Dabbous M K, Haney L, Nicolson G L, Eckley D, Woolley D E
Department of Biochemistry, University of Tennessee, Memphis 38163.
Br J Cancer. 1991 Jun;63(6):873-8. doi: 10.1038/bjc.1991.192.
Mast cells were shown to accumulate around the periphery of the invasive and metastatic rat mammary adenocarcinoma (MTLn3), and histological evidence of mast cell degranulation was observed during the later stages of this model. To assess the physiological role of mast cells in vivo we have used the mast cell-stabilising compound FPL 55618 applied i.p. daily at 1 mg kg-1 for 23 days. Using groups of 12 rats we have found that this compound inhibited tumour growth at the primary site by as much as 70% in most of the treated animals compared with the control group which received equivalent volumes of saline. When the drug treatment was stopped after 23 days, tumour growth of the test group accelerated over the next 7 days and reached a similar tumour size to that of control animals. Histological studies of the tumour and contiguous host tissue at day 24 of the experiment revealed numerous extra-tumoural mast cells often showing signs of degranulation at several sites around the tumour periphery in the control animals. Such observations were not seen in those animals receiving FPL 55618 where, in contrast to controls, numerous intact mast cells were often seen within the tumour mass. Following cessation of the MC-stabilising treatment progressive mast cell activation was evident within 2-4 days, primarily at the tumour periphery. In vitro studies have shown that drug concentrations equivalent to five times the in vivo dose had no effect on the proliferative rate or viability of the MTLn3 cells. Moreover, the proliferative rate of these cells in culture was significantly increased when exposed to soluble mast cell products. Thus our data indicate that a mast cell-stabilising compound has significant benefits in reducing tumour growth in vivo, an observation which supports the concept that mast cell:tumour cell interactions are important for the growth and invasive properties demonstrated by this model of breast carcinoma.
肥大细胞在侵袭性和转移性大鼠乳腺腺癌(MTLn3)的周边积聚,并且在该模型的后期观察到肥大细胞脱颗粒的组织学证据。为了评估肥大细胞在体内的生理作用,我们使用了肥大细胞稳定化合物FPL 55618,每天腹腔注射1 mg kg-1,持续23天。在每组12只大鼠的实验中,我们发现与接受等量生理盐水的对照组相比,在大多数接受治疗的动物中,该化合物可使原发部位的肿瘤生长抑制多达70%。当在23天后停止药物治疗时,试验组的肿瘤生长在接下来的7天内加速,并达到与对照动物相似的肿瘤大小。在实验第24天对肿瘤及相邻宿主组织进行的组织学研究显示,在对照动物的肿瘤周边多个部位,有大量肿瘤外肥大细胞,常显示出脱颗粒迹象。在接受FPL 55618的动物中未观察到此类现象,与对照组相反,在肿瘤块内常可见大量完整的肥大细胞。在停止肥大细胞稳定治疗后,2 - 4天内肥大细胞的活化逐渐明显,主要发生在肿瘤周边。体外研究表明,相当于体内剂量五倍的药物浓度对MTLn3细胞的增殖率或活力没有影响。此外,当暴露于可溶性肥大细胞产物时,这些细胞在培养中的增殖率显著增加。因此,我们的数据表明,一种肥大细胞稳定化合物在体内减少肿瘤生长方面具有显著益处,这一观察结果支持了肥大细胞与肿瘤细胞相互作用对该乳腺癌模型所表现出的生长和侵袭特性很重要这一概念。