W Biernat

University of Lodz, Łódź, Lodz Voivodeship, Poland

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Publications (60)92.96 Total impact

  • Article: [Papillary glioneuronal tumor].
    W Biernat, P P Liberski
    Polish journal of pathology: official journal of the Polish Society of Pathologists 02/2001; 52(4 Suppl):111-2. · 0.35 Impact Factor
  • Article: [Primitive neuroectodermal tumor].
    W Biernat
    Polish journal of pathology: official journal of the Polish Society of Pathologists 02/2001; 52(4 Suppl):125-34. · 0.35 Impact Factor
  • Article: [Melanocytic tumors of the central nervous system (melanocytoma, melanoma malignum)].
    W Biernat
    Polish journal of pathology: official journal of the Polish Society of Pathologists 02/2001; 52(4 Suppl):173-5. · 0.35 Impact Factor
  • Article: [Germ cell OUN tumors].
    W Biernat
    Polish journal of pathology: official journal of the Polish Society of Pathologists 02/2001; 52(4 Suppl):183-9. · 0.35 Impact Factor
  • Article: [Congenital neoplasms].
    W Biernat
    Polish journal of pathology: official journal of the Polish Society of Pathologists 02/2001; 52(4 Suppl):191-203. · 0.35 Impact Factor
  • Article: [Glioblastoma multiforme].
    W Biernat
    Polish journal of pathology: official journal of the Polish Society of Pathologists 02/2001; 52(4 Suppl):23-8. · 0.35 Impact Factor
  • Article: [Central neurocytoma].
    W Biernat
    Polish journal of pathology: official journal of the Polish Society of Pathologists 02/2001; 52(4 Suppl):87-94. · 0.35 Impact Factor
  • Article: [Atypical teratoid/rhabdoid tumor (AT/RT)].
    W Biernat
    Polish journal of pathology: official journal of the Polish Society of Pathologists 02/2001; 52(4 Suppl):139-40. · 0.35 Impact Factor
  • Article: [Malignant lymphoma of the central nervous system (lymphoma malignum)].
    W Biernat
    Polish journal of pathology: official journal of the Polish Society of Pathologists 02/2001; 52(4 Suppl):177-82. · 0.35 Impact Factor
  • Article: January 2000: 12 year old boy with recent onset seizures.
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    ABSTRACT: A 12-year old boy presented with new onset of seizures and a CT scan showed a left frontal lobe tumor which was removed completely. Neuropathological examination showed a pleomorphic ganglion cell tumor with necrosi, and endothelial proliferation. The diagnosis was extraventricular atypical neurocytic neoplasm ("cystic ganglioneurocytoma").
    Brain Pathology 05/2000; 10(2):313-4, 319. · 3.99 Impact Factor
  • Article: Ductal sebaceoma (sebomatricoma).
    W Biernat, S Biernat
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    ABSTRACT: We present a case of an unusual tumour arising in the forehead of a 52-year-old female. The tumour, diagnosed as sebaceoma (or sebomatricoma), showed predominantly differentiation towards ductal protion of the sebaceous gland. It was marked in tissue sections as areas of "poroid" cells and the tumour required differentiation from poroma. Focal areas of necrosis en masse in the present tumour contributed further difficulties in to the differential diagnosis. As single multivacuolar sebocytes were found and no cuticular cells could be identified, the tumour was diagnosed as ductal sebaceoma (sebomatricoma). The aspects of morphological distinction between sebomatricomas and poromas are presented with its clinical implications.
    Polish journal of pathology: official journal of the Polish Society of Pathologists 02/2000; 51(1):55-7. · 0.35 Impact Factor
  • Article: Retiform/racemiform neoplasm with features of clear cell hidradenoma.
    W Biernat, J Pytel
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    ABSTRACT: We report a case of a 78-year-old woman with a tumor of the left cheek. The tumor was a well-circumscribed cystic/solid nodule with a racemiform and reticulated pattern of growth of its epithelial cells, and mucinous and fibrocytic stroma. The epithelial cords and strands were continuous with the apocrine lining of large cystic structures. The main bulk of the epithelial component was formed by the proliferation of clear cells. This tumor is an example of an unusual benign neoplasm with racemiform and retiform patterns having a histogenetical link with the folliculo-sebaceous-apocrine unit.
    American Journal of Dermatopathology 11/1999; 21(5):479-82. · 1.20 Impact Factor
  • Article: A case history of glioma progression.
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    ABSTRACT: Low-grade diffuse astrocytomas have an intrinsic tendency for malignant progression but the factors determining the kinetics of this process are still poorly understood. We report here the case of a male patient who developed a fibrillary astrocytoma at the age of 33 years and who underwent six surgical interventions over a period of 17 years without radiotherapy or chemotherapy. The first three biopsies spanned a period of 11 years and led to the diagnosis of low-grade, diffuse astrocytoma (WHO grade II), with a growth fraction (MIB-1 labeling index) of 2.3-3.7%. The fourth to sixth biopsies showed histological features of anaplastic astrocytoma (WHO grade III), with growth fractions between 5.0 and 10.5%. The fraction of gemistocytic neoplastic astrocytes also increased, from 0.3% in the first biopsy to 17.5% in the last biopsy and preceded the increase in proliferative activity and transition to anaplastic astrocytoma. The fraction of tumor cells immunoreactive to BCL-2 increased from 0.3% to 8.2%. A p53 mutation in codon 273 (CGT-->TGT, Arg-->Cys) was identified in the first biopsy and persisted throughout the course of the disease. However, the fraction of cells with p53 protein accumulation increased significantly during progression, from 3.2% in the first biopsy to 13.7% in the last. The absence of additional genetic alterations (PTEN mutations, loss of chromosome 10 and 19q) may be responsible for the slow progression and lack of glioblastoma features even after a 17-year disease duration.
    Acta Neuropathologica 05/1999; 97(5):525-32. · 9.32 Impact Factor
  • Article: Cytogenetic and proliferative potentials in meningiomas.
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    ABSTRACT: Cytogenetic analysis and Ki-67 staining index (SI) were performed on the series of 51 meningiomas, to estimate the relationship between the extent of chromosomal changes and the growth potential of tumors. The tumors were classified according to histological subtype (22 meningiotheliomatous, 15 transitional, 12 fibroblastic and 2 angiomatous) and grade (40 benign, 5 atypical and 6 malignant ones). There was no significant difference in the complexity of chromosomal changes among the histologically distinct tumor subtypes. In contrast, there was a significant association between the number of chromosomal abnormalities and tumor grade. Normal karyotypes were found in 50% and complex in 20% of benign tumors. All grade II or III tumors revealed complex karotype. The tumors classified as benign revealed significantly lower mean Ki-67 SI than atypical or malignant ones (1.6%, 7.4% and 14.7%, respectively). However, within tumors classified as benign, mean Ki-67 SI of these with normal or simple karyotypic changes did not differ significantly from those with complex karyotype (1.6% and 0.9%, respectively). Thus, the extent of genome abnormalities in meningiomas, measured on the chromosomal level, does not relate directly to their proliferative potential.
    Polish journal of pathology: official journal of the Polish Society of Pathologists 02/1999; 50(4):243-8. · 0.35 Impact Factor
  • Article: The methods of molecular genetic analysis applied for the diagnosis of brain tumors.
    W Biernat
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    ABSTRACT: The basic knowledge of most commonly used molecular methods applied for the diagnosis of neoplasms of the central nervous system is shortly reported.
    Folia neuropathologica / Association of Polish Neuropathologists and Medical Research Centre, Polish Academy of Sciences 02/1999; 37(3):131-2. · 1.23 Impact Factor
  • Article: Dysembryoplastic neuroepithelial tumor (DNT): an ultrastructural study of six cases.
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    ABSTRACT: We report six cases od DNT with a detailed ultrastructural characteristics. The patient age ranged from 7 to 16 years (mean 12), the location was temporal in three cases and frontal, temporooccipital and parietooccipital in each of one remaining cases. The predominant clinical feature in each case was history of episodes of intractable seizures. Histopathologically, the neoplasms were multinodular, each nodule was well-circumscribed and was composed of glioneuronal elements embedded in the variable amount of myxoid matrix. The oligodendroglial-like cells (OLC) predominated in the nodules with some accompanying mature neurons. The nodules were frequently surrounded by small calcifications which could be found also within the tumors. OLCs were immunoreactive for S-100 protein and neurons had the expression of synaptophysin and neurofilament proteins. Ultrastructurally, each tumor consisted of three major elements: neoplastic cells (OLC), elongated processes forming neuropil-like structure and expanded "mucoid" extracellular space: the latter gave an impression of cellular elements floating within it. Neoplastic cells had round, oval or elongated nuclei, no discernible nucleoli and a relatively narrow rim of the cytoplasm. Some nuclei were irregular and invaginated and pseudoinclusions were observed; a part of cytoplasm sequestered within pseudoinclusions often appeared degenerated with large blabs and electron-lucent vesicles, some of these contained in turn semicircular profiles of unknown significance. The second element consisted of innumerable cellular processes. Some of these were elongated and formed stacks connected by symmetrical symmetric or asymmetric adhesive plaque junctions. The others had shorter "neck" containing microtubules, these extended into bullous extensions. Dense-cored vesicles were occasionally observed, in both cytoplasm of neoplastic cells and within processes. In one cell, cross-sectioned annulate lamellae were found. In cytoplasm of a few cells, unusual inclusions reminiscent ribosome-lamellae complexes were observed. These were cylindrical resembling "laboratory tubes" with a cone-like endings. At higher power, walls of the "tubes" resolved into layered structures composed of several laminae; between laminae, ribosome-like structures were visible.
    Folia neuropathologica / Association of Polish Neuropathologists and Medical Research Centre, Polish Academy of Sciences 02/1999; 37(3):167-70. · 1.23 Impact Factor
  • Article: PTEN (MMAC1) mutations are frequent in primary glioblastomas (de novo) but not in secondary glioblastomas.
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    ABSTRACT: Loss of heterozygosity (LOH) on chromosome 10 is the most frequent genetic alteration associated with the evolution of malignant astrocytic tumors and it may involve several loci. The tumor suppressor gene PTEN (MMAC1) on chromosome 10q23 is mutated in approximately 30% of glioblastomas (WHO Grade IV). In this study, we assessed the frequency of PTEN mutations in primary glioblastomas, which developed clinically de novo, and in secondary glioblastomas, which evolved from low-grade (WHO Grade II) or anaplastic astrocytomas (WHO Grade III). Nine of 28 (32%) primary glioblastomas contained a PTEN mutation and an additional case showed a homozygous PTEN deletion. This indicates that after overexpression/amplification of the EGF receptor, loss of PTEN function is the most common alteration in primary glioblastomas. In this series, 5 of 28 (18%) primary glioblastomas showed both a PTEN mutation and EGFR amplification. In contrast, only 1 of 25 (4%) secondary glioblastomas contained a PTEN mutation, and none of them showed a homozygous PTEN deletion. The secondary glioblastoma with a PTEN mutation developed from an anaplastic astrocytoma that already carried the mutation. The observation that secondary glioblastomas have a p53 mutation as a genetic hallmark but rarely contain a PTEN mutation supports the concept that primary and secondary glioblastomas develop differently on a genetic level.
    Journal of Neuropathology and Experimental Neurology 08/1998; 57(7):684-9. · 4.26 Impact Factor
  • Article: p53 mutations in sweat gland carcinomas.
    W Biernat, A Peraud, L Wozniak, H Ohgaki
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    ABSTRACT: Sweat gland carcinomas are rare skin tumours and little is known about their etiology and molecular basis. In this study, we analyzed p53 mutations in 16 sweat gland carcinomas with different histologic types, including 2 spiradenocarcinomas, 1 composed adnexal carcinoma, 5 porocarcinomas, 2 eccrine hidradenocarcinomas, 2 syringocystadenocarcinomas, 1 sclerosing sweat gland carcinoma, 1 adenoid cystic carcinoma, 1 cylindrocarcinoma and 1 apocrine adenocarcinoma. Single-stranded conformation polymorphism (SSCP) analyses followed by direct DNA sequencing revealed that 5 carcinomas (31%) contained a p53 mutation, 4 of which were G:C-->A:T transition mutations and 1 of which was a deletion. Three G:C-->A:T mutations were located at dipyrimidine sequences on the antisense strand (2 spiradenocarcinomas, 1 eccrine hidradenocarcinoma), suggesting that UV light may play a role in the development of sweat gland carcinomas. In 2 spiradenocarcinomas, p53 mutations were present in the carcinoma but not in the adenoma portions, suggesting that p53 mutations may be associated with malignant progression in these rare adnexal tumours.
    International Journal of Cancer 05/1998; 76(3):317-20. · 5.44 Impact Factor
  • Article: Desmoplastic cerebral astrocytoma of infancy: a case report.
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    ABSTRACT: We report a case of desmoplastic cerebral astrocytoma of infancy (DCAI), in a 7-month-old boy. DCAI belongs to a group of recently described central nervous system (CNS) tumors, which also includes desmoplastic infantile ganglioglioma (DIG), pleomorphic xanthoastrocytoma (PXA) and dysembryoplastic neuroepithelial tumor (DNT), all characterized by relatively favorable prognosis and occurring mostly in children and young adults. DCAI is a rare neoplasm arising in the cerebral hemispheres within the first two years of life, and histologically is characterized by dense fibrous desmoplasia. In our case, CT scan presents a massive partially cystic tumor of the left cerebral hemisphere with an enlargement of the ventricular system. Histologically, the tumor was composed of cells arranged in fascicles and whorls forming storiform pattern. Immunohistochemical stainings for glial fibrillary acidic protein proved glial histogenesis of this tumor, while no cells were unequivocally immunopositive for neuron specific enolase, neurofilament proteins and synaptophysin what excludes a diagnosis of DIG--a similar entity but containing also a neuronal elements. Our studies, comprising a complete clinical, radiological, histopathological and immunohistochemical data, correspond to a cases of DCAI published before and it is the first one described in Poland.
    Folia neuropathologica / Association of Polish Neuropathologists and Medical Research Centre, Polish Academy of Sciences 02/1998; 36(1):45-51. · 1.23 Impact Factor
  • Article: Mutations of TP53, amplification of EGFR, MDM2 and CDK4, and deletions of CDKN2A in malignant astrocytomas.
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    ABSTRACT: We investigated the frequency and mutual relationship of molecular alterations in 33 malignant astrocytomas (28 glioblastomas and 5 anaplastic astrocytomas). The genetic alterations analyzed were: deletion of CDKN2a/p16 gene, TP53 mutations, and amplification of EGFR, MDM2 and CDK4. The most common genetic alteration was EGFR amplification which was revealed in 15 cases (45%). TP53 mutation was identified in 9 cases (27%) and CDKN2/p16 deletion was detected in 13 cases (41%). Either MDM2 and CDK4 amplifications were less frequent, as they were identified in 4 (12%) and 1 (3%) case, respectively. Of the 15 cases showing the amplification of EGFR, 9 had CDKN2/p16 deletion (60%, p = 0.04). On the other hand, CDKN2/p16 deletion and EGFR amplification rarely occurred with TP53 mutations (2 of 14 cases with CDKN2/p16 deletion, 14%). These results confirm the existence of at least two different pathways leading to the formation of a glioblastoma.
    Polish journal of pathology: official journal of the Polish Society of Pathologists 02/1998; 49(4):267-71. · 0.35 Impact Factor