Knowledge about hereditary cancer of women with family histories of breast, colorectal, or both types of cancer.

Usually, the mass media do not address hereditary cancer and their risk factors, nor are these topics discussed at the community level. We used an informative guide on cancer and hereditary cancer, followed by a questionnaire on these topics to investigate the relevant knowledge among women at high risk for hereditary breast and/or colorectal cancer from a population-based cohort. The cohort was composed of 81 Brazilian women with positive family histories of breast and/or colorectal cancer. Strauss and Corbin's Grounded Theory was used for qualitative analysis. The average age of the cohort was 49.9 years old. Three participants (3.9%) were illiterate, 45 (59.2%) had attended elementary school, 14 (18.4%) had secondary school, and 14 (18.4%) held higher education degrees. A total of 47 (54.3%) volunteers were unable to fully understand the information provided in the guide because they did not know the meaning of words such as metastasis, malignant, hereditary, sporadic, or oncogenetics. Notwithstanding, the acceptance of the educational tool utilized was satisfactory, and it enhanced the volunteers' interest in a better understanding of cancer and heredity. Thereby, we concluded that the low knowledge of this important subject and the unawareness about fundamental terms required for the comprehension of this specific type of neoplasm made us believe that the use of the informative guide can provide a great value when used previously to the genetic counseling consultations. Besides, educational tools of easy understanding should be part of everyday clinical practice, from primary to specialized patient care.

Early expression of iepsilon, CD23 (FcepsilonRII), IL-4Ralpha, and IgE in the human fetus.

BACKGROUND: A major predictor of childhood atopy is the concentration of IgE in the cord blood, but whether the source of cord blood IgE is maternal or fetal remains unclear. OBJECTIVE: We sought to determine the pattern of in situ IgE production during ontogeny. METHODS: Ninety-seven fetal, 142 natal, and 96 childhood samples were analyzed by using reverse transcription PCR for transcription of VDJCepsilon, Iepsilon, and CD23. Thirty-eight fetal liver samples were analyzed for the IL4RA genotype. RESULTS: IL-4Ralpha, CD23a, CD23b, and sterile Iepsilon transcripts were present as early as 8 weeks' gestation. VDJCepsilon transcripts were found in second-trimester fetal liver and third-trimester cord blood, although they were rare. VDJCepsilon transcripts were more common in the blood of children 9 months and older. Sequence analysis suggested that fetal VDJCepsilon was the product of selection. All fetal livers actively transcribing Iepsilon, VDJCepsilon, and IL-4Ralpha contained at least one copy of the atopy-associated IL4RA*A1902G polymorphism. CONCLUSION: The human fetus contains B cells that are primed to undergo IgE class switching from the earliest stages of ontogeny and can produce endogenous IgE by 20 weeks' gestation. However, IgE-producing cells are rare until 9 months after birth.

IgM heavy chain complementarity-determining region 3 diversity is constrained by genetic and somatic mechanisms until two months after birth.

Due to the greater range of lengths available to the third complementarity determining region of the heavy chain (HCDR3), the Ab repertoire of normal adults includes larger Ag binding site structures than those seen in first and second trimester fetal tissues. Transition to a steady state range of HCDR3 lengths is not complete until the infant reaches 2 mo of age. Fetal constraints on length begin with a genetic predilection for use of short DH (D7-27 or DQ52) gene segments and against use of long DH (e.g., D3 or DXP) and JH (JH6) gene segments in both fetal liver and fetal bone marrow. Further control of length is achieved through DH-specific limitations in N addition, with D7-27 DJ joins including extensive N addition and D3-containing DJ joins showing a paucity of N addition. DH-specific constraints on N addition are no longer apparent in adult bone marrow. Superimposed upon these genetic mechanisms to control length is a process of somatic selection that appears to ensure expression of a restricted range of HCDR3 lengths in both fetus and adult. B cells that express Abs of an "inappropriate" length appear to be eliminated when they first display IgM on their cell surface. Control of N addition appears aberrant in X-linked agammaglobulinemia, which may exacerbate the block in B cell development seen in this disease. Restriction of the fetal repertoire appears to be an active process, forcing limits on the diversity, and hence range of Ab specificities, available to the young.