Our experiences with combination of enzyme therapy and laser therapy in enthesopathies.

The present communication brings a contribution to the confrontation of two treatment methods in enthesopathies (painful overload syndromes). In group A, 26 patients were treated by a combination of systemic enzyme therapy (SET) and non-invasive laser therapy. In group B, 13 persons were treated only by therapeutic laser. The average age in group A and B was of 39.3 and 41.8 years, respectively. The representation of men and women in the two groups was almost identical. The intensity of the pain prior to the treatment and after the treatment, specified by each patient with the help of a ten-grade scale, was evaluated by the variance analysis. The combined treatment by the SET and therapeutic laser was statistically significantly more efficient (p = 0.02). On the other hand, there was also a significant difference between the two groups in baseline values of average pain intensities. These values were of 7.0 and 5.2 in groups A and B, respectively. The average value of the pain intensity in all the 39 patients was of 6.6 prior to the treatment and it was reduced to 3.5 after the treatment.

Retinoid X receptor suppresses transformation by the v-myb oncogene.

The v-myb oncogene of avian myeloblastosis virus causes acute monoblastic leukemia in vivo and transforms myelomonocytic cells in culture. Retinoids are potent regulators of proliferation and differentiation in various cell types, and they can initiate differentiation in certain types of leukemic cells. However, the BM2 v-myb-transformed chicken monoblastic cell line is resistant to retinoic acid treatment. We found that overexpression of the retinoid X receptor confers sensitivity of BM2 cells to retinoic acid, resulting in induction of growth arrest and terminal differentiation. In contrast, the frequency of apoptosis was not affected by the retinoid X receptor in this cell type. We also demonstrated that suppression of transformation by v-Myb results from the negative effect of retinoid X receptor on v-Myb transactivation function, similar to that previously described for the retinoic acid receptor. The retinoid X receptor-induced inhibition of transactivation by v-Myb seems to be enhanced by a cell type-specific factor(s), which is not required by retinoic acid receptor.

Oncoprotein v-Myb and retinoic acid receptor alpha are mutual antagonists.

The process of hematopoiesis is critically dependent on correct interactions of multiple regulatory molecules and transcription factors. We have studied the interactions of the v-Myb and retinoic acid receptor proteins which have opposing effects on hematopoiesis. While v-myb acts as a transforming oncogene preventing differentiation of monoblasts to macrophages, RAR alpha functions as an anti-oncogene arresting the growth of v-myb-transformed cells and allowing their final myeloid differentiation steps to occur. We found that the retinoic acid receptor alpha inhibits v-Myb transformation by suppressing the expression of v-Myb target genes typified by the mim-1 gene. Conversely, v-Myb protein interferes with RAR alpha transactivation function as well as with retinoic acid-induced apoptosis of HL-60 cells. These results demonstrate that retinoic acid receptor and v-Myb proteins act in antagonistic ways and reciprocally modify each other's functions.

A possible cross-talk of retinoic acid- and TPA-driven myeloid differentiation pathways.

Retinoic acid (RA) and phorbol esters are important regulators of cellular proliferation and differentiation processes which are capable of arresting growth and inducing differentiation of various leukemic cells. We have studied and compared the effects of these agents on the line of v-myb oncogene-transformed chicken monoblasts BM2. We found that although there are differences in the differentiation kinetics and cell cycle stop points, the differentiation pathways induced by RA and phorbol esters seem to be significantly interconnected.