PubMed · 5453536
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R Hervé, P Sergent. [Cervical mucus].. https://pubmed.ncbi.nlm.nih.gov/5453536/
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Prophylactic vaccination has made an essential contribution to the improvement of human health over the 20th century. However, we still lack efficient vaccines against major human diseases such as malaria or tuberculosis. Today, the design of therapeutic vaccines referred to as 'pharmaccines' is actively investigated in order to treat diseases such as cancer. In that context, novel ways to rationalize and accelerate vaccine discovery are needed. A series of advances in the fields of molecular biology and computer science, have greatly accelerated the rate at which candidate vaccine antigens can be discovered. In this review, we will present and discuss how applied genome research may facilitate antigen discovery and the design of new prophylactic and therapeutic vaccines.
The use of recombinant factor VIIa (rFVIIa) is on the increase, not only to treat haemophilic patients with inhibitors, but also patients with other clotting disorders. However, the most appropriate method of monitoring this treatment remains a question that has yet to be resolved. We studied 24 plasma samples from patients receiving rFVIIa treatment (three had haemophilia A with inhibitors, and three a congenital FVII deficiency) and compared the results obtained from the FVII:C and FVIIa assays. Although a good correlation between the two methods was obtained (r = 0.91), the values of the FVII:C method were 1.63 higher than those of the FVIIa method, with a relatively wide margin in the interval of the FVII:C/FVIIa ratios obtained [95% confidence interval (CI) 1.38--1.88, range 0.68--3.68]. This interval became wider when we compared values of over 6 IU mL(-1), which led us to conclude that the two methods cannot be considered equivalent. As the FVIIa method specifically measures FVIIa, and FVII:C assay is known to have a wide interlaboratory variability, we believe that the FVIIa assay would be more suitable for the monitoring of rFVIIa treatment.
Twenty years ago the fetal antigen hypothesis was proposed as a potential mechanism by which women are naturally immunized against cancer antigens by antigens from their fetus. Evidence from recent clinical studies shows that a high percentage of parous woman, but not nulliparous women, show evidence of immunization to antigens found on breast, ovarian and endometrial cancer cells. I suggest that this maternal immunization also affects the fetus, causing early immune rejection of fertilized ova that express cancer-related genotypes. Additional cancers, and perhaps even other types of genetic diseases, may be involved in this mechanism.