Intralesional bleomycin injection (IBI) treatment for haemangiomas and congenital vascular malformations.

Successful treatment of vascular anomalies has eluded the physician until now, despite various treatments utilised. Bleomycin has been successfully used in intralesional injection treatment of cystic hygromas and haemangiomas, based specifically on a high sclerosing effect on vascular endothelium. In a prospective study of 95 patients, the effectiveness of intralesional bleomycin injection (IBI) treatment in haemangiomas and vascular malformations was evaluated and documented. Complete resolution or significant improvement occurred in 80% of all patients treated. Complete resolution occurred in 49% of haemangiomas, 32% of venous malformations, and 80% of cystic hygromas. Significant improvement occurred in 38% of haemangiomas, 52% of venous malformations, 13% of cystic hygromas and 50% of lymphatic malformations. Of the six patients who presented with a painful lesion, four experienced complete resolution and two had significant improvement to treatment. Local complications encountered were superficial ulceration occurring in 2 patients, and cellulitis in 1 of the 95 patients. Systemic complications were flu-like symptoms in three patients and partial, transient hair loss in two patients. None of the patients presented with haematological toxic effects or signs of pulmonary involvement (fibrosis, hypertension). IBI is an effective treatment in haemangiomas and vascular malformation lesions, obviating the need for invasive primary surgery or systemic treatment regimens in 80% of cases, and allowing for limited need of secondary surgical or adjunctive procedures in cases with a moderate result.

Some effects of linoleic acid and gamma-linolenic acid on the proliferation of human hepatoma cells in culture.

In previous communications the growth-suppressive effect of gamma-linolenic acid (GLA) dissolved in sodium carbonate in the culture media of malignant cells has been reported. In this study we show that linoleic acid (LA), the fatty acid precursor of GLA, had no growth-suppressive effect on human hepatoma cells in culture while a similar concentration of GLA suppressed malignant cell growth in culture by 69% after 10 days. This growth-suppressive effect must therefore be seen as an effect of GLA and not as a 'soap' effect. It has also been shown that the growth rate of human hepatoma cells in culture to which GLA was added daily for 5 consecutive days remained suppressed after the withdrawal of GLA from the growth medium for a further 5-day period. The striking difference between GLA and LA as regards growth suppression of human hepatoma cells in culture appears to imply a metabolic block in the hepatoma cells, involving the enzyme delta-6-desaturase, in the conversion of LA to GLA and thence via dihomo-gamma-linolenic acid to the prostaglandins of the 1 series.

The effect of gamma-linolenic acid on the growth of human osteogenic sarcoma and oesophageal carcinoma cells in culture.

A statistically highly significant growth-suppressive effect of the prostaglandin precursor gamma-linolenic acid (GLA) on MG63 human osteogenic sarcoma and oesophageal carcinoma cells in culture was found. In view of the results reported on the growth-suppressive effect of GLA on cancer cells in culture, on transplanted mammary tumours in rats and in primary liver cancer patients, it would appear that further investigation of the effects of this fatty acid on cancer cell growth both in vitro and in vivo is warranted.

The reversibility of cancer: evidence that malignancy in melanoma cells is gamma-linolenic acid deficiency-dependent.

Certain metabolic abnormalities are common to all malignant cells, and Horrobin proposed that the underlying cause is the inability of cancer cells to produce prostaglandin E1 (PGE1). This appears to be due to the lack of the enzyme delta-6-desaturase which converts the essential fatty acid, linoleic acid, to gamma-linolenic acid (GLA), from which PGE1 is then synthesized. Our studies strongly support this contention. Addition to GLA to cancer cells, thus bypassing the block in the metabolic pathway, results in very marked, statistically highly significant inhibition of growth, while having no effect at all on normal cells. Our finding of the regression of cancer through such proposed normalization offers preliminary hope for a new effective and harmless approach to the treatment of cancer.

Some effects of gamma-linolenic acid on cultured human oesophageal carcinoma cells.

Cells of two continuous human oesophageal carcinoma lines were treated by the addition of gamma-linolenic acid (GLA) at concentrations of 10-60 micrograms/ml culture medium. After 7 days of exposure to GLA, pronounced morphological changes became evident and culminated in cell death. GLA-mediated effects were time- and dose-dependent and varied slightly with the degree of histological differentiation of the lines tested. These findings may have clinical implications.

The reversibility of cancer: evidence that malignancy in human hepatoma cells is gamma-linolenic acid deficiency-dependent.

A further critical test of Horrobin's hypothesis that malignancy in cells may be dependent on gamma-linolenic acid (GLA) deficiency, has revealed that GLA supplementation produces a highly significant reduction in the growth rate (up to 87%) of a cultured human hepatoma cell line, compared with the growth rate of untreated hepatoma cells. This supports our previous suggestion that this hypothesis requires urgent further investigation at all levels including trials in human cancer patients.