Biomedical subjects

Naoya Nakamura

Publications and source records attributed to Naoya Nakamura.

At least 19 recordsLinked to original sources

PubMed2007

CD10-MUM1+ follicular lymphoma lacks BCL2 gene translocation and shows characteristic biologic and clinical features.

CD10 and MUM1 are representative B cell differentiation markers. Follicular lymphoma (FL) is usually positive for CD10 and negative for MUM1. In this study, however, we compared 22 FLs with peculiar phenotype CD10-MUM1+ with 119 typical CD10+MUM1- FLs. All CD10-MUM1+ FL patients exhibited follicular structure with follicular dendritic meshwork, and a high rate of somatic hypermutation and ongoing mutation, similar to typical FL. However, CD10-MUM1+ FLs were encountered frequently in the elderly compared with CD10+MUM1- typical FLs (67.0 versus 58.7 years, P < .01), showed high grade (grade 3A or 3B) morphology (91% versus 17%, P < .001), diffuse proliferation (59% vs 19%, P < .001), and lacked BCL2/IGH translocation (5% versus 92.5%, P < .001), which is the most characteristic aberration in FL, and 88% showed BCL6 gene abnormalities (translocation or amplification). Our results indicate that CD10-MUM1+ FL is different from typical FL with respect to biologic and clinical features.

Aged↗

PubMed2007

Prognostic impact of chromosomal alteration of 3q27 on nodal B-cell lymphoma: correlation with histology, immunophenotype, karyotype, and clinical outcome in 329 consecutive patients.

Rearrangements involving the BCL6 gene are found in 30% of diffuse large B-cell lymphomas (DLBCLs). We evaluated the clinical characteristics and prognoses of patients with B-cell lymphoma carrying 3q27 translocations. Among the 59 patients having 3q27 translocation, 10.9% had follicular lymphoma (FL) and 23.1% had DLBCL. It is of interest that the prognostic significance was not found between FL and DLBCL with 3q27 translocations. Progression-free survival (PFS) rate was significantly higher in the FL patients with 3q27 translocation than in those with 18q21 translocation. PFS rate was significantly higher in the DLBCL patients with 3q27 translocation than in those with 18q21 translocation. These findings suggest that the presence of 3q27 translocation is a significant prognostic factor in DLBCL.

Adult↗

PubMed2006

Deviated VH4 immunoglobulin gene usage is found among thyroid mucosa-associated lymphoid tissue lymphomas, similar to the usage at other sites, but is not found in thyroid diffuse large B-cell lymphomas.

It remains unclear whether or not diffuse large B-cell lymphomas of extranodal sites arise from mucosa-associated lymphoid tissue (MALT) lymphomas. We studied the clinicopathological features of MALT lymphoma and diffuse large B-cell lymphoma in the thyroid gland, with special reference to VH usage of immunoglobulin gene rearrangement, to clarify the relationships between these two types of lymphomas. In addition, t(11; 18) (q21; q21) translocation was examined by multiplex reverse transcription-polymerase chain reaction. We examined 58 patients with primary thyroid lymphoma: 31 (male seven and female 24) with MALT lymphoma and 27 (male three and female 24) with diffuse large B-cell lymphoma. Interestingly, the sequence of VH genes revealed that the two subtypes differed significantly in their use of the VH4 family (P < 0.05). Of the seven MALT lymphomas, three used the VH4 family and the other four used the VH3 family, whereas eight out of nine diffuse large B-cell lymphoma used the VH3 family, one used the VH1 family, and none used the VH4 family. It was also interesting that, in one diffuse large B-cell lymphoma patient with MALT lymphoma, the diffuse large B-cell lymphoma component used the VH3 family and the MALT lymphoma component used the VH4 family. These data imply that, in a subset of cases, these two subtypes do not share a common origin and that at least some diffuse large B-cell lymphomas have a de novo origin. No t(11; 18) (q21; q21) was detected in thyroid lymphomas, which are different from MALT lymphoma of the stomach, lungs, large intestine and ocular adnexa. This strongly indicated that the presence of t(11; 18) (q21; q21) in MALT lymphoma is organ-specific.

Adult↗

PubMed2006

t(8;14)(q24;q32) in two patients with CD10-negative primary thyroid diffuse large B-cell lymphoma.

Diffuse large B-cell lymphoma (DLBCL) with the 8q24 translocation is occasionally seen in the gastrointestinal tract, but has rarely been reported in the thyroid gland. We experienced two cases of primary thyroid DLBCL having t(8;14)(q24;q32). The immunophenotype and karyotype of Case 1 (66-year-old female) and Case 2 (70-year-old female) were: CD10-, CD20+, BCL-2+/add(13)(q34), t(8;14)(q24;q32) and CD10-, CD20-, CD79a+, BCL-2-/t(8;14)(q24;q32), respectively. Although long-term complete remission could be achieved in both of our patients by conventional chemotherapy with/without radiation therapy, accumulation of further such cases is necessary to develop a standard treatment protocol and also to elucidate the pathogenesis of t(8;14)(q24;q32)-positive primary thyroid DLBCL.

Aged↗

PubMed2005

Expression of BAFF-R (BR 3) in normal and neoplastic lymphoid tissues characterized with a newly developed monoclonal antibody.

BAFF-receptor (BAFF-R) is required for the successful maturation and survival of B-cells. We developed an anti-human BAFF-R monoclonal antibody (mAb), 8 A 7. The reactivity of 8 A 7 in normal and neoplastic tissue was examined by performing immunohistochemistry on paraffin-embedded sections. 8 A 7 reacted with lymphocytes in the mantle and marginal zones, but not with lymphocytes in the interfollicular area. Lymphocytes in the germinal centers were found to be negative or occasionally weakly positive for 8 A 7. BAFF-R expression was found only in B-cell lymphoma (44/80, positive cases/examined cases): B-lymphoblastic lymphoma 0/3, B-chronic lymphocytic leukemia/small lymphocytic lymphoma 4/4, mantle cell lymphoma 9/11, follicular lymphoma 10/14, diffuse large B-cell lymphoma (DLBCL) 11/25, marginal zone B-cell lymphoma 8/10, lymphoplasmacytic lymphoma 2/2, plasma cell myeloma 0/2, and Burkitt lymphoma 0/9, but not in T/NK cell lymphomas (0/19) or Hodgkin lymphoma (0/10). BAFF-R was expressed in most low-grade B-cell neoplasms and a small number of DLBCL, suggesting that BAFF-R may play an important role in the proliferation of neoplastic lymphoid cells. Thus, the mAb is very useful for further understanding of both healthy B-cell biology and its pathogenic neoplasms.

Antibodies, Monoclonal↗

PubMed2005

Primary pulmonary plasmacytoma involving bilateral lungs and marked hypergammaglobulinemia: differentiation from extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue.

A 71-year-old woman was referred to our hospital because of hyperproteinemia and serum M-protein (IgG-lambda type). Chest computed tomographic (CT) scan revealed a tumor in each lung and transbronchial lung biopsy was performed. Histopathological examination showed monotonous medullary proliferation of morphologically mature plasma cells. These cells were cIgG+, cIg-lambda+, CD 20+, CD 79 a+, CD 138+, cIg-kappa-, and CD3-. Since there were very few non-neoplastic plasma cells and small lymphocytes in addition to the absence of reactive lymph follicles and fibrosis, the patient was diagnosed as having plasmacytoma. There was no proliferation of plasma cells in the bone marrow. Thus, the lesion was finally characterized as primary pulmonary plasmacytoma. Treatment with melphalan/prednisolone resulted in considerable decrease in the serum IgG level and regression of the pulmonary tumors. The effectiveness of the chemotherapy could confirm our diagnosis, although MALT-type lymphoma with plasmacytic differentiation cannot be completely ruled out.

Aged↗

PubMed2005

Primary breast diffuse large B-cell lymphoma shows a non-germinal center B-cell phenotype.

Primary breast diffuse large B-cell lymphoma has a poor prognosis relative to other extranodal diffuse large B-cell lymphoma. Recently, diffuse large B-cell lymphoma has been subclassified as germinal center B-cell-like and nongerminal center B-cell types using tissue microarrays. The 5-year overall survival rate of the germinal center B-cell group is better than that of the nongerminal center B-cell group. To elucidate the reason for which primary breast diffuse large B-cell lymphoma has a poor clinical outcome, we investigated 15 patients with primary breast diffuse large B-cell lymphoma (stage IE; 13 cases, stage IIE; two cases) by immunohistochemistry using various markers including CD10, Bcl-6, MUM1 and MIB-1 and by molecular analysis of the immunoglobulin heavy chain gene variable region. Immunohistochemistry showed 0/15 (positive cases/examined cases) for CD10, 5/15 for Bcl-6, 15/15 for MUM1, 10/15 for Bcl-2, 2/15 for CD5 and 4/15 for CD40. The expression pattern of CD10(-) MUM1(+) in primary breast diffuse large B-cell lymphoma corresponded to the nongerminal center B-cell group. Moreover, the MIB-1 index was distributed from 60 to 95% with a mean of 79%, indicating a high proliferation of the lymphoma cells. The immunoglobulin heavy chain gene variable region of primary breast diffuse large B-cell lymphoma had a mutation frequency of 1-10% (seven cases) and 0-1 additional mutations in ongoing mutation analysis (five cases). Primary breast diffuse large B-cell lymphoma had characteristics of the nongerminal center B-cell group. In conclusion, primary breast diffuse large B-cell lymphoma has a nongerminal center B-cell phenotype and has a high MIB-1 index. These features might therefore be associated with poor prognosis.

Aged↗

PubMed2005

Atypical Burkitt lymphoma arising from follicular lymphoma: demonstration by polymerase chain reaction following laser capture microdissection and by fluorescence in situ hybridization on paraffin-embedded tissue sections.

A 77-year-old man with disseminated lymphadenopathy was referred to our hospital. An inguinal lymph node biopsy specimen had the appearance of composite lymphoma consisting of follicular lymphoma and atypical Burkitt lymphoma. The bone marrow was involved, and chromosomal analysis of the marrow showed t(8;14) and t(14;18) in identical cells. The patient underwent systemic chemotherapy but died of lymphoma 4 months later. Polymerase chain reactions performed on cells obtained from follicular and diffuse components by laser capture microdissection showed the two components to be clonally identical. Moreover, fluorescence in situ hybridization performed on paraffin-embedded tissue sections demonstrated an immunoglobulin heavy chain (IGH)/BCL2 translocation signal in both follicular and diffuse components, but an IGH/c-MYC translocation signal in only the diffuse component. Accordingly, the atypical Burkitt lymphoma arose from the follicular lymphoma as a consequence of the additional IGH/c-MYC translocation, then involving the bone marrow.

Aged↗

PubMed2005

CD5+ diffuse large B-cell lymphoma consists of germline cases and hypermutated cases in the immunoglobulin heavy chain gene variable region.

CD5+ diffuse large B-cell lymphoma (DLBCL) has recently been identified as a subgroup with different clinical characteristics from CD5- DLBCL and as having a poorer outcome than CD5- DLBCL. Data regarding differences in gene alteration between CD5+ and CD5- DLBCL have accumulated. In this article, we report an analysis of the immunoglobulin heavy-chain gene variable region (VH) gene in 35 cases of CD5+ DLBCL and compare these cases with those with the germline of the VH gene (GL-VH) and those with a somatically hypermutated VH gene (HM-VH). When the CD5+ DLBCL cases were subdivided with a cutoff value of 98% homology in the VH gene, there were 7 cases (20%) of GL-VH and 28 cases (80%) of HM-VH. The proportion of GL-VH cases in CD5+ DLBCL was more than that in CD5 DLBCL. Although we found no significant difference in pretreatment clinical parameters between the GL-VH and HM-VH subgroups, there was a tendency for the GL-VH subgroup to show lower incidences of elevation of lactate dehydrogenase and >1 site of extranodal involvement compared to the HM-VH subgroup. The overall survival curve of the HM-VH subgroup showed a rapid decline followed by a plateau, whereas that of the GL-VH subgroup declined constantly after 5 years, suggesting that GL-VH disease may not be curable by standard therapies. These findings suggest that CD5+ DLBCL with GL-VH shares clinical features with mantle cell lymphoma, the cellular origin of which has been considered to be pre-germinal center B-cells. We therefore propose that analysis of the VH gene is important for predicting the clinical course of CD5+ DLBCL.

CD5 Antigens↗

PubMed2005

Expression of CD29 on lymphoma cells and/or CD36 on microvascular endothels correlates with high serum LDH level in diffuse large B-cell lymphomas (DLBCLs) and is frequent in de novo CD5-positive DLBCLs.

Our previous study demonstrated that CD29 and CD36 mRNAs were overexpressed in de novo CD5-positive diffuse large B-cell lymphomas (CD5+ DLBCLs) compared with CD5-negative (CD5-) DLBCLs. CD29 was expressed on lymphoma cells, and CD36 on microvascular endothels. In the present study, we analyzed the clinicopathological significance of CD29 and microvascular CD36 (mvCD36) expression in many cases of DLBCLs. CD29 and CD36 expression was examined by immunohistochemistry on frozen sections of 159 specimens, consisting of 120 cases of CD5-DLBCL, 14 cases of de novo CD5+ DLBCL, 11 cases of follicular lymphoma, 8 cases of mantle cell lymphoma, and 6 cases of reactive lymphoid hyperplasia. Three cases of CD5- intravascular large B-cell lymphomas (IVLs) with hepatic intrasinusoidal infiltration were also examined. CD29+ and/or mvCD36+ DLBCL cases had significantly higher serum LDH levels compared with CD29- mvCD36- DLBCL cases. The number of CD29+ and mvCD36+ cases, and the number of CD29+ or mvCD36+ cases, were significantly higher in de novo CD5+ DLBCLs than in CD5- DLBCLs. The frequencies of CD29 and mvCD36 expression were low in follicular lymphomas, and mvCD36 was negative in reactive lymphoid hyperplasias. Liver biopsies of three IVL cases showed that CD29 was positive on lymphoma cells, and, that CD36 was expressed on hepatic sinusoids. The present study supports the notion that CD29 and/or mvCD36 expression manifests the aggressive feature of a subset of DLBCLs because of its correlation with high serum LDH levels. Furthermore, CD29 and mvCD36 expression should be evaluated in relation to the intravascular growth pattern of lymphoma cells.

Biomarkers, Tumor↗

PubMed2004

HBL-3 cell line, derived from precursor B-cell lymphoblastic leukemia, lacks somatic hypermutation of immunoglobulin heavy chain variable region genes.

Somatic mutation (SM) analysis provides a useful tool for understanding the stages at which neoplastic differentiate from normal B-cells. B-cell precursor neoplasms are considered to be somatically premutational. However, the variable frequency of SM of the variable region (VH) genes has been described in cases of precursor B-cell acute lymphoblastic leukemia (PB-ALL). To better characterize PB-ALL based on the differentiation stage, we investigated the SM of the VH genes expressed by tumor cells of the surface immunoglobulin (sIg)(-) HBL-3 cell line derived from childhood PB-ALL. In the HBL-3 cell line, the rearranged Ig heavy chain VH gene sequence showed no SM in the complementarity-determining regions of 1, 2, and 3, or in the framework regions of 1, 2, and 3 relative to the putative germline VH gene sequences. In addition, the VH segment of HBL-3 cells showed no intraclonal sequence heterogeneity, indicating ongoing SM. Our data demonstrated that HBL-3 cells express unmutated and developmentally regulated rearrangement of VH genes at the stage of B-cell precursor cells. HBL-3 cells, which are derived only from the sIg(-) PB-ALL, showed that SM cannot be recognized in VH genes of tumor cells before the expression of sIg.

Base Sequence↗

PubMed2004

Gammadelta T-cell large granular lymphocyte (LGL) leukemia with spontaneous remission.

T-cell large granular lymphocyte (LGL) leukemia is a clonal disorder with an indolent clinical course. In July 1995, a 46-year-old Japanese man was admitted to our hospital because his anemia had progressed. He had a white blood cell count of 3.9 x 10(9)/L with 75% lymphocytes, which were intermediate to large and had almost round nuclei and azurophilic granules, and anemia with a red blood cell count (RBC) of 2.69 x 10(12)/L, hemoglobin (Hb) of 9.5 g/dL, and hematocrit (Hct) of 28.3%. Electron microscopic examination showed that most of the lymphocytes had a parallel tubular array and dense core granules in their cytoplasm. Flow cytometry and Southern blotting of the T-cell antigen receptor (TCR) genes using the peripheral blood species showed monoclonal proliferation of LGLs with a CD3+, TCRgammadelta+, CD4-, CD8-, CD16+, CD56-, CD57-, HLA-DR+ phenotype, and a TCR gamma gene rearrangement, respectively, suggesting that the patient was diagnosed as having gammadelta T-cell LGL leukemia. He had no symptoms, organomegaly, or skin lesions. About 1.5 years after diagnosis, the anemia gradually improved with disappearance and appearance of a rearranged band in the TCR-gamma gene and TCR-beta gene, respectively. About 7 years after diagnosis, the anemia improved completely with a RBC of 5.01 x 10(12)/L, Hb of 14.8 g/dL, and Hct of 44.3%, and he was in complete remission without TCR-beta and -gamma gene rearrangements. He had received no therapy. This is the first report of spontaneous remission of gammadelta T-cell LGL leukemia.

Blotting, Southern↗

PubMed2004

A common clonal origin of nodal marginal zone B-cell lymphoma and plasma cell myeloma demonstrating different immunophenotypes: a case report of composite lymphoma.

We demonstrated an 83-year-old male case of composite lymphoma. Before 18 years, he was diagnosed with nodal marginal zone B-cell lymphoma in the cervical lymph node. Peripheral blood showed anemia and IgA (kappa)-type monoclonal gammopathy (IgA; 3,625 mg/dL). Bone marrow aspiration biopsy exhibited plasma cell myeloma, in which atypical plasma cells were positive for cytoplasmic IgA (kappa) and atypical lymphoid cells intermingled were positive for CD20. In contrast, cervical lymph node biopsy revealed nodal marginal zone B-cell lymphoma, in which lymphoma cells were positive for cytoplasmic IgG (lambda). Southern blotting analysis of the IgH gene showed same clonal rearrangement band in both lymph node and bone marrow samples and additional band in the bone marrow. Sequence analyses of the IgH gene showed an identical sequence of CDR3 in both samples. Thus, we demonstrated a common clonal origin of composite lymphoma comprising nodal marginal zone B-cell lymphoma and plasma cell myeloma. Nodal marginal zone B-cell lymphoma recurred in cervical lymph node and involved into the bone marrow, differentiating into plasma cell myeloma in which Ig isotype switched and monoclonal gammopathy developed. Sequence analysis of the IgH gene was a powerful tool for determination of clonal origin.

Aged↗

PubMed2003

Richter syndrome in B-cell chronic lymphocytic leukemia.

Richter syndrome (RS) is well known as a secondary high-grade lymphoma, mostly diffuse large B-cell lymphoma (DLBCL) developed in patients with B-cell chronic lymphocytic leukemia (B-CLL). In this review, we describe clinicopathological, histological, immunophenotypical and genetic findings of RS. The patients with RS, regardless of transformation of pre-existing clone or de novo malignant clone, were resistant to conventional combined chemotherapy and died within months of diagnosis. Molecular techniques can provide convincing results for the clonal relationship of RS to pre-existing B-CLL. When RS carries a same rearrangement band or a same sequence as B-CLL by Southern blotting or nucleotide sequence analyses of immunoglobulin heavy and/or light chain genes, it is suggested to that RS transforms from original B-CLL. These analyses have showed that approximately two-thirds of RS cases evolved from a B-CLL clone. How and where does the B-CLL clone evolve to RS? The genetic alteration of transforming B-CLL clone into RS has been addressed. Abnormalities of chromosomes 11 and 14 were most frequently involved in RS, but non-specific. In addition, RS does not include chromosomal translocation between Ig locus and oncogenes or rearrangements of bcl-6 gene, both of which were found in some de novo DLBCL. Several candidates, such as mutation of p53 gene and abnormalities of cyclin dependent kinase inhibitor, have been proposed to play an important role in the transformation of a part of B-CLL. However, there is still uncertainty as to how B-CLL progresses or develops into RS.

Clone Cells↗

PubMed2003

Involvement of the chromosomal translocation t(11;18) in some mucosa-associated lymphoid tissue lymphomas and diffuse large B-cell lymphomas of the ocular adnexa: evidence from multiplex reverse transcriptase-polymerase chain reaction and fluorescence in situ hybridization on using formalin-fixed, paraffin-embedded specimens.

The chromosomal translocation t(11;18) is a unique chromosomal aberration associated with mucosa-associated lymphoid tissue lymphoma. API2 and MALT1 genes have been identified around this translocation. We attempted to find chromosomal abnormalities focusing mainly on the t(11;18) translocation in formalin-fixed, paraffin-embedded tissues of ocular adnexal lymphoproliferative disorders using multiplex reverse transcriptase-polymerase chain reaction and/or two-color interphase fluorescence in situ hybridization. By these methods, the t(11;18) translocation was detected in 1 of 8 patients with reactive lymphoid hyperplasia (13%), 3 of 23 with mucosa-associated lymphoid tissue lymphoma (13%), and 2 of 14 with diffuse large B-cell lymphoma with/without mucosa-associated lymphoid tissue lymphoma (14%). Moreover, we performed fluorescence in situ hybridization analysis to detect any numerical aberration of chromosomes 3, 7, 12, and 18 on some specimens nonselectively. No numerical chromosomal abnormalities were detected in 3 cases of reactive lymphoid hyperplasia, whereas three of four cases of mucosa-associated lymphoid tissue lymphoma and all four cases of diffuse large B-cell lymphoma with/without mucosa-associated lymphoid tissue lymphoma components exhibited one or more abnormalities. These findings indicate a possibility that at least in the ocular adnexa, some diffuse large B-cell lymphomas are derived from mucosa-associated lymphoid tissue lymphomas.

Adult↗

PubMed2003

Microelectrode array on folding polyimide ribbon for epidural mapping of functional evoked potentials.

This paper describes a flexible polyimide microelectrode ribbon with a bending structure for epidural recording. Bending the ribbon establishes good electro-mechanical contact of the electrodes to the cortex. Impedance spectroscopy and noise measurements in vitro were used to characterize the electrodes. Our in vivo experiments then successfully achieved synchronized neuronal activity and evoked potential patterns useful for understanding brain function and for finding cortical function.

Action Potentials↗

PubMed2003

Histogenesis of CD5-positive and CD5-negative B-cell neoplasms on the aspect of somatic mutation of immunoglobulin heavy chain gene variable region.

The immunoglobulin heavy chain (IgH) gene of B-cells dramatically alters twice in their differentiation to memory or plasma cells; VDJ recombination at B-cell precursor and somatic hypermutation, class switch recombination and receptor revision at germinal center (GC) B-cells. Among them, somatic hypermutation of the IgH gene variable region (VH gene) is a powerful tool for detection of B cell differentiation. B-cells and B-cell neoplasms have been divided into following; 1) pre-GC B-cells and neoplasms with a germline VH gene and 2) GC and post-GC B-cells and neoplasms with a somatically mutated VH gene. In this article, we review normal B-cell differentiation and histogenesis of various types of B-cell neoplasms on the aspect of somatic mutation of the rearranged VH gene. In particular, differences between CD5+ and CD5- B-cell neoplasms, using our own data of over 100 cases with B-cell neoplasms, are discussed. Although CD5+ B-cells are included in pre-GC B-cells for the reason of germline VH gene in most of CD5+ B-cells, an about 5% of CD5+ B-cells show somatically mutated VH gene. The rearranged VH gene of CD5+ B-cell neoplasms shows heterogeneity, whereas CD5- B-cell neoplasms possess somatically mutated VH gene with a mean of 8 approximately 12%. Both CD5+ B-cell chronic lymphocytic leukemia and CD5+ diffuse large B-cell lymphoma display that about half of cases show a germline or low frequency of somatic mutation and the others possess somatically mutated VH gene. CD5+ mantle cell lymphoma constitutes most cases with germline and a small number of cases with mutated VH gene. Therefore, CD5- B-cells & CD5- B-cell neoplasms are distinct from CD5+ B-cells and CD5+ B-cell neoplasms in somatic mutation of VH gene. It suggests that each of CD5- and CD5+ B-cells independently has its own differentiation.

B-Lymphocytes↗

PubMed2002

Ovarian follicular lymphoma: a case report and review of the literature.

Primary ovarian lymphoma is extremely rare, and such a case is reported here. The patient was a 54-year-old Japanese female with abnormal genital bleeding. Pelvic CT and MRI showed a right ovarian tumor with a diameter of 7 cm and an irregular border. With the diagnosis of a right ovarian tumor, the patient underwent a simple hysterectomy and bilateral salpingo-oophorectomy. Microscopic examination of the right ovarian tumor revealed vaguely nodular growth of small lymphoid cells. They were CD10+, Bcl-2+, Cyclin D1- and CD21-, although CD21+ follicular dendritic cell clusters were present as a background component in each vague nodule. A conventional cytogenetic analysis revealed t(14;18)(q32;q21), and somatic hypermutation of the variable region of the immunoglobulin heavy chain gene (IgH) was confirmed by direct sequencing of subcloned DNA samples derived from PCR amplicons. These findings led us to characterize the lesion as follicular lymphoma, grade 1. The patient was free of detectable disease 9 months after initiation of post-surgical chemotherapy. Since the prognosis for primary ovarian lymphoma is relatively favorable in many cases, it is important to establish therapeutic methods for the cure of this disease using chemotherapy and radiotherapy without radical surgery.

Antineoplastic Combined Chemotherapy Protocols↗