Cyclooxygenase-2 Pathway Correlates with VEGF Expression in Head and Neck Cancer. Implications for Tumor Angiogenesis and Metastasis

This review presents an atlas of the histology of the normal physiological states of the human breast including prenatal, prepubertal, and pubertal development, adult resting gland, pregnancy, lactation, and postinvolution. The aim is to produce a pictorial overview of the main stages in development and the common findings in the adult that are considered to be within the range of normality. Unlike inbred strains of animals, in humans it is clear that the chronology of ductal and lobular development is not predictable, either in the fetus, the infant, the peripubertal breast, or the adult. This is probably due to the individual variation in hormone levels both in utero and after birth. For many of the developmental time points there are very little data available. In this review we indicate the current state of knowledge of human breast development and some of the main similarities and differences with the rodent, the main animal model. The major phases of growth and development are described and accompanied by photographs that are representative of each stage. Stress is placed on terminology as there is confusion in the literature. This article is written as an accessory to the companion review on breast cancer.

Human Breast Development

Prognostic significance of cyclooxygenase-2 pathway and angiogenesis in head and neck squamous cell carcinoma

Exercise-induced muscle damage (EIMD) occurs primarily from the performance of unaccustomed exercise, and its severity is modulated by the type, intensity, and duration of training. Although concentric and isometric actions contribute to EIMD, the greatest damage to muscle tissue is seen with eccentric exercise, where muscles are forcibly lengthened. Damage can be specific to just a few macromolecules of tissue or result in large tears in the sarcolemma, basal lamina, and supportive connective tissue, and inducing injury to contractile elements and the cytoskeleton. Although EIMD can have detrimental short-term effects on markers of performance and pain, it has been hypothesized that the associated skeletal muscle inflammation and increased protein turnover are necessary for long-term hypertrophic adaptations. A theoretical basis for this belief has been proposed, whereby the structural changes associated with EIMD influence gene expression, resulting in a strengthening of the tissue and thus protection of the muscle against further injury. Other researchers, however, have questioned this hypothesis, noting that hypertrophy can occur in the relative absence of muscle damage. Therefore, the purpose of this article will be twofold: (a) to extensively review the literature and attempt to determine what, if any, role EIMD plays in promoting skeletal muscle hypertrophy and (b) to make applicable recommendations for resistance training program design.

Does exercise-induced muscle damage play a role in skeletal muscle hypertrophy?

• The in vivo administration of a prostaglandin-synthetase inhibitor inhibited or reduced tumor growth in cancer patients and experimental animals. Indomethacin, a prostaglandin-synthetase inhibitor and nonsteroidal anti-inflammatory agent commonly used in the management of arthritic patients, acted as an immune adjuvant by decreasing the production of prostaglandins. Seven cases demonstrated that indomethacin taken in the usually recommended dosages causes regression and stabilization of head and neck cancer. The following factors were also considered in this study: prostaglandin production, a survey of other reports of solid neoplasm response to prostaglandin-synthetase inhibitor administration, drug toxicity, irradiation therapy and metastases, the need for tumor biopsy, and the role that reduction in inflammation plays in tumor shrinkage. ( Arch Otolaryngol 1981;107:658-663)

BasilA. Stoll

Papers

Health care in south africa

Indomethacin in breast cancer.

Brain catecholamines and breast cancer: a hypothesis.

Prenatal influences and breast cancer

"false-positive" œstrogen-receptor assay in breast cancer