Disease relevance of Anaplasia

• PURPOSE: To evaluate the effect of the combination of vincristine, dactinomycin, and doxorubicin with (regimen J) or without (regimen DD-RT) cyclophosphamide on the relapse-free survival of children with stages II to IV Wilms' tumor and focal or diffuse anaplasia [1].
• Histologically, rhabdoid meningiomas usually exhibit signs of anaplasia, a high mitotic activity, and a markedly increased MIB-1 labeling index [2].
• These findings demonstrate that the lack of functional p53 in ret/PTC1 mice promotes anaplasia and invasiveness of thyroid carcinomas [3].
• These mice were crossed with p53-/- mice to investigate whether loss of p53 would promote anaplasia and metastasis of ret/PTC1-induced thyroid tumors [3].
• In astrocytic tumors, p27 decreases with advancing anaplasia and is almost absent in glioblastomas [4].

High impact information on Anaplasia

• A semiquantitative immunohistochemical method demonstrated that expression of the p21 antigen in a carcinoma strongly correlated with nuclear anaplasia and was inversely related to the degree of glandular differentiation [5].
• Our data further supported the association between HVH-2 and cervical anaplasia and indicated that CMV may also be implicated in its etiology [6].
• These results indicate that progression to anaplasia is associated with clonal expansion of cells which have acquired a p53 mutation [7].
• CONCLUSION: We conclude that children with focal anaplasia have an excellent prognosis when treated with vincristine, doxorubicin, and dactinomycin [1].
• A critical observation from histopathological studies is that there is progressive loss of GFAP expression with increasing astrocytic anaplasia [8].

Chemical compound and disease context of Anaplasia

• The addition of cyclophosphamide to the three-drug treatment regimen improved the 4-year relapse-free survival rate of children with stage II to IV diffuse anaplasia [1].
• The disappearance of the CK-M subunit of creatine kinase and decreasing levels of creatine kinase were demonstrated with increasing anaplasia [9].
• The inhibitory effect of retinyl acetate may be related to the effect of retinoids on epithelial cell differentiation and/or reversal of carcinogen-induced anaplasia [10].
• The levels of uPA and PAI-1 were correlated with tumour size, degree of anaplasia, steroid receptor status and number of positive nodes [11].
• CONCLUSIONS: Preoperative chemotherapy followed by nephron sparing surgery is indicated in patients with bilateral Wilms tumor, while in those with diffuse anaplasia nephron sparing surgery is contraindicated [12].

Biological context of Anaplasia

• Thirty-four Wilms' tumors with nephrogenic rests and/or areas of anaplasia were microdissected from paraffin sections to determine whether and at what stage loss of heterozygosity (LOH) occurred, using polymerase chain reaction-based polymorphic markers at 11p13, 11p15, and 16q [13].
• Six cases are reported (four gliosarcomas and two glioblastomas) in which the epithelial-like areas of glial anaplasia showed focal squamous cell differentiation, characterized by the development of epithelial whorls, keratin pearls and immunopositivity for cytokeratin [14].
• Ki-67 expression was correlated significantly with histologic grade only in the clinicopathologic factors (P <.0001), and in the histologic factors, with necrosis, mitosis, and anaplasia [15].
• These observations suggest that elevated ras p21 antigen expression is important in the development of both cirrhotic nodules and HCC, but that after tumor development, its sustained elevation is no longer necessary for cell proliferation and progression through the grades of anaplasia [16].
• Our observations show that complex chromosome abnormalities and telomeric associations are observed in tumors that histologically display a certain degree of anaplasia [17].

Anatomical context of Anaplasia

• The results of these studies clearly show a disparity between the forms of hCG found in the normal placenta and pregnancy sera, as previously reported, and those found in the neoplastic trophoblast with varying degrees of anaplasia [18].
• HER2 is not expressed in adult glial cells, but its expression increases with the degree of astrocytomas anaplasia [19].
• The diagnosis of thymoma was used for circumscribed and invasive neoplasms of thymic epithelium without anaplasia [20].

Gene context of Anaplasia

• Loss of p53 promotes anaplasia and local invasion in ret/PTC1-induced thyroid carcinomas [3].
• In astrocytic neoplasms, the number of cells expressing glial fibrillary acidic protein (GFAP) is inversely proportional to the extent of anaplasia [21].
• Increased vimentin expression associated with a decrease of GFAP immunoreactivity correlated with anaplasia and short survival [22].
• No change in vimentin- or GFAP-IF expression with increasing anaplasia was seen [23].
• In gliomas, contrary to many malignancies, cyclin D1 is rarely amplified, but together with other cyclins, it increases with anaplasia [24].

Analytical, diagnostic and therapeutic context of Anaplasia

• Using the log-rank test (median observation time 94 months) a significantly worse prognosis (disease-free survival, overall survival) relation was found with larger tumors, nodal involvement, anaplasia, rising proliferation activity, and lack of steroid receptors [25].

References