By Roger S. Kirby MD FRCS(Urol) FEBU
This can be a condensed model of the author's profitable Atlas of Prostatic Disease. The emphasis is on a succinct description of prostatic illness in a mostly illustrative layout. The publication covers the motives, prognosis and staging of prostate melanoma, benign prostatic hyperplasia and prostatitis. The sections on therapy were more advantageous via the addition of algorithms to summarize the decision-making strategy.
Men's healthiness is now an incredible public future health factor and prostatic affliction could have an incredible influence at the caliber of lifetime of many males. This booklet will supply a handy precis for urologists, basic care physicians and nurse practitioners
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Extra info for An illustrated pocketbook of prostatic diseases
Identification of this process of invasion can be facilitated by the use of immunocyto-chemistry to delineate basal cells and the cytokeratin of the basement membrane (see Figure 3). Once invasion has occurred, the histological grading of the malignancy is accomplished by use of Gleason’s technique27, which is based on the tendency of a given tumor to form gland-like structures (Figure 35). Because of the marked heterogeneity of prostatic cancers, the Gleason score is calculated as the sum of the two most dominant histological patterns within a given cancer.
A mutation (Figure 18), resulting in a single base-pair change, causes an inability to separate GTP from the ras p21 protein, thereby locking it permanently in its activated form. The result is a continuing inappropriate signal for cell proliferation (Figure 19). Another oncogene, c-erb B-2, acts through a different mechanism. A point mutation of DNA segment coding for c-erb B-2 results in the production of a distorted version of the EGF receptor. This mutant protein has no external component, with the result that the internal component continually signals the need for cell division, regardless of the presence or absence of EGF signal molecules15.
Normally, the p53 protein is involved in the regulation of cell division. Mutation or deletion of the gene thus encourages uncontrolled cell division suppressor genes16, the best examples of which are the p53 and retinoblastoma tumor suppressor genes17,18. The p53 protein encoded by the former gene acts as an important regulator of cell division. Point mutation or complete deletion of this gene permits abnormal cell proliferation to occur (Figure 20). The p53 tumor suppressor gene has also been implicated as an important factor in the development of other cancers, including lung, breast, colon and bladder neoplasms19,20.
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