Breast cancer, desmoid tumours, and familial adenomatous polyposis—a unifying hypothesis

Benson, JR; Baum, Michael

doi:10.1016/0140-6736(93)92700-4

Cited by 30 publications

(9 citation statements)

References 19 publications

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“…The importance of mesenchymal growth factor production in epithelial tumours has recently been re-emphasised (Benson and Baum, 1993). The effect of stromal IL6 production on ICAM-1 expression in the epithelial cells reflects one of many intercellular signalling a n d induction events likely to b e involved in tumour development.…”

Section: Discussionmentioning

confidence: 99%

Regulation of ICAM‐1 (CD54) expression in human breast cancer cell lines by interleukin 6 and fibroblast‐derived factors

Hutchins

Steel

1994

Intl Journal of Cancer

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Four human breast cancer cell lines (T47D, ZR-75-1, MCF7D and HS578T) were examined for the effects of cytokines on expression of cell surface antigens. Interferon (IFN)gamma up-regulated the expression of ICAM-I (CD54) in all the cell lines and coordinately up-regulated both CD54 and CD40 expression in T47D. Tumour necrosis factor (TNF)alpha, interleukin (IL)1 alpha, IL1 beta and IL6 also up-regulated the expression of CD54 in all the cell lines but CD40 was unaffected. Levels of expression of CD11a, CD18, CD49b, CD58 and CD71 were unaltered by these cytokines. Conditioned medium (CM) generated from human fibroblasts, and in particular from foetal cells, was highly effective in up-regulating expression of ICAM-1 but not of CD40 in the breast cancer cell lines. ICAM-1 induction correlated with IL6 bioactivity in these CMs. Combinations of IL6 with other cytokines, such as IL1, resulted in further increases in ICAM-1 expression. Our observations suggest that IL6 is involved in intercellular signalling between mesenchyme and breast cancer epithelium.

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Section: Discussionmentioning

confidence: 99%

Regulation of ICAM‐1 (CD54) expression in human breast cancer cell lines by interleukin 6 and fibroblast‐derived factors

Hutchins

Steel

1994

Intl Journal of Cancer

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“…This growth factor is involved in cellular proliferation and differentiation during development, and defective TGF-P signalling may be implicated in carcinogenesis (Roberts et al, 1988). Specific roles for TGF-# in malignant predisposition and progression have been proposed, owing either to loss of sensitivity to TGF-# (Tucker et al, 1984) or defective intrinsic production by stromal cells, leading to reduced negative paracrine influences upon neighbouring epithelial cells (Benson and Baum, 1993 sample of a patient with benign breast disease, and these were considered to be normal skin fibroblasts. Specimens of tissue, collected at surgery, were washed immediately in RPMI-1640 medium following collection and excess fat trimmed off.…”

mentioning

confidence: 99%

Synthesis and secretion of transforming growth factor beta isoforms by primary cultures of human breast tumour fibroblasts in vitro and their modulation by tamoxifen

Benson

Wakefield²,

Baum³

et al. 1996

Br J Cancer

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Summary Tamoxifen may mediate its effect in early breast cancer in part via an oestrogen receptor (ER)-independent pathway by directly stimulating fibroblasts to produce the negative paracrine growth factor transforming growth factor (TGF)-f,. We have previously shown that secretion of this factor is induced 3-to 30-fold in human fetal fibroblasts in vitro, and by stromal fibroblasts in vivo following tamoxifen treatment of ERpositive and ER-negative breast cancer patients. Primary cultures of breast tumour fibroblasts have been exposed to tamoxifen for 48 h, and rates of secretion of TGF-fl, and TGF-fl2 measured using a quantitative immunoassay. Fibroblast strains derived from malignant and benign tumours produced and secreted similar amounts of TGF-flp, but benign breast tumour fibroblasts secreted significantly higher levels of TGF-f32 compared with fibroblasts of malignant origin. Tamoxifen did not induce any consistent increase in TGF-,B secretion into the conditioned medium, but immunofluorescence analysis for the intracellular form of TGF-f3, revealed evidence of increased immunoreactive protein in tamoxifen-treated fibroblasts, which is localised to the nucleus. Therefore synthesis of TGF-fl, appears to be stimulated by tamoxifen, but increased secretion may be abrogated in vitro. Furthermore, using immunocytochemistry and transient transfection with an ER-responsive reporter construct, no ER was demonstrable in these fibroblasts supporting the proposed ER-independent paracrine pathway.

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“…It is known that NSAIDs are able to inhibit tumor angiogenesis [31,32]. On the other hand, stromal-epithelial interactions are determinant during development of neopla 262 Tonell i/V alanzano/Dolara Sulindac in FAP sia, and evidence is now arising of interac tions both in early phases and during tumor progression [44], In fact, colonic carcinoma cells cultured with fibroblasts respond to mes enchymal factors which stimulate growth and promote differentiation [45].…”

Section: Possible Mechanisms Of Action Of Sulindacmentioning

confidence: 99%

Sulindac Therapy of Colorectal Polyps in Familial Adenomatous Polyposis

Tonelli

Valanzano²,

Dolara³

1994

Dig Dis

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Familial adenomatous polyposis (FAP) is characterized by multiple adenomatous colorectal polyps, some of which progress to adenocarcinoma in the absence of surgery. Colectomy with ileorectal anastomosis still remains much in use, although strict surveillance of the rectal stump is necessary to prevent rectal cancer. After 1983, sulindac has been used to control rectal polyps in about 90 FAP patients, at doses of 150-400 mg/day. The treatment was well tolerated, and regression of the polyps was frequently observed. However, recurrence of polyps was sometimes observed, and the onset of rectal cancer during sulindac therapy was also reported. A review of the literature and the personal experience of the authors are here presented, discussing the pharmacological profile and possible mechanisms of action of sulindac.

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Breast cancer, desmoid tumours, and familial adenomatous polyposis—a unifying hypothesis

Cited by 30 publications

References 19 publications

Regulation of ICAM‐1 (CD54) expression in human breast cancer cell lines by interleukin 6 and fibroblast‐derived factors

Regulation of ICAM‐1 (CD54) expression in human breast cancer cell lines by interleukin 6 and fibroblast‐derived factors

Synthesis and secretion of transforming growth factor beta isoforms by primary cultures of human breast tumour fibroblasts in vitro and their modulation by tamoxifen

Sulindac Therapy of Colorectal Polyps in Familial Adenomatous Polyposis

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