Serum insulin-like growth factor-I levels in patients with small cell lung cancer

Vm, Macaulay; Jd, Teale; Mj, Everard; Gp, Joshi; Jl, Millar; Ie, Smith

doi:10.1016/0277-5379(88)90135-6

Cited by 12 publications

(6 citation statements)

References 9 publications

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“…We also measured circulating levels of IGF-I. We have shown that serum IGF-I levels do not correlate with tumour bulk in patients with SCLC (Macaulay et al, 1988b) and we used this parameter not as a tumour marker but rather as a measure of the endocrine effects of octreotide, as reported in acromegaly (Lamberts et al, 1988 (Carney et al, 1985;Duchesne et al, 1987;Macaulay et al, 1987) (Miller et al, 1981) and by serial serum levels of NSE and IGF-I. Side effects were graded as mild (grade 1), moderate (2), or severe (3).…”

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confidence: 99%

Experimental and clinical studies with somatostatin analogue octreotide in small cell lung cancer

Macaulay

Smith²,

Everard³

et al. 1991

Br J Cancer

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Summary We have detected somatostatin receptors (SSR) by autoradiography in 3/4 established small cell lung cancer (SCLC) cell lines but not in two non-SCLC cell lines. The growth of 1/3 SSR positive SCLC cell lines was significantly inhibited by the long-acting somatostatin analogue octreotide statin) 10-9M. We treated 20 SCLC patients with octreotide 250 gg three times daily for I week prechemotherapy (six patients) or at relapse after chemotherapy (14). Octreotide was well tolerated, and serum insulin-like growth factor-I levels were suppressed to 62±7% of pre-treatment levels. However there was no evidence of anti-tumour activity measured by tumour bulk or serum levels of neuron-specific enolase. In one patient metastatic skin nodules were shown to be SSR positive before and at the end of 2 weeks octreotide. Despite this the patient had progressive disease, and tumour cells obtained by fine needle aspirate before and after treatment showed no growth inhibition when cultured with octreotide immediately or following establishment as a cell line. In summary we saw little correlation between SSR expression and growth inhibition by octreotide, either in vitro or clinically.Somatostatins are a family of 14-and 28-residue neuropeptides which regulate peptide secretion from the pituitary, gut and pancreas (Bloom & Polak, 1987;Frohman & Krieger, 1987). Somatostatin receptors (SSR) are expressed by these so-called 'SS target tissues', and by tumours arising from them including pituitary adenomas and pancreatic insulinomas (Reubi et al., 1982;1984). Natural SS-14 is of limited therapeutic use here because of its short plasma half-life (3 min) and diverse action (Moreau & DeFeudis, 1987;Schally, 1988). Systematic structure/activity studies have led to the development of potent octapeptide SS analogues with prolonged and selective activity. One of these, octreotide (SMS 201-995, Sandostatin) has pharmacological effects in vivo for up to 9 h and is 45-70 times more potent than SS-14 at inhibiting growth hormone release (Plewe et al., 1987;Schally, 1988). In patients with acromegaly, carcinoid syndrome, insulinomas and other gastroenteropancreatic tumours, octreotide produces clinical improvement in parallel with suppression of inappropriate peptide secretion, and in some cases reduction in tumour bulk Wood et al., 1985;Kvols et al., 1986;Lamberts et al., 1987;Comi, 1989;Maton, 1989). Octreotide and other octapeptide SS analogues have also shown experimental evidence of antiproliferative activity in some common solid tumours, including cancers of the breast, exocrine pancreas, colon and prostate (Setyono-Han et al., 1987;Schally, 1988;Parmar et al., 1989;Weber et al., 1989). Growth inhibition here could be mediated directly, via SSR which have been detected on breast, pancreas and prostate cancers (Reubi et al., 1987;Setyono-Han et al., 1987;Srkalovic et al., 1990), or indirectly via suppression of local or circulating levels of growth factors (Schally, 1988).There is some evidence that SS may play a role in growth regulat...

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confidence: 99%

Experimental and clinical studies with somatostatin analogue octreotide in small cell lung cancer

Macaulay

Smith²,

Everard³

et al. 1991

Br J Cancer

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“…Although lung carcinogenesis can largely be attributed to tobacco smoke carcinogens such as the very potent NNK, and the IGF-IR has been found to be highly expressed in most lung tumor samples and cell lines, the interaction between IGF-IR and the tobacco carcinogen, NNK, has not been investigated [16][17][18][19]. As both the IGF-IR and NNK promote lung tumorigenesis, it is con- ceivable that these two tumor promoters interact to augment lung tumor development.…”

Section: Discussionmentioning

confidence: 95%

“…It seems evident that the added carcinogenic effects of NNK allow for an IGF-IR-dependent increase in tumor size during lung tumorigenesis. Considering that the IGF-IR has been found to be overexpressed in many lung cancer cell lines and human tumor tissue extracts, it is not surprising to find that the endogenous murine IGF-IR is overexpressed in NNK derived tumors given that the majority of lung cancer cases are caused by tobacco smoke carcinogens [16][17][18][19]. Further studies using molecular targets that block the IGF-IR pathway in NNK derived tumorigenesis would be useful to investigate whether or not the IGF-IR is an essential pathway of NNK induced carcinogenesis.…”

Section: Discussionmentioning

confidence: 97%

“…This receptor is often overexpressed in many common cancers, such as breast, colon and lung cancer. For example, in lung cancer the IGF-IR has been found to be overexpressed in most NSCLC and SCLC cell lines, and in almost all lung tumor tissue extracts [16][17][18][19]. Overexpression and activation of the IGF-IR signaling pathways has been found to be associated with many aspects of the malignant phenotype such as mitogenesis, survival, transformation and metastasis [20][21][22].…”

Section: Introductionmentioning

confidence: 97%

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The function of IGF-IR in NNK-mediated lung tumorigenesis

2011

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“…Epidermal growth factor (EGF) is elevated in the serum of some patients with stomach cancer (23), cancer of the tongue (24), and ovarian cancer (25), but unchanged or decreased in other cancers (26)(27)(28). Insulinlike growth factors, (IGF) have been reported to be elevated in the plasma of some breast cancer patients (29) and ovarian cancer patients (25), but not in other cancers (30,31). Elevated serum levels of hepatocyte growth factor (HGF) have been reported in hepatocellular carcinoma as well as in nonmalignant liver diseases (32).…”

Section: Othermentioning

confidence: 99%

Biomarkers of gene expression: growth factors and oncoproteins.

Brandt‐Rauf

1997

Environ Health Perspect

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This article reviews the literature on the application of methods for the detection of growth factors, oncogene proteins, and tumor-suppressor gene proteins in the blood of humans with cancer or who are at risk for the development of cancer. The research summarized here suggests that many of these biomarker assays can be used to distinguish between diseased and nondiseased states and in some instances may be able to predict susceptibility for future disease. Thus, these biomarkers could be valuable tools for monitoring at-risk populations for purposes of disease prevention and control. -Environ Health Perspect 105(Suppl 4): 807-816 (1997)

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Serum insulin-like growth factor-I levels in patients with small cell lung cancer

Cited by 12 publications

References 9 publications

Experimental and clinical studies with somatostatin analogue octreotide in small cell lung cancer

Experimental and clinical studies with somatostatin analogue octreotide in small cell lung cancer

The function of IGF-IR in NNK-mediated lung tumorigenesis

Biomarkers of gene expression: growth factors and oncoproteins.

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