By using the method of clonal analysis the evidence to prove that Hemophagocytic syndrome (HPS) is reactive or malignant was investigated to probe into the pathogenesis of HPS and its relations with clinical prognosis. The macrophages abnormally proliferated in bone marrow were isolated. Electrophoresis analysis was made after DNA extraction, enzyme restriction of human ardrogen receptor (HUMARA) genetic locus, and PCR amplification. In the 9 specimens, clonal proliferation was found in 2 cases and nonclonal proliferation in 7. Among the 7 cases of nonclonal proliferation, 3 were voluntarily discharged without clinical outcome, 2 cases fully recovered after 2–3 week treatment of large dose gamma globulin intravenous drip and hormone therapy, 1 case died at the 43th day after the hormone and anti-infection therapy, and one case was found to have granular leukoblast in peripheral blood after 3 weeks and diagnosed as having M2a after bone puncture. For the two patients with clonal proliferation, one obtained remission after chemotherapy and the other was died after 32 days without chemotherapy. It was concluded that there do exist clonal or malignant proliferation in HPS, so not every case is reactive.
The role of bcl-2 in the pathogenesis of colorectal tumor were studied. The expression of bcl-2 in the colorectal carcinoma and incisional edge tissue of tumor was detected by using SABC method. The results showed that the positive rate of bcl-2 was 69.6% in colorectal carcinoma and 47.6% in the incisional edge tissue respectively, with the difference being very significant (P=0.001). Bcl-2 positive rate was associated with Dukes' stage, but had nothing to do with histological classification. It was concluded that bcl-2 might play a significant role in the development of colorectal carcinoma.