BACKGROUND African‐American women have had a lower incidence, yet higher mortality rate from breast cancer compared with White‐American women. African‐American women also have had a higher risk for early‐onset, high‐grade, node‐positive, and hormone receptor‐negative disease. Similar features have characterized hereditary breast cancer, prompting speculation that risk factors could be genetically transmitted. Further evaluation of this theory required the study of breast cancer among women from sub‐Saharan Africa because of their shared ancestry with African‐American women. METHODS Publications from 1988 to 2004 of English‐language literature on breast cancer in Africa were reviewed. RESULTS Women from sub‐Saharan Africa were found to have a low incidence of breast cancer. This was partly explained by a largely protective reproductive history, including late menarche, early menopause, high parity with prolonged breastfeeding, irregular menses, and fewer ovulatory cycles. The average age at diagnosis, however, was approximately 10 years younger than breast cancer patients of western nations, and disease stage distribution was shifted toward more advanced disease, which resulted in higher mortality rates. These features were found to be similar to data on breast cancer in African‐American women. Mutations in BRCA1 and BRCA2 have been reported in African‐American women, but the extent of the contribution of BRCA1 and BRCA2 to breast cancer burden in Africa was uncertain. Limited financial resources lead to suboptimal cancer data collection, as well as delayed diagnosis and treatment of many African breast cancer patients. CONCLUSIONS Parallels between breast cancer burdens of African‐American and sub‐Saharan–African women were provocative, indicating the need for further exploration of possible genetically transmitted features related to estrogen metabolism and/or breast cancer risk. Cancer 2005. © 2005 American Cancer Society.

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The authors discovered a significant increase of low mineralized, immature bone and a significant decrease of highly mineralized, mature bone in the irradiated regenerate. These findings corroborate the authors' hypothesis that radiation induces a diminution in cell function, impairing optimal bone regeneration. Overall densitometrics, however, were unchanged according to micro-computed tomographic measurements, despite documented significant changes in biomechanical and histologic metrics. An optimal radiation dose must now be sought that demonstrates a higher degree of reproducible degradation, but not irreversible destruction, in all three outcomes. Such an approach will allow formulation of therapeutic interventions designed to enhance mandibular distraction osteogenesis so that it may be used as a viable reconstructive option.

The lowered breaking load in mandibular distraction osteogenesis following radiation therapy reflects the reduced biomechanical quality of the regenerate, despite evidence of radiographic union. These data show that radiographic union is not an adequate outcome measure for regenerate healing and support the need to define quantitative bone-healing metrics in mandibular distraction osteogenesis following radiation therapy before implementation in head and neck reconstruction.