM forskolin, 10 μM GTPλS, or 10 mM NaF, five- to 20-fold more cAMP was accumulated in RK1-derived membranes than in LK1-derived membranes. With the same membrane fractions, upon treatment with Mn++, which directly stimulates the catalytic unit, a high level of cAMP was accumulated both in RK1 and LK1, indicating that the catalytic function inducible by Mn++ was similar in both clones. There was no significant difference in the level of expression of G protein α2, αi (at least αi1 and αi2), and β subunits between LK1 and RK1. Cholateextracts of the membrane protein of LK1 and RK1 reconstituted the adenylyl cyclase activity of the cyc variant of S49 lymphoma cells to the same level. Therefore, it is inferred that the defect in LK1 resides in the interaction of stimulatory G proteins and the actual catalyst.

Additional Material: 6 Ill.