Expression of insulin-like growth factor-I and -II genes in human smooth muscle tumours.

Höppener, Jo W.M.; Mosselman, Sietse; Roholl, P. J. M.; Lambrechts, Caro; Slebos, Robert J. C.; Pagter-Holthuizen, P. de; Lips, Cornelis J.M.; Jansz, H.S.; Sussenbach, J.S.

doi:10.1002/j.1460-2075.1988.tb02954.x

Cited by 113 publications

(43 citation statements)

References 33 publications

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“…Identification of IGF-II as a tumour suppressor in this system is surprising because in the clinical situation levels of IGF-II mRNA are often much higher in tumours than in the surrounding adult host tissue in which they are found (Scott et al, 1985, Su et al, 1989Cariani et al, 1988;Hoppener et al, 1988;Daughaday et al, 1988;Tricoli et al, 1986 In sporadic Wilms' tumour , hereditary…”

Section: Discussionmentioning

confidence: 99%

“…This observation is particularly striking in the case of a group of developmental neoplasms, hepatoblastoma, embryonal nephroblastoma (Wilms' tumour), adrenocortical carcinoma and rhabdomyosarcoma (Scott et al, 1985), but elevated expression is also seen in hepatocellular carcinoma (Su et al, 1989;Cariani et al, 1988), leiomyoma & leiomyosarcoma (Hoppener et al, 1988;Daughaday et al, 1988), colon carcinoma, and liposarcoma (Tricoli et al, 1986) together with fibrosarcomas (Schofield et al, 1989). One common feature of all these tumours is that the presumed foetal counterparts of all these cell types make significant quantities of IGF-II mRNA and protein (Han et al, 1988;Hill, 1990) while their normal adult counterparts do not.…”

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confidence: 99%

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Tumour suppression associated with expression of human insulin-like growth factor II

Schofield

Lee²,

Hill³

et al. 1991

Br J Cancer

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Recent circumstantial evidence has implicated Insulin-like growth factor II in the genesis of several tumour types, notably developmental tumours (Scott et al., 1985; Schofield & Tate, 1987; Wilkins et al., 1989). This type of tumour, thought to originate during the defective differentiation of organ precursors (Miereau et al., 1987), often expresses greatly elevated levels of mRNA for IGF-II, a known mitogen for these cells and abundantly expressed in their presumed normal counterparts (Scott et al., 1985; Schofield & Tate, 1987; Gray et al., 1987). It has been proposed that continued, inappropriate expression of this gene drives tumour growth by an autocrine mechanism. In order to examine the potential role of IGF-II in the growth of tumour cells an IGF-II cDNA was introduced into a retroviral expression vector, and used to infect a cloned fibroblast cell line. Expression of IGF-II conferred a degree of serum independence of growth in cell culture, however, when cells were injected into nude mice as subcutaneous grafts, clones expressing IGF-II from the retrovirus were found to have a greatly increased (five fold) latency of sarcoma formation. After a prolonged lag all cell lines eventually gave rise to tumours in which the introduced IGF-II genes had either been lost or inactivated, suggesting that in this system IGF-II acts as a tumour suppressor gene. Images Figure 2 Figure 4

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Tumour suppression associated with expression of human insulin-like growth factor II

Schofield

Lee²,

Hill³

et al. 1991

Br J Cancer

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“…IGF-I, but not IGF-II, was mitogenic in leiomyoma cell cultures . The levels of IGF-I mRNA were reported higher in leiomyomas than in the myometrium in two studies (Boehm et al 1990;Hoppener et al 1988), whereas two other studies concluded that the levels were not significantly different (Gloudemans et al 1990;Vollenhoven et al 1993). Increased IGF-I peptide has been detected in some, but not all, leiomyomata compared with myometrium in immunohistochemical studies (Dixon et al 2000).…”

Section: Growth Factors Identified In Fibroidsmentioning

confidence: 97%

Etiology and pathogenesis of uterine leiomyomas: a review.

Flake

Andersen

Dixon

2003

Environ Health Perspect

494

392

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Uterine leiomyomas, or fibroids, represent a major public health problem. It is believed that these tumors develop in the majority of American women and become symptomatic in one-third of these women. They are the most frequent indication for hysterectomy in the United States. Although the initiator or initiators of fibroids are unknown, several predisposing factors have been identified, including age (late reproductive years), African-American ethnicity, nulliparity, and obesity. Nonrandom cytogenetic abnormalities have been found in about 40% of tumors examined. Estrogen and progesterone are recognized as promoters of tumor growth, and the potential role of environmental estrogens has only recently been explored. Growth factors with mitogenic activity, such as transforming growth factor-β 3, basic fibroblast growth factor, epidermal growth factor, and insulin-like growth factor-I, are elevated in fibroids and may be the effectors of estrogen and progesterone promotion. These data offer clues to the etiology and pathogenesis of this common condition, which we have analyzed and summarized in this review.

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“…The most obvious candidates are the insulin-like growth factors, Which are single chain polypeptides evolutionary related to insulin. Elevated levels of IGF mRNA have been found in a number of tumour types of mesenchymal origin, associated with hypoglycaemia (Tricoli et al, 1986;Hoppener et al, 1988;Schofield et al, 1989). Animals bearing the MAC16 adenocarcinoma show a progressive decrease in blood glucose levels as weight loss increases.…”

Section: Discussionmentioning

confidence: 99%

Tumour-associated hypoglycaemia in a murine cachexia model

Tisdale²

1992

Br J Cancer

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SummaryAnimals bearing a cachexia-inducing tumour, the MAC16 adenocarcinoma, showed a progressive decrease in blood glucose levels with increasing weight loss, while animals bearing a histologically similar tumour, the MAC13 adenocarcinoma, showed no change in either body weight or blood glucose levels with growth of the tumour. The effect of the MAC16 tumour on blood glucose levels appeared to be unrelated to food intake, glucose consumption by the tumour, or to the production of increased levels of IGF-I and IGF-II mRNA by the tumour cells. The relationship between the induction of cachexia and alteration in blood glucose levels remains unknown.A high rate of glucose consumption under both anaerobic and aerobic conditions is a characteristic feature of both experimental (Weber et al., 1961;Weber, 1977) and human tumours (Nolop et al., 1987). Alterations in glucose metabolism in tumour cells are associated with an increased intracellular concentration of glucose, which is tightly coupled with an over-expression of facilitative glucose transporter genes (Yamamoto et al., 1990), an increased transcription of the hexokinase gene (Johansson et al., 1985), as well as alterations in isoenzyme profiles of the enzymes involved in glycolysis (Weber et al., 1961). The enhanced glucose transport is not insulin-dependent, since hypoglycaemia often develops in both tumour-bearing animals (Bibby et al., 1987) and cancer patients (Heber et al., 1985) with normal or even decreased blood insulin levels. The architecture of solid tumours also plays an important role in determining the metabolic substrate for energy production. Large solid tumours tend to have a poor blood supply, and consequently become hypoxic, in which case glucose will become the predominant metabolic substrate, since the Embden-Meyerhof pathway is the only means of ATP production in the absence of oxygen.We have recently reported studies on glucose utilisation by tumour and host tissues in NMRI mice bearing the MAC16 colon adenocarcinoma, which is capable of inducing cachexia in recipient animals (Mulligan & Tisdale, 1991). Glucose consumption by the tumour was second only to brain and the increased demand for glucose was met by a decrease in glucose utilisation by host organs and in particular the brain. This study further investigates changes in blood glucose levels and the possible role of insulin-like growth factors (IGF) in the MAC16 model. Since antibodies to both mouse IGFI and IGFII were not readily available, we have chosen to measure their production in the MAC16 tumour indirectly, through the study of gene expression. Materials and methodsPure strain NMRI mice were bred in our own colony and were fed on a rat and mouse breeding diet (Pilsbury, Birmingham, UK) and water ad libitum. Fragments (1 x 2 mm) of either the MAC16 or MAC13 tumour were implanted into the flank of male NMRI mice (starting weight 28 g) by means of a trocar as described (Bibby et al., 1987

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Expression of insulin-like growth factor-I and -II genes in human smooth muscle tumours.

Cited by 113 publications

References 33 publications

Tumour suppression associated with expression of human insulin-like growth factor II

Tumour suppression associated with expression of human insulin-like growth factor II

Etiology and pathogenesis of uterine leiomyomas: a review.

Tumour-associated hypoglycaemia in a murine cachexia model

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