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At least 1,603 records · Page 89Linked to original sources
PubMed1998

Phenotypic and genotypic analyses of blastic cell population suggest that pure B-lymphoblastic leukemia may arise from myelodysplastic syndrome.

The case history of a 70-year-old man with myelodysplastic syndrome terminated into acute leukemia in 22 months is presented. The leukemic cells exhibited multifocal acid phosphatase positivity and expressed TdT, CD45, CD34 and HLA-DR but not myeloid, monocytic or megakaryocytic differentiation antigenes. The genotypic analysis revealed clonal immunoglobulin heavy chain gene rearrangement. These phenotypic and genotypic analyses of the blastic cell population suggest that myelodysplastic syndrome may transform to pure acute lymphoblastic leukemia of B-cell origin.

Acid Phosphatase↗
PubMed2003

Expression of a prototypic anti-colorectal cancer polyclonal antibody library in mammalian cells.

We describe the production of a prototypic polyclonal antibody library (PCAL), a standardized mixture of full-length IgG polyclonal antibodies for which the genes are available. The PCAL was generated by mass transfer of heavy and light chain variable region gene pairs, selected for binding to human colorectal cancer cells, from a Fab phage display vector to a mammalian IgG expression vector. Following transfection of the IgG vector library into Sp2/0 myeloma cells, clones were characterized for IgG expression and binding to the colorectal cancer cells by ELISA, and for diversity by DNA fingerprinting, nucleotide sequencing, and immunoblot analysis. The results showed that 76-84% of the library clones produce IgG and of those 72-79% bind antigen. Furthermore, preliminary analysis showed clonal diversity at both the DNA and antigen-binding levels. When depleted of reactivity to normal tissue, polyclonal antibody libraries to cancer cells may be efficacious for cancer therapy.

Animals↗
PubMed1997

The clinical diversity and role of chemotherapy in lymphoproliferative disorder in liver transplant recipients.

BACKGROUND/AIMS: Post-transplant lymphoproliferative disorder is a well-documented complication with an incidence ranging from 2 to 10%, depending on the organ transplanted. Yet despite our increased understanding of the pathophysiology of this disease and the various treatments available, the mortality remains high at 60-80%. We present the clinical and histological features of ten adult liver transplant recipients with post-transplant lymphoproliferative disorder presenting over a 15-year period and review the therapeutic options. METHODS: CD20/CD45RO immunostaining was used for T/B-cell markers; polymerase chain reaction and in-situ hybridisation for Epstein-Barr virus genome detection; kappa/lambda immunostaining and gene rearrangement analysis for clonality. RESULTS: There were six females and four males (age range 24-56) with onset of post-transplant lymphoproliferative disorder-symptoms ranging from 3 to 72 months post transplant. Sites of post-transplant lymphoproliferative disorder included liver (n=4), lymph nodes (n=5), bone marrow (n=2), lungs (n=2), kidneys (n=2), brain, ovaries,: and pancreas (n=1). All lesions were classified as high-grade lymphoma, of B-cell lineage (9 tested); Epstein-Barr virus genome was detected in 7/10 cases. Three tumours were monoclonal; four were polyclonal and three undetermined. Treatment included immunosuppression reduction, antiviral therapy with acyclovir and/or chemotherapy (CHOP or VAPEC-B). Survival times for those patients not treated with chemotherapy were from 9 days to 30 months, whereas those receiving chemotherapy had remission times of 4 to 48 months. CONCLUSIONS: Longer-term remissions can be achieved in patients treated with systemic chemotherapy, although not without morbidity. Clonality assessment is important but treatment decisions should be based primarily on clinical features of progression, as polyclonal tumours can behave as aggressively as monoclonal tumours.

Adult↗
PubMed1984

The growth of concanavalin-A activated, Lyt selected subsets in IL-2 containing supernatants.

The growth properties of Con A activated, Lyt selected splenic T lymphocytes were examined by limiting dilution analysis and clonally by single cell picking. Under the conditions used, a comparable frequency of Lyt 1+ and Lyt 2+ cells grew after Con A activation in the presence of Con A rat spleen supernatant. At a clonal level, however, the growth of these subsets differed qualitatively and quantitatively. While Lyt 2+ cells obtained clone sizes of several hundred cells, Lyt 1+ clone sizes were usually less than 100 cells, and many clones aborted their growth after a few days. Morphologically, the Lyt 1+ cell was smaller and usually showed fewer pseudopodial protusions as compared to the Lyt 2+ cell.

Animals↗
PubMed2000

Anaplastic large-cell lymphoma associated with acquired ichthyosis.

Anaplastic, CD30(+), large-cell lymphoma (ALCL) is a subtype of non-Hodgkin's lymphoma that accounts for 2% to 8% of all lymphomas. Its most common form is a classical systemic type, which involves multiple nodal and extranodal sites, including the skin. Malignant lymphoproliferative disorders, especially Hodgkin's disease, are known rarely to be associated with acquired ichthyosis, whereas only 1 case of ALCL has been reported to be associated with acquired ichthyosis. We describe a 74-year-old Japanese man with ALCL, involving lymph nodes and the skin, who exhibited acquired ichthyosis. The clinical and histopathologic findings were recorded, and immunophenotyping, T-cell receptor (TCR), and immunoglobulin gene rearrangement were determined. Clinically, right axillary and bilateral inguinal lymph nodes were palpable. The cutaneous eruptions were multiple pinkish and yellow colored, up to thumb-sized nodules, some of which were ulcerated. Histologically, the right axillary lymph node showed proliferation of anaplastic large cells in the paracortical and sinusoidal areas. Both the lymph node and skin showed pleomorphic proliferation of lymphoid cells with a mixture of mononuclear cells having oval, embryo-shaped, reniform, and lobulated nuclei, binucleated Reed-Sternberg-like cells, and multinucleated cells, with giant anaplastic and wreath-shaped nuclei. Immunophenotyping of the neoplastic cells revealed that they were positive for CD30 (Ber-H2), CD15 (Leu-M1), CD45 (LCA), and CD45RO (UCHL-1). Southern blot analysis demonstrated clonal rearrangement of the TCR beta region. In contrast, no novel bands were detected with the immunoglobulin heavy chain JH probe. Several months after the detection of the axillary nodes, an ichthyosiform, scaly eruption developed over almost the entire body of the patient. Histologically, it showed orthokeratotic, slight hyperkeratosis of the epidermis without a granular layer or with only a single layer of cells in the granular layer. Several kinds of lymphoproliferative diseases are associated with acquired ichthyosis, including Hodgkin's disease, multiple myeloma, and lymphomatoid papulosis. This is the second case report of acquired ichthyosis associated with ALCL. Although a common pathomechanism is suspected of underlying the development of acquired ichthyosis in these diseases, it is still unexplained.

Aged↗
PubMed1992

Methylation of the DXS255 hypervariable locus 5' CCGG site may be affected by factors other than X-chromosome activation status.

Differences in the methylation status of certain cytosine residues between active and inactive X chromosomes can be used to determine X-inactivation in females heterozygous for X-linked restriction fragment length polymorphisms. We have studied methylation patterns in 105 females heterozygous at the DXS255 locus by Southern blotting of PstI and MspI or HpaII double digests and hybridization with the probe M27B. Unequivocal patterns of unilateral or bilateral X-inactivation were obtained in 15/64 and 49/64 cases, respectively. In the remaining 41 cases the results were unclear due to the absence of HpaII digestion of one or both PstI fragments. In 7 samples an unequivocal digestion pattern was demonstrated on repeat analysis, suggesting that the initial ambiguous pattern was due to incomplete HpaII digestion. In certain individuals, methylation at the 5' CCGG DXS255 locus may be affected by factors other than X-inactivation, making analysis of clonality with the M27B probe impossible. These individuals should be clearly identified in studies of clonality.

Blotting, Southern↗
PubMed1995

Biological aspects of multiple myeloma.

Although considerable progress has been made towards understanding many aspects of myeloma, the myeloma stem cell and the factors that drive the disease remain elusive. Recent developments in the molecular analysis of clonality have helped to confirm the presence of pre-switch B cells that are of the same clone as the myeloma plasma cells. The role of these cells in myelomagenesis has not been demonstrated, and the isotypic heterogeneity of the clonally-relevant cells suggests that the pre-switch B cells are pre-malignant progenitors of the tumour cells. Thus, the circulating clonal B cells appear to be the earliest progenitors of the mature, monoclonal plasma cells. IL-6, and possibly other cytokines, are involved in driving this process. The role of IL-6 in myeloma is complex and more involved than its proposed growth factor function. In the absence of IL-6, dependent cells become apoptotic. Increased IL-6 signalling also leads to apoptosis of myeloma cells, possibly as a result of terminal differentiation. In the presence of exogenous IL-6, the IL-6 receptor appears to be the rate-limiting factor in the pathway's activity. IL-6 may regulate the survival of myeloma cells by stimulating c-myc transcription, possibly from the P0 promoter. The high levels of c-myc transcripts and protein could regulate myeloma cell proliferation and apoptotic death by controlling p53 expression and, through it, the expression of the Rb and BAX genes. Proliferative signalling in myeloma cells is likely to be intrinsic, within the tumour cell compartment. Molecules such as CD28 and B7, both expressed by less mature myeloma cells, could represent one such self-self stimulatory mechanism, with IL-6, possibly through stimulation of c-myc expression, providing the signals for survival and differentiation.

B7-1 Antigen↗
PubMed2001

The clonality of tumor-infiltrating lymphocytes in African Kaposi's sarcoma.

BACKGROUND: African Kaposi's sarcoma (KS) lesions contain human herpesvirus-8 (HHV-8) and Epstein-Barr virus (EBV), both of which are associated with various types of non-Hodgkin's lymphomas and are known to produce several factors suspected of lymphomagenic potential. The aim of this study was to evaluate tumor-infiltrating lymphocytes for the evidence of clonal expansion in African KS. METHODS: We used polymerase chain reaction (PCR)-based assays to determine the clonality of tumor-infiltrating lymphocytes in African KS lesions and compared the results to similar studies of patient-matched uninvolved skin and peripheral blood. RESULTS: T cells were polyclonal in all samples tested. Peripheral blood B cells were also polyclonal; however, a minority of lesional and uninvolved skin samples exhibited evidence of restricted B-cell clonality. Correlation with immunohistological analysis revealed that this clonal B-cell restriction was secondary to the sparse nature of lesional B cells rather than their clonal overgrowth. CONCLUSIONS: We conclude that, despite the putative lymphomagenic potential of HHV-8 and EBV and their co-existence in African KS lesions, tumor-infiltrating lymphocytes in these cases do not show evidence of clonal expansion that might be an early manifestation of lymphoma. Nevertheless, these studies are a case in point that sparse lymphoid subpopulations in lesional and uninvolved extranodal tissues can give rise to restricted clonal patterns that must be interpreted carefully to avoid the misdiagnosis of occult lymphoma.

Africa↗
PubMed1997

Establishment and characterization of a human stroma-dependent myeloma cell line (MM5.1) and its stroma-independent variant (MM5.2).

Although IL-6 has been identified as a major growth factor in multiple myeloma (MM), it is believed that maintenance of tumor growth in vivo depends on one or more additional stroma-derived factors. We describe a new human myeloma cell line (MM5.1) that can be maintained in the presence of bone marrow-derived stromal cell layers, and not only when cultured with exogeneous IL-6. This cell line expresses the same immunoglobulin kappa light chain RNA sequence as the patient's original tumor cells, has a plasma cell morphology and expresses plasma cell antigens (cytoplasmic kappa light chain, CD38, BB4). Without the presence of stromal factors, MM5.1 cells become apoptotic. A low proliferative effect was observed in the presence of oncostatin M (OSM) but other cytokines (IL-10, IL-11, stem cell factor (SCF) and leukemia inhibitory factor (LIF)) had no effect at all. We observed that MM5.1 cells also grow when physically separated from stromal cell layers by a 0.45 microm microporous membrane or when cultured in conditioned medium from stromal marrow cells. Unexpectedly, the growth in stromal supernatants was markedly inhibited by an anti-IL-6 antiserum and an anti-IL-6 receptor transducer chain (gp130) mAb in a dose-dependent manner. This implies that MM5.1 cells are IL-6 responsive only when exposed to one or more additional soluble factor(s) derived from bone marrow stroma. Coculturing MM5.1 cells with IL-6 and cytokines that were described to increase the IL-6 responsiveness of myeloma cells (G-CSF, GM-CSF and IL-3) had no effect on the growth or survival. A strong proliferative effect was observed when MM5.1 cells were cultured with IL-6 and soluble IL-6 receptor (sgp80). However no sgp80 could be detected in stromal supernatants using a sensitive immunoassay. This indicates that sustained proliferation of the MM5.1 cell line depends on a combination of IL6 and at least one, thus far unidentified, stroma-derived factor. After more than 1 year in continuous culture, we could obtain a variant of the line (MM5.2) that shows an improved growth rate and grows stroma independently. Molecular analysis revealed clonal identity with the early passage form and Epstein-Barr virus antigen expression was negative. The two variants of this cell line offer a useful model to identify molecular mechanisms involved in clonal evolution towards stroma-independent growth of myeloma cells.

Adipose Tissue↗
PubMed2000

New definition of remission in childhood acute lymphoblastic leukemia.

The extent of clearance of leukemic cells from the blood or bone marrow during the early phase of therapy is an independent prognostic factor in acute lymphoblastic leukemia (ALL). Several methods are available to measure the minimal residual disease (MRD) remaining after initial intensive chemotherapy. The most promising are flow cytometric detection of aberrant immunophenotypes and polymerase chain reaction analysis of clonal antigen-receptor gene rearrangements. When applied together, these techniques enable one to monitor MRD in virtually all cases of ALL. Patients who achieve an 'immunologic' or 'molecular' remission (ie leukemic involvement of <0.01% of nucleated bone marrow cells at the end of remission induction therapy) are predicted to have a better clinical outcome than patients whose remission is defined solely by morphologic criteria. In studies to date, patients with MRD at a level of 10(-2) or more at the end of induction have fared almost as poorly as those with > or =5% blast cells in the bone marrow (ie induction failures). Sequential monitoring of MRD can improve the clinical utility of risk assessment still further. Additional studies are needed to determine the critical levels of MRD at various times of treatment and whether therapeutic intervention based on MRD findings can improve clinical outcome.

Child↗
PubMed1998

Transformation of NIH3T3 fibroblasts by the c-Kit receptor tyrosine kinase: effect of receptor density and ligand-requirement.

Ectopic expression of the normal murine receptor tyrosine kinase, c-Kit, in NIH3T3 cells induced many phenotypic changes characteristic of transformation including anchorage-independent growth, focus formation and tumorigenicity in nude mice. Although transformation was largely dependent on the presence of recombinant murine Steel Factor (SLF), the ligand to the c-Kit receptor, anchorage independent growth did occur at a low frequency in the absence of added factor, and this could not be inhibited by neutralising antibodies or by SLF anti-sense mRNA. Clones from factor-independent colonies in semi-solid agar displayed a narrow range of c-Kit surface protein levels (4.3-6.4 x 10(4) receptors/cell) which was relatively high compared with the pool from which they were derived. Analysis of a larger series of random clones derived from adherent cultures expressing different levels of c-Kit demonstrated a positive correlation between SLF-dependent, anchorage-independent growth and c-Kit protein and mRNA expression levels (respectively, Rs = 0.58, P < 0.01; and Rs = 0.53, P < 0.01) with consistent colony formation observed with clones having > 2.5 x 10(4) receptors/cell. Interestingly, two of the three clones expressing the highest levels of c-Kit protein and mRNA produced few or no colonies in the presence or absence of SLF. Sequential overexpression of human c-KIT in NIH3T3 cells using a dihydrofolate reductase (DHFR)-encoding vector and gene co-amplification through methotrexate selection, which resulted in pools expressing up to 1.5 x 10(5) receptors/cell, confirmed that high receptor densities resulted in a decrease in colony numbers. Thus, analysis of clonal and selected populations has indicated that an optimal level of c-Kit is required for transformation of NIH3T3 cells in the presence of SLF, and that some ligand-independent transformation occurs.

3T3 Cells↗
PubMed1999

An improved micro-method for obtaining chromosome preparations from individual haemopoietic colonies.

A robust method for obtaining chromosome preparations from individual haemopoietic colonies in semi-solid media is described. The accumulation of metaphases and the hypotonic treatment of cells were carried out in the culture dish and individual colonies were transferred onto poly-L-lysine-treated slides and fixed stepwise prior to staining. The technique produced high yields of well-spread metaphases facilitating clonal cytogenetic analysis.

Animals↗
PubMed2000

p53 intronic point mutation, aberrant splicing and telomeric associations in a case of B-chronic lymphocytic leukaemia.

We report a case of chronic lymphocytic leukaemia (CLL) with telomeric associations and a p53 intronic point mutation. Karyotypic analysis revealed clonal and non-clonal telomeric associations, accompanied by clonal cytogenetic abnormalities and also in isolation. The p53 mutation, which occurred at the invariant base pair -2 of the splice acceptor site in intron 7 resulted in the abolition of correct splicing of exon 7 to exon 8. Multiple aberrant splice products were characterized, all of which differed from wildtype in the DNA binding domain. Fluorescence in situ hybridization demonstrated that the clone retained two copies of the p53 gene and wild-type p53 transcript was detected on cloning of reverse transcriptase polymerase chain reaction (RT-PCR) product, indicating that one wild-type allele remained. However, a plasmid clone with correct splicing at the exon 7/8 boundary, but with a 21 bp deletion in exon 8, was also found at low frequency. This finding indicates clonal evolution, resulting in complete loss of wild-type p53. The intronic point mutation was not present in DNA extracted from cervical tissue indicating that it was a leukaemic phenomenon. This is the first case of an intronic point mutation to be reported in CLL. This mutation led to chaotic p53 expression and, interestingly, occurred in a case showing telomeric associations, a rare phenomenon in B-CLL.

Amino Acid Sequence↗
PubMed2002

Establishment and characterization of a Kaposi's sarcoma-associated herpesvirus- and Epstein-Barr virus-negative malignant lymphoma cell line (OHK) with primary effusion lymphoma immunophenotype.

A novel cell line, designated OHK, was established from ascites of a 59-year-old Japanese woman with diffuse large B-cell lymphoma showing a peculiar serosal tropism, as seen in primary effusion lymphomas (PEL). OHK exhibited a large pleomorphic morphology with irregular nuclei and distinct nucleoli, and included immunoblastic and Reed-Sternberg-like giant cells. On ultrastructural examination, rich intermediate filaments, and well-developed Golgi apparati and rough endoplasmic reticulum, were seen. Immunophenotypically, OHK lacked T and B cell-associated antigens, and had CD10, CD30, CD33 and CD138 antigens. Although OHK cells did not express immunoglobulin (Ig) protein, Southern blot analysis demonstrated clonal rearrangements of Ig heavy and light chain genes. These observations suggest that OHK cells are derived from preterminally differentiated B cells, and that they have features of PEL. Kaposi's sarcoma-associated herpesvirus and Epstein-Barr virus were not detected. OHK displayed hyperploid karyotypes with multiple structural abnormalities, and produced some cytokines such as macrophage-colony-stimulating factor (M-CSF), granulocyte-CSF, interleukin 6 and transforming growth factor beta 1. In particular, vascular endothelial growth factor (VEGF), whose stimulation of vascular permeability is thought to be critical to the pathogenesis of PEL, was also produced in large quantities. These results indicate that OHK may be a useful tool for the investigation of PEL.

Ascitic Fluid↗
PubMed2001

The use of nonhuman primate models to improve gene transfer into haematopoietic stem cells.

Primitive haematopoietic progenitor and stem cells (HSC) have been pursued as highly desirable targets for genetic therapy as technology allowing safe and controllable transfer of exogenous genes into eukaryotic cells was developed a decade ago. Retroviral vectors have been used for the majority of preclinical and clinical studies directed at these cells, because these vectors have a number of the necessary properties, including chromosomal integration, helper-free production systems, and lack of toxicity. Until recently, however, results with these vectors in clinical trials and large animal models indicated efficiency of gene transfer as a major hurdle to be overcome. We have focused on using the rhesus macaque autologous transplantation model to optimize gene transfer to primitive haematopoietic cells, and investigate questions regarding in vivo stem cell behaviour, in a system with proven predictive value for human haematopoiesis. By optimization of transduction conditions using standard vectors, gene transfer efficiency to primitive repopulating cells has reached the clinically relevant range of 5-20% long-term. Alternative vector systems, have also yielded promising results. We have also found that relatively simple manipulation of cell cycle status prior to reinfusion of marked cells results in significantly improved engraftment of transduced cells: this finding may have an impact particularly in the nonablative setting. The high level marking has permitted insertion site analysis and clonal tracking in vivo. Inverse PCR and/or a ligation-mediated PCR procedure have demonstrated that a large number of transduced clones (over 50) contribute to multiple lineages in vivo for up to at least 2 years post-transplantation. Thus far we have little evidence for rapid clonal succession or lineage-restricted engraftment of transduced cells. These and other advances should result in successful gene therapy for a variety of acquired and congenital disorders affecting HSCs and their progeny lineages.

Animals↗
PubMed1999

Evidence for sequence selection within the non-structural 5A gene of hepatitis C virus type 1b during unsuccessful treatment with interferon-alpha.

Resistance of the hepatitis C virus (HCV) to interferon-alpha (IFN-alpha) therapy in patients with hepatitis C may be genetically controlled by an IFN sensitivity-determining region (ISDR) within the non-structural 5A (NS5A) gene. To assess whether HCV 1b strains carrying a 'resistant' type of ISDR are selected during unsuccessful IFN therapy, we analysed the evolution of the NS5A quasispecies, as detected by the clonal frequency analysis technique, and of the ISDR sequence by nucleotide sequence determination, in 11 patients showing no virological response during two consecutive cycles of IFN-alpha therapy. IFN-resistant patients had a homogeneous ISDR quasispecies with sequences identical to those described as 'resistant-' or 'intermediate-' type ISDR. After retreatment with IFN, further selection towards a homogeneous viral population was observed and 10 out of 11 patients had only one variant of HCV with no or just one single amino acid mutation within the ISDR sequence. Treatment and retreatment with IFN was associated in our non-responder patients with evolution of the ISDR quasispecies towards a rather homogeneous viral population carrying a conserved or minimally mutated ISDR motif, supporting the idea that this motif may be relevant for IFN resistance in HCV 1b-infected individuals.

Adult↗
PubMed2006

Productive replication of hepatitis C virus in perihepatic lymph nodes in vivo: implications of HCV lymphotropism.

BACKGROUND & AIMS: The pathogenesis of chronic hepatitis C is poorly understood. This study examines the ability of hepatitis C virus (HCV) to infect, replicate in, and produce progeny virus from perihepatic lymph nodes in vivo. METHODS: Lymph node (LN) biopsy specimens were taken from 20 patients with HCV genotype 1 infection and end-stage liver disease and 20 noninfected negative controls. Sections were probed with HCV RNA strand-specific riboprobes and antibodies specific for HCV core and nonstructural region 3 antigens plus B-cell (CD20) and T-cell (CD2) antigens. In a selected case, HCV quasispecies in serum, peripheral blood mononuclear cells, liver, and perihepatic lymph nodes were analyzed by clonal frequency analysis and sequencing. RESULTS: HCV infection was confirmed in 17 of 20 (85%) of lymph node specimens by in situ hybridization, and HCV replication was confirmed in 50% of cases by detection of HCV replicative intermediate RNA. HCV core and nonstructural 3 antigens were detected in lymph nodes by immunocytochemistry. Infected cell phenotypes were primarily CD20 B cells, although other cell types were positive for HCV replication markers. Quasispecies analysis in one case indicated that 68% of variants circulating in serum were also present in lymphoid tissues, and only 40% of serum variants were identified in liver, documenting a major contribution of lymphoid replication to HCV viremia. CONCLUSIONS: HCV lymphotropism provides new insights into the complex pathobiology of chronic hepatitis C in humans. We demonstrate for the first time a major contribution of extrahepatic HCV replication to circulating virus in serum (viremia).

Antigens, CD20↗
PubMed2001

[Cancer register for cervix carcinoma--useful and necessary?].

During the last two decades, cancer research has shifted from using cell lines and animal models to using methods and models that use human tissues from defined tumors. DNA and RNA can be analysed from fresh tissue from samples obtained at surgery, biopsy, cytologies or necropsy as well as from paraffin-embedded material. Archival material has several advantages: not only it is from individuals for whom disease process has been documented, but also data may available about the outcome as well as the response to treatment. Material available from well-controlled clinical trails would enable a wide range of hypotheses to be tested. Laser microdissection allows to sample cellular material from histopathologic well documented areas of the tumor, including special differentiated areas. It is necessary to establish tumor registries, especially in gynecologic oncology to get material from well described tumors for molecular profiling, the molecular analysis of clonality in tumors and malignant progression. At the Leipzig University a cervical tumor registry has been established in March 1979. Until the end of December of the year 2000 1,030 cases of surgically treated cervical cancer from stage pT1b1 up to pT2b including paraffin blocks and original histologic slides were collected. First evaluation up to the end of 1996 (n = 919) has shown, that 27.2% of the patients represented with histological proven pelvic lymph node metastases. The majority of cases were staged pT1b1 (52.1%), followed by stage pT2b (23.9%), pT1b2 (9.7%) and pT2a (9.5%). In 44 cases stage was not documented. In about 95.2% datas about the follow up of the patients were available. In conclusion, tumor registries are helpful in establishing and controlling uniform criteria for the accurate determination of prognostic factors and exact histopathologic evaluation can ideally be combined with new tools in molecular pathology, i.e. histopathology meets genomics.

DNA, Neoplasm↗