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At least 19 recordsLinked to original sources
PubMed2006

Bilateral Wilms' tumor with anaplasia: lessons from the National Wilms' Tumor Study.

PURPOSE: The purpose of this study was to evaluate whether initial diagnostic technique influenced the ability to identify anaplastic histology, to determine the time interval to diagnosis of anaplasia, and to delineate the incidence of discordant pathology in bilateral Wilms' tumor. We hypothesized that delay in diagnosis of anaplasia could affect time to appropriate surgery and intensive multimodality therapy. METHODS: One hundred eight-nine children were enrolled in the fourth National Wilms' Tumor Study with synchronous bilateral tumors, 27 of whom were eventually shown to have anaplastic histology. Initial diagnostic technique, time interval to diagnosis of anaplasia, and the incidence of discordant pathology were determined. RESULTS: Anaplasia was identified in 0 of 7 tumors by core needle biopsy, 3 of 9 tumors by open wedge biopsy, and in 7 of 9 cases by partial or complete nephrectomy. The mean duration of first chemotherapy regimen (DD or EE) was 20, 39, and 36 weeks, respectively, before anaplasia was identified at second surgery. Discordant pathology between bilateral tumors was identified on final tissue diagnosis in 20 patients. Only 4 patients had anaplastic tumors in both kidneys. CONCLUSIONS: Core needle biopsy did not identify anaplasia in 7 of 7 children. Open biopsy or partial/complete nephrectomy identified anaplasia at initial diagnostic procedure in 10 of 18 children. Twenty of 24 patients at final tissue diagnosis had discordant pathology between the 2 kidneys. Earlier interval incisional biopsy or resection may identify anaplastic histology and limit the duration of chemotherapy targeted to favorable histology for children with bilateral Wilms' tumor and anaplasia.

Adult↗
PubMed1996

Focal versus diffuse anaplasia in Wilms tumor--new definitions with prognostic significance: a report from the National Wilms Tumor Study Group.

Anaplasia, defined by the presence of extreme nuclear and mitotic atypia, is a potent marker of adverse prognosis in Wilms tumor (WT). Anaplastic WT cells apparently have increased resistance to therapy rather than increased aggressiveness. The distribution of anaplasia should therefore have critical prognostic relevance. The original definitions for focal anaplasia (FA) and diffuse anaplasia (DA) were based on quantitative rather than topographical criteria and lacked prognostic significance. A new definition was developed based on the distribution of anaplastic changes within the tumor: FA applies only to tumors with anaplasia confined to one or a few discrete loci within the primary tumor, with no anaplasia or marked nuclear atypia elsewhere. This revised definition was evaluated in 165 cases with anaplastic WT entered on the third and fourth National Wilms Tumor Study. Only three relapses and one death occurred among 39 cases with FA, regardless of tumor stage, a result comparable to that for nonanaplastic WT. Eight children with metastases at diagnosis and FA in the primary tumor were alive and free of relapse; 22 of 23 children with stage IV DA WT died of tumor. This new definition reinforces the importance of carefully documenting the exact site from which each tumor section is obtained.

Anaplasia↗
PubMed1999

New definitions of focal and diffuse anaplasia in Wilms tumor: the International Society of Paediatric Oncology (SIOP) experience.

BACKGROUND: Unlike the original definitions of focal (FA) and diffuse anaplasia (DA) in Wilms tumor (WT), recently redefined FA and DA proved to be of prognostic significance. The aim of the study was to analyze WT from the SIOP file, the majority of which were treated with preoperative chemotherapy, in order to investigate whether chemotherapy influenced the presence of anaplasia, whether the new definitions were applicable to these tumors, and whether they were of prognostic significance. PROCEDURE: The unilateral anaplastic WT of children up to 16 years of age from the SIOP 6 and 9 nephroblastoma trials and studies were first classified according to the original definitions and analyzed. Then they were reclassified and analyzed according to the new definitions. RESULTS: Anaplasia was diagnosed in 86 (5.5%) of 1,554 unilateral WT. The age at diagnosis ranged from 9 to 175 months (median, 63) and more than half of children were over 5 years of age. From 15% to 85% of the tumor mass showed chemotherapy-induced changes. Blastemal anaplasia was seen in 74, stromal in 23, and epithelial in 22 cases. According to the original definitions, FA was diagnosed in 55 (64%) and DA in 31 (36%) cases. In total, 48% children were alive and well, including 53% with FA and 39% with DA (P = 0.23). When reclassified, 39 old FA cases were moved to the new DA group, resulting in 70 (81%) DA and 16 (19%) FA cases. The female-to-male ratio for FA changed from 1.9:1 to 1:1 while remained unchanged for DA. The percentage of FA stage I cases increased from 31% to 44%, while it decreased from 25% to 6% for stage III. For other stages it remained virtually unchanged. The overall 4-year actual survival was 75% for FA and 41% for DA (P = 0.03). CONCLUSIONS: Preoperative chemotherapy did not obliterate or produce anaplasia. The new definitions were applicable to pretreated cases and they were of prognostic significance.

Adolescent↗
PubMed2004

Histopathological and molecular prognostic markers in medulloblastoma: c-myc, N-myc, TrkC, and anaplasia.

Several molecular and histopathological prognostic markers have been proposed for the therapeutic stratification of medulloblastoma patients. Amplification of the c-myc oncogene, elevated levels of c-myc mRNA, or tumor anaplasia have been associated with worse clinical outcomes. In contrast, high TrkC mRNA expression generally presages longer survival. The goal of this study was to evaluate the prognostic value of c-myc, N-myc and TrkC expression in medulloblastomas and compare them to histopathological classification. We used in situ hybridization to measure expression of these molecular markers. c-myc mRNA was detected in 18 of 59 (31%) cases, and was significantly associated with shorter patient survival times on both univariate and multivariate analyses (p = 0.04). The presence of c-myc mRNA was also significantly associated with tumor anaplasia. While survival rates were higher for patients with low N-myc or high TrkC expression, these differences were not statistically significant. The group of patients with either moderate or severely anaplastic tumors showed only a trend towards shorter survival (p = 0.11). However, severe anaplasia alone was significantly prognostic (p = 0.002). Given the prognostic import of c-myc, we investigated 2 potential mechanisms by which its expression might be regulated: Wnt signaling and Mxi-1 mutation. Nuclear translocation of beta-catenin, a marker of Wnt pathway activation, was more common in medulloblastomas with high c-myc than in tumors overall, but the difference was not statistically significant. No Mxi-1 mutations were detected in the 22 cases examined. The association we describe between c-myc expression, tumor anaplasia, and worse clinical outcomes provides further evidence for the importance of this oncogene in medulloblastoma pathobiology.

Active Transport, Cell Nucleus↗
PubMed2005

[Methods of statistical analysis in differential diagnostics of the degree of brain glioma anaplasia during preoperative stage].

The authors proposed a possible preoperative diagnostics of the degree of supratentorial brain gliom anaplasia using statistical analysis methods. It relies on a complex examination of 934 patients with I-IV degree anaplasias, which had been treated in the Institute of Neurosurgery from 1990 to 2004. The use of statistical analysis methods for differential diagnostics of the degree of brain gliom anaplasia may optimize a diagnostic algorithm, increase reliability of obtained data and in some cases avoid carrying out irrational operative intrusions. Clinically important signs for the use of statistical analysis methods directed to preoperative diagnostics of brain gliom anaplasia have been defined

Adult↗
PubMed2004

Prognostic significance of anaplasia and angiogenesis in childhood medulloblastoma: a pediatric oncology group study.

The purpose of this study was to investigate whether quantitative assessment of cytologic anaplasia and angiogenesis may predict the clinical prognosis in medulloblastoma and stratify the patients to avoid both undertreatment and overtreatment. Medulloblastomas from 23 patients belonging to the Pediatric Oncology Group were evaluated with respect to some prognostic variables, including histologic assessment of nodularity and desmoplasia, grading of anaplasia, measurement of nuclear size, mitotic cell count, quantification of angiogenesis, including vascular surface density (VSD) and microvessel number (NVES), and immunohistochemical scoring of vascular endothelial growth factor (VEGF) expression. Univariate and multivariate analyses for prognostic indicators for survival were performed. Univariate analysis revealed that extensive nodularity was a significant favorable prognostic factor, whereas the presence of anaplasia, increased nuclear size, mitotic rate, VSD, and NVES were significant unfavorable prognostic factors. Using multivariate analysis, increased nuclear size was found to be an independent unfavorable prognostic factor for survival. Neither the presence of desmoplasia nor VEGF expression was significantly related to patient survival. Although care must be taken not to overstate the importance of the results of this single-institution preliminary report, pathologic grading of medulloblastomas with respect to grading of anaplasia and quantification of nodularity, nuclear size, and microvessel profiles may be clinically useful for the treatment of medulloblastomas. Further validation of the independent prognostic significance of nuclear size in stratifying patients is required.

Adolescent↗
PubMed1976

Histochemistry of oxidoreductases, enzymatic polymorphism and anaplasia of neuroectodermal tumors.

Oxidoreductases were studied histochemically in 162 cases of neuroectodermal tumors. In order of decreasing activity in the cytoplasma these enzymes could be arranged as follows: NADH diaphorase, lactate dehydrogenase, NADPH diaphorase, glutamate dehydrogenase, glucose-6-phosphate dehydrogenase, isocitrate dehydrogenase, succinate dehydrogenase, malate dehydrogenase. The weak activity of Krebs cycle enzymes and the relatively strong activity of other oxidoreductases, particularly of lactate dehydrogenase, permits to conclude that glycolysis prevails over oxidative processes in neuroectodermal tumor cells. But this should not be interpreted as a decrease of the Krebs cycle enzymes in astrocytoma and oligodendroglioma cells as compared with their parent cells because the latter themselves display a weak activity of these enzymes. A real decrease of Krebs cycle enzyme activity was established only for tumors, the parent cells of which are characterized by a strong (in choroid-papillomas) or moderate (in ependymomas) activity of these enzymes. Many neuroectodermal tumors, in particular those of astrocytic origin, demonstrate a certain correlation between the amount of cytoplasm and oxidoreductase activity. This results in enzymatic polymorphism of the tumor tissue. A certain similarity was established of the oxidoreductase activity in tumor cells and in reactive hypertophic astrocytes. This indicates that both tumor cells and reactive astrocytes may in certain conditions utilize similar mechanisms of increased metabolism. The oxidoreductase activity correlates not with the grade of anaplasia but with different directions of anaplasia reflected in different variants of neuroectodermal tumors. The concept "anaplasia" includes not only certain degrees of dedifferentiation of tumor cells but, as it has been shown histochemically, also an increase of metabolic processes in the tumor cell cytoplasma.

Anaplasia↗
PubMed1981

[Quantitative electron microscopic and cytological analysis of breast cancer of various degrees of anaplasia].

Electron microscopic and cytological study of mammary carcinoma cells of different degrees of anaplasia was carried out using morphometric methods in 15 patients with infiltrating carcinoma of this localization and correlation of cytological and histological data. The results showed the quantitative ultrastructural characteristics of the infiltrating mammary carcinoma reflecting the level of development of granular reticulum and polyribosomal apparatus to differ significantly depending on the degree of the tumor anaplasia established by cytological and histological studies with a light microscope. The cytological signs showing the maximum correlation with the ultrastructural changes in cells were found to include the numbers of "naked" nuclei, sizes of the cells and nuclei, number of nucleoli in the cell. Combinations of these signs typical for mammary carcinoma of different degrees of anaplasia are described.

Anaplasia↗
PubMed1997

Age and the risk of anaplasia in magnetic resonance-nonenhancing supratentorial cerebral tumors.

BACKGROUND: It is often assumed that a cerebral lesion that is nonenhancing on a magnetic resonance imaging study with gadolinium contrast is a low grade tumor. Some physicians recommend observation rather than biopsy for such lesions. METHODS: The authors prospectively evaluated the incidence of anaplastic tumor histology in a consecutive series of patients who presented to a neuro-oncology service with a nonenhancing mass of the cerebral hemisphere. RESULTS: During a 5-month period, the authors evaluated 31 patients who had a nonenhancing lesion in the cerebral hemisphere on initial magnetic resonance images. Thirty patients underwent stereotactic biopsy (27%) or open resection (73%). The median patient age was 36 years (range, 6-63 years). There was no mortality or permanent neurologic morbidity from surgery. Twenty-eight patients had pathologic confirmation of diagnosis while their lesions were still nonenhancing. Of these patients, 9 (32%) had Grade 3 lesions (anaplastic astrocytoma or oligoastrocytoma), 13 (43%) had Grade 2 lesions (astrocytoma, oligodendroglioma, or oligoastrocytoma), and 2 (7%) had Grade 1 lesions (dysembryoplastic neuroepithelial tumors). Two additional patients (ages 33 and 59 years) who developed enhancement within their lesions during preoperative periods of observation had glioblastomas at surgery. Logistic regression was used to relate patient age to the risk of anaplasia in a nonenhancing cerebral mass lesion. Older age predicted a significantly higher risk of anaplasia (P = 0.025). The model predicted that nonenhancing cerebral masses in patients older than 44 years were more likely to be anaplastic tumors than low grade tumors. There was no "safe" age below which low grade histology could be confidently assumed. CONCLUSIONS: Magnetic resonance-nonenhancing cerebral lesions may be histologically anaplastic, even in young patients. The risk of anaplasia in magnetic resonance-nonenhancing lesions increases significantly with patient age.

Adolescent↗
PubMed1988

Anaplasia in unilateral Wilms' tumor: a report from the National Wilms' Tumor Study Pathology Center.

Fifty-eight unilateral anaplastic Wilms' tumors entered on the Third National Wilms' Tumor Study (NWTS-3) were reviewed. The favorable outcome of stage I anaplastic tumors was confirmed. In stage II-IV tumors, the extent and severity of anaplasia were not of prognostic importance. However, two histologic features were correlated with extremely poor outcome; anaplasia in extrarenal tumor sites (P = .016) and predominantly blastemal tumor pattern (P = .020). The importance of these features in predicting relapse and death for children with anaplastic Wilms' tumor was supported by the study of 47 additional anaplastic Wilms' tumor cases from NWTS-2. These results emphasize the importance of examining sites of extrarenal spread in anaplastic Wilms' tumors. Cytologic criteria for anaplasia and clues to its recognition are reviewed, and the potential clinical and biological implications of our findings are discussed.

Cell Transformation, Neoplastic↗
PubMed2006

Medulloblastoma: histopathologic and molecular markers of anaplasia and biologic behavior.

Large cell/anaplastic (LC/A) medulloblastoma (MB) is a recently recognized variant of medulloblastoma known to be associated with an advanced stage and a poor prognosis. Although Eberhart et al. suggested histopathologic grading of medulloblastoma in 2002, no consensus has been reached in terms of determining the criteria of an LC/A variant, and its biological behavior continues to be the subject of debate. We retrospectively analyzed 74 cases (range 0.25-15 years) of MB clinicopathologically using the criteria established by Eberhart et al. The LC/A variant was identified in 16 cases (22% of MB cases), five of which showed a poor outcome. Most LC/A variant cases revealed synaptophysin immunoexpression (75%), but no epidermal growth factor receptor (EGFR) expression. Expression of synaptophysin, NeuN, GFAP, p53, c-erbB2, and EGFR did not differ in LC/A and non-LC/A variants. Seven of the 74 cases of medulloblastoma showed erbB2 amplification by FISH, four of which were LC/A variants. N-myc amplification was observed in only one LC/A variant, but no c-myc amplification was found. In patients younger than 10 years, the LC/A variant showed a significantly poorer outcome than the non-LC/A variant (P = 0.02), while no difference was found in older patients. Multivariate analysis revealed only metastasis on MRI and p53 expression, but not anaplasia as unfavorable prognostic factors. Our study suggests that prognostic implications of anaplasia in medulloblastoma are uncertain, and that the reproducibility of the histopathologic criteria of the LC/A variant should be reassessed before they can be applied in practical use.

Adolescent↗
PubMed2000

Loss of p53 promotes anaplasia and local invasion in ret/PTC1-induced thyroid carcinomas.

Papillary thyroid carcinomas in humans are associated with the ret/PTC oncogene and, following loss of p53 function, may progress to anaplastic carcinomas. Mice with thyroid-targeted expression of ret/PTC1 developed papillary thyroid carcinomas that were minimally invasive and did not metastasize. These mice were crossed with p53-/- mice to investigate whether loss of p53 would promote anaplasia and metastasis of ret/PTC1-induced thyroid tumors. The majority of p53-/- mice died or were euthanized by 17 weeks of age due to the development of thymic lymphomas, soft tissue sarcomas, and testicular teratomas. All ret/PTC1 mice developed thyroid carcinomas, but tumors in p53-/- mice were more anaplastic, larger in diameter, more invasive, and had a higher mitotic index than tumors in p53+/+ and p53+/- mice. Thyroid tumors did not metastasize in any of the experimental p53+/+ and p53+/- mice </=28 weeks of age or p53-/- mice </= 17 weeks of age; however, an older (170-day-old) male p53-/- mouse used to maintain the colony developed anaplastic thyroid carcinoma with liver metastases. These findings demonstrate that the lack of functional p53 in ret/PTC1 mice promotes anaplasia and invasiveness of thyroid carcinomas.

Anaplasia↗
PubMed2003

Spontaneous anaplasia in pilocytic astrocytoma of cerebellum.

We report a cystic cerebellar astrocytoma with a mural nodule that contained an additional focus of astrocytoma with the histological features of anaplasia, and showed up to 48% of aneuploid and 3% S-phase cells on flow cytometry. This focus was detectable on the enhanced, as well as non-enhanced T1 and T2 images. This appears to be the first case of pilocytic astrocytoma of cerebellum with focal anaplasia detected on histological and radiological studies.

Anaplasia↗
PubMed2005

Anaplasia is rare and does not influence prognosis in adult medulloblastoma.

Histopathologic grading based on increasing anaplasia predicts clinical behavior of pediatric medulloblastomas. The present study was aimed at grading 86 medulloblastomas of adult patients (aged 18 and older) by anaplasia and analyzing the predictive power. Nodularity, desmoplasia, nuclear size, nuclear pleomorphism, necrosis, and endothelial proliferations have been evaluated. Morphometric analysis of nuclear size was performed using the Eclipse Net program. Patients treated with standard postoperative radiotherapy (35 Gy to craniospinal axis and 50 Gy to posterior fossa) were considered for correlation with survival. Pathologic data and total survival were compared by Kaplan-Meier and logrank analysis. No correlation was found between total survival duration and individual pathologic features. Cooccurrence of nuclear pleomorphism, large nuclear diameter, microvascular proliferations, and necroses did not predict outcome. Severe nuclear pleomorphism was found in 4 of 86 cases; the only large-cell medulloblastoma was from an 18-year-old patient. Histopathologic factors have no clinical use for stratification of patients in risk groups. The histologic spectrum of medulloblastoma in adults is different from that in children.

Adult↗
PubMed2003

Anaplasia and grading in medulloblastomas.

The variable clinical outcomes of medulloblastoma patients have prompted a search for markers with which to tailor therapies to individuals. In this review, we discuss clinical, histological and molecular features that can be used in such treatment customization, focusing on how histopathological grading can impact both patient care and research on the molecular basis of CNS embryonal tumors. Medulloblastomas span a histological spectrum ending in overtly malignant large cell/anaplastic lesions characterized by increased nuclear size, marked cytological anaplasia, and increased mitotic and apoptotic rates. These "high-grade" lesions make up approximately one quarter of medulloblastomas, and recur and metastasize more frequently than tumors lacking anaplasia. We believe anaplastic change represents a type of malignant progression common to many medulloblastoma subtypes and to other CNS embryonal lesions as well. Correlation of these histological changes with the accumulation of genetic events suggests a model for the histological and molecular progression of medulloblastoma.

Anaplasia↗
PubMed2006

c-myc overexpression causes anaplasia in medulloblastoma.

Both anaplasia and increased c-myc gene expression have been shown to be negative prognostic indicators for survival in medulloblastoma patients. myc gene amplification has been identified in many large cell/anaplastic medulloblastoma, but no causative link between c-myc and anaplastic changes has been established. To address this, we stably overexpressed c-myc in two medulloblastoma cell lines, DAOY and UW228, and examined the changes in growth characteristics. When analyzed in vitro, cell lines with increased levels of c-myc had higher rates of growth and apoptosis as well as significantly improved ability to form colonies in soft agar compared with control. When injected s.c. into nu/nu mice, flank xenograft tumors with high levels of c-myc in DAOY cell line background were 75% larger than those derived from control. Overexpression of c-myc was required for tumor formation by UW228 cells. Most remarkably, the histopathology of the Myc tumors was severely anaplastic, with large areas of necrosis/apoptosis, increased nuclear size, and macronucleoli. Indices of proliferation and apoptosis were also significantly higher in Myc xenografts. Thus, c-myc seems to play a causal role in inducing anaplasia in medulloblastoma. Because anaplastic changes are often observed in recurrent medulloblastoma, we propose that c-myc dysregulation is involved in the progression of these malignant embryonal neoplasms.

Anaplasia↗
PubMed2006

[The effect of mammographic screening on tumor size, axillary node status and the degree of histologic anaplasia].

UNLABELLED: Breast cancer is the most frequent malignant tumor in women in Hungary. Significant reduction of mortality has been brought about not only by the increasing efficiency of complex therapy but also by regular mammographic screening. Of the histopathological data of 633 patients operated with primary breast tumor at the 1st Surgical Clinic of the Debrecen Medical University between January 1st 2000 and December 31st 2004, the authors analyzed tumor diameter, axillary node status and the degree of histologic anaplasia and compared them with the data of mammographic screening. RESULTS: Of the "screened"patients, 70.7% were diagnosed with T1 size tumors, 28.5% with T2 size, and 0.8% with tumors bigger than that. In the "unscreened" patients, our findings were 44.3%, 45.9% and 9.8% respectively. Within T1 tumors, Tla tumors were found in 11%, TIb in 37.6% and T1c in 51.4% in the "screened" group of patients, while the "unscreened" group's results were 2.3%, 12.6% and 85% respectively. 72.7% of the "screened" patients and 56.2% of the "unscreened" patients were found to be axillary node-negative. A study of the degree of histologic anaplasia showed G-I tumors in 15.6%, G-IIs in 62.1% and G-IIIs in 22.3% of the "screened" patients. The corresponding values for the "unscreened" patients were 6.1%, 53.8% and 40.1%, respectively. The differences were highly significant (p < 0.001) in all the parameters investigated. The authors have found a significant increase in the proportion of node-negative patients and patients with smaller tumors even after the first round of mammographic screening and at less than 50% participation. It is to be hoped that a 20% reduction in mortality can be achieved by further increasing the rate of participation.

Adult↗
PubMed1984

Condyloma acuminatum in Rochester, Minn, 1950-1978. II. Anaplasias and unfavorable outcomes.

A total of 746 patients residing in Rochester, Minn, received the diagnosis of condyloma acuminatum between 1950 and 1978. Anaplasia was present in six and subsequently developed in 36 patients during follow-up examination in 42 patients (one male and 41 female). One had invasive squamous cell carcinoma (vulva), six had severe dysplasias, 21 had moderate to mild dysplasias, and 14 had carcinomas in situ (CIS), of which 11 were cervical. In the female patients, 37 of the anaplasias were cervical and the other four were vulval or vaginal. The 11 cervical CIS amounted to 3.8 times the expected number of 2.9, based on an earlier study of cervical cancer incidence in the community. The risk of cervical CIS developing among patients with condyloma is significantly higher than expected. Neither laryngeal papilloma nor other unfavorable outcomes substantially affected the conceptus of 51 pregnancies in women with concurrent condyloma. There appears to be an association between condyloma and genital malignant neoplasms and a relationship of condyloma with sexually transmitted disease and warts.

Anaplasia↗