common isochromosome is the X sex chromosome. Acrocentric autosomal chromosomes 13, 14, 15, 21, and 22 are also common candidates for isochromosome formation. Chromosomes containing smaller arms are more likely to become isochromosomes because the loss of genetic material in those arms can be tolerated. Turner syndrome Turner syndrome is a condition in females in which there is partial or complete loss of one X chromosome. This causes symptoms such as growth and sexual development problems. In 15% of Turner syndrome patients, the structural abnormality is isochromosome X, which is composed of two copies of the q arm (i(Xq)). A majority of i(Xq) are created by U-type strand exchange. A breakage and reunion in the pericentric region of the p arm results in a dicentric isochromosome. Some of the p arm can be found in this formation of i(Xq), but a majority of the genetic material on the p arm is lost so it is considered absent. Since the p-arm of the X chromosome contains genes that are necessary for normal sexual development, Turner's syndrome patients experience phenotypic effects. Alternatively, the increase in dosage of genes on the q arm may be involved in a 10-fold increase in risk of i(Xq) Turner's patients developing autoimmune thyroiditis, a disease in which the body creates antibodies to target and destroy thyroid cells. Neoplasia Neoplasia is uncontrolled cell growth, resulting in the creation of a tumour. In many different forms of neoplasia, isochromosome 17q is the most frequent neoplasia associated isochromosome and corresponds with poor patient survival. Unique DNA sequences, known as low copy repeats, occur in the pericentric region of the p arm, so a crossover event in that area can create a dicentric isochromosome through U-type strand exchange. The neoplasia created from i(17q) is caused by a decrease and increase in gene dosage from the monosomy of the p arm and trisomy of the q arm, respectively. Many candidate tumour suppressor genes are found on the lost p arm, allowing the tumour cell population to be maintained. It is debated whether the loss of tumour suppressor gene p53, located on 17p, is involved in the central pathogenesis of some neoplasia. The presence of one p53 gene can be functionally active, but its relation to other oncogenes can alter its expression levels when present only in one copy. Since the genetic sequences involved in i(17q) neoplasia are large, it is difficult to