Dysplasia markers

P53 Normal p53 protein has an extremely short half-life and is found in small quantities inside cells. As such, p53 cannot be detected in normal cells using immuno-histochemistry. The p53 protein from abnormal p53 genes has a longer half-life than normal p53 protein, builds up inside cells, and can be detected with anti-p53 antibodies. In theory, p53 overexpression, as a surrogate marker for p53 gene mutations, is an immunohis-tochemical test for neoplasia (dysplasia). However, this is not the case in practice because correlation between staining and gene abnormalities is not precise. ... 

Andersen SN, Rognum TO, Bakka A, Clausen OP. Ki-67 a useful marker for the evaluation of dysplasia in ulcerative colitis. Mol Pathol. 1998 51 327-332. 

Weston AP, Banerjee SK, Sharma P, et al. p53 protein overexpression in low grade dysplasia (LCD) in Barrett s esophagus immunohistochemical marker predictive of progression. Am J Gastroenterol. 2001 96 1355-1362. 

Hamden P, Eardley I, Joyce AD, Southgate J. Gytokeratin 20 as an objective marker of urothelial dysplasia. Br J Urol. 1996 78 870. 

Cortical dysplasia consists of disrupted cortical architecture and abnormally enlarged cells, some with IFIC staining of neurons, some with GFAP-positive astrocytes, and some individual cells that stain for both glial and neuronal markers.Cortical tubers, seen with tuberous sclerosis, are cortical dysplasias. Other dys-plastic abnormalities are described in the Neuronal Tumors section earlier in this chapter. 

Saqi A, Pasha TL, McGrath CM, et al. Overexpression of pl6INK4A in liquid-based specimens (SurePath) as marker of cervical dysplasia and neoplasia. Diagn Cytopathol. 2002 27 365-370. 

H. pylori and the associated chronic inflammation are thought to initiate a cascade of events leading to atrophic gastritis, metaplasia, dysplasia, and cancer (Fignre 10.2). Once progression to dysplasia occurs, continued infection is probably uimecessary for continuation of the neoplastic sequence. In fact, the atrophic stomach may itself be unsuitable for continued H. pylori infection, and markers of infection may be negative at the time of diagnosis." ... 

The risk factors for developing EAC still remain unclear. As we better understand the epidemiology of the disease, we will be better able to screen patients and prevent the progression to advanced EAC. Further research into better noninvasive screening methods for BE, less invasive methods to survey for dysplasia, vahdation of biological markers to identify those at risk to develop EAC, and use of chemotherapeutic and endoscopic ablation techniques will hopefully result in a better prognosis for patients presenting with EAC in the future. 

The precancerous lesions termed aberrant crypts (AC) have been developed as an early marker for colon carcinogenesis (21). Upon treatment with colon carcinogens mice and rats develop early preneoplastic changes in the crypts of the colon that are easily observable under light microscope after methylene blue staining. Histological examination of AC foci confirmed their dysplasia nature, and are considered precursors to colon cancer (22-25). 

The studies mentioned above suggest that flow-cytometric and p53 abnormalities may be earlier and more specific markers for cancer development than the histologic finding of dysplasia. Nevertheless, these markers do not yet provide sufficient additional information to justify their routine application in clinical practice. Indeed, none of the biomarkers listed in the table provides such information. Despite the problems, at this time, the finding of dysplasia remains the most appropriate biomarker for the clinical evaluation of patients with Barrett s esophagus. 

Yet, there is no direct correlation between the degree of dilatation and renal function. The best marker of renal obstructive dysplasia and probable poor renal function is probably hyperechoic parenchyma with macrocysts within it (Blane et al. 1991). 

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