[Primary cutaneous histiocytic sarcoma].
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Biomedical subjects
Publications and source records attributed to Xiao-ge Zhou.
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OBJECTIVE: To study the clinical and pathologic features of post-transplant lymphoproliferative disorders (PTLD), and to investigate the clinical significance of this diagnosis. METHODS: Four cases of PTLD were studied by routine light microscopy, immunohistochemistry and in-situ hybridization and polymerase chain reaction. The clinical data and follow-up information were also reviewed. RESULTS: In the 4 cases, 3 cases occurred in renal transplant recipients and 1 in bone marrow transplant patient. In the 3 post-renal transplant patients, 2 had polymorphic PTLD and 1 had monomorphic PTLD. The post-bone marrow transplant case was classified as "early" lesion of PTLD. Epstein-Barr virus (EBV) was detected in 2 cases. All the 4 cases studied had received cyclosporine A and steroids after transplantation. The duration between organ transplantation and diagnosis of PTLD from case 1 to case 4 was 42, 7, 129, 2 months. One of the polymorphic PTLD cases belonged to clinical stage II and subsequently died of the disease. Other cases belonged to clinical stage I and were alive for 5 to 40 months after diagnosis of PTLD. CONCLUSIONS: PTLD is a lymphoproliferative disease with distinctive morphologic and clinical characteristics. An association with EBV at least in some cases is observed. The prognosis of PTLD correlates with clinical stage. It may respond to reduction in dosage of immunosuppressive agents.
OBJECTIVE: To study the expression of CDX2 in normal and tumor tissues, and to evaluate the value of CDX2 immunostaining in the diagnosis of gastrointestinal adenocarcinoma. METHOD: Seventy-six samples of normal tissue and 612 samples of tumor tissue were studied by tissue microarray technology and immunohistochemistry for CDX2. RESULTS: CDX2 was strongly expressed in surface epithelium of 13 samples of normal intestine and in ductal epithelium of 8 samples of normal pancreas, as well as in 47 samples (92.2%) of colonic adenocarcinoma and 58 samples (66.9%) of gastric adenocarcinoma. As for other tumor types, there was only weak or patchy CDX2 positivity. The positivity rates were as follows: ovarian mucinous adenocarcinoma 15.6% (10/64), pancreatic cancer 33.3% (3/9), thyroid cancer 27.3% (3/11) and extrahepatic biliary cancer 25% (4/16). On the other hand, primary tumors of breast, prostate, kidney, adrenal and liver were negative for CDX2. CONCLUSIONS: CDX2 is expressed mainly in normal epithelium of intestinal tract and small pancreatic ducts, as well as in primary adenocarcinoma of gastrointestinal tract. CDX2 may thus play an important role in distinguishing primary non-intestinal adenocarcinoma from metastatic adenocarcinoma of gastric or colorectal primary.
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OBJECTIVE: To describe the relative frequency, morphologic features, immunophenotype and clinical data of different types of B-cell non-Hodgkin lymphoma (B-NHL) and to evaluate the practical application of the 2001 World Health Organization (WHO) classification of lymphoid neoplasms. METHODS: 369 documented cases of B-NHL were further subtyped according to the 2001 WHO classification of lymphoid neoplasms, on the basis of hematoxylin and eosin staining, immunohistochemistry and in-situ hybridization techniques. RESULTS: Amongst the 369 cases of B-NHL studied, 353 cases could be further classified into 11 subtypes. Diffuse large B-cell lymphoma, extranodal marginal zone lymphoma and follicular lymphoma were the commonest subtypes, accounting for 51.2% (189 cases), 14.9% (55 cases) and 10.6% (39 cases) of all cases respectively. Tumors in lymph nodes were seen in 158 cases (42.8%) and in extra node in 211 cases (57.2%). B-cell prolymphocytic leukemia and hairy cell leukemia were not identified. When comparing the diagnosis based on morphologic examination alone with the diagnosis based on both morphology and immunophenotype, there was a 80% concordance rate. Immunohistochemical study was helpful in reaching the correct diagnosis in many cases and could improve the overall diagnostic accuracy by about 20%. CONCLUSIONS: Amongst cases of B-NHL, diffuse large B-cell lymphoma is the commonest subtype, followed by MALToma and follicular lymphoma. While morphologic examination forms the basis for lymphoma diagnosis, immunohistochemical study also plays an important role in further subtyping. A combination of both modalities are sufficient for arriving at an accurate diagnosis in most cases of B-NHL, in keeping with the recommendation of the 2001 WHO classification of lymphoid neoplasms.
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OBJECTIVE: To investigate the histopathological classification and clinical features of ocular adnexal lymphoproliferative lesions. METHODS: The clinical, histomorphological and immuno-histochemical features of 112 cases of ocular adnexal lymphoproliferative lesions (116 paraffin specimens) were studied retrospectively. The lesions were classified according to the World Health Organization classification of tumors of haematopoietic and lymphoid tissues (2001). RESULTS: This group of patients' ages averaged at 49. The mean duration between the onset of the symptoms and the time of presentation was 22 months. Sixteen patients (14.3%) had bilateral lesions. Proptosis or local orbital mass was presented in 69 cases (61.6%). Reactive lymphoid hyperplasia was diagnosed in 11 cases (9.8%) and atypical lymphoid hyperplasia in 10 cases (8.9%). The rest 91 cases (81.3%) were diagnosed as lymphoma, among which 74 cases (81.3%) were extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT-EMZL). CONCLUSIONS: MALT-EMZL is the most frequent type of ocular lymphoproliferative lesions in ocular adnexa. The ocular adnexal lymphoproliferative lesions show an indolent course clinically, tending to affect the old. Bilateral case is not uncommon.
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OBJECTIVE: To assess the utility of P504S immunohistochemistry in the diagnosis and differential diagnosis of prostatic adenocarcinoma. METHODS: Light microscopy and immunohistochemistry examinations (EnVision staining) were performed in 117 cases of prostatic adenocarcinoma, PIN, AAH, ASAP, BPH and normal prostatic tissue to correlate the morphology and protein expression of P504S, 34betaE12, and P63. RESULTS: Seventy-one of the 78 (91%) cases of prostatic adenocarcinoma stained positive for P504S, with strong cytoplasmic granular staining in most cases, and a weak or intense granular staining along the circumferential luminal and apical cell border membrane in a few cases. Negative P504S immunostaining was observed in 7 of 78 (9%) cases of prostatic adenocarcinoma, all of which were clear cell type prostatic adenocarcinoma. Cases of PIN (9 cases), AAH (6 cases) and ASAP (2 cases) showed various expression levels of P504S. Sixty-five of 68 (96%) cases of normal prostates and BPH were negative for P504S and basal cell hyperplasia cases were also negative. CONCLUSIONS: P504S is a useful marker for microscopic diagnosis of prostatic adenocarcinoma, and immunohistochemistry study using a combination of P504S and 34betaE12/p63 may be of greater benefit in aiding the differential diagnoses.
In classical Hodgkin lymphoma the malignant Hodgkin/Reed-Sternberg (HRS) cells characteristically constitute only a small minority of the tumour load. Their origin has been debated for decades, but on the basis of rearrangement and somatic hypermutations of their immunoglubulin (Ig) genes, HRS cells are now ascribed to the B-cell lineage. Nevertheless, phenotypically HRS cells have lost their B cell identity: they usually lack common B cell-specific surface markers such as CD19 and CD79a as well as Ig gene transcripts. Here we demonstrate that Ig promoters as well as both intronic and 3' enhancer sequences are transcriptionally inactive in HRS cell lines. This inactivity correlates with either reduced levels or even a complete lack of several B cell-specific transcription factors required for their expression: Oct-2, OBF-1, PU.1, E47/E12, PAX-5 and EBF. Moreover, we demonstrate that PU.1 and PAX-5 are significantly down-regulated in HRS cells in pathological specimens from primary tumour tissues. However, forced expression of these transcription factors can activate regulatory sequences of silenced B cell marker genes, and in one instance also transcription from a silenced endogenous locus. Thus, HRS cells are dedifferentiated B cells with global down-regulation of B cell-specific genes.
BACKGROUND: Bladder cancer is characterized by genomic instability. In this study, we investigated whether genome-wide screening using single-nucleotide polymorphism (SNP) arrays could detect allelic imbalance (loss or gain of at least one allele) in bladder cancers. METHODS: For microarray analysis, DNA was isolated from microdissected bladder tumors and leukocytes from 11 patients. The stage T1 tumor (connective tissue invasive) and the subsequent stage T2-4 tumor (muscle invasive) were available from eight of these patients, and only the first muscle-invasive stage T2-4 tumor was available from three of the 11 patients. The microarray contained 1494 biallelic polymorphic sequences. For microsatellite analyses, DNA was isolated from tumors and leukocytes of nine patients with primary T2-4 tumors and 13 patients with Ta (noninvasive) tumors. All statistical tests were two-sided. RESULTS: We assigned a genotype to 1204 loci, 343 of which were heterozygous. Allelic imbalance was detected in known areas of imbalance on chromosomes 6, 8, 9, 11, and 17, and a new area of imbalance was detected on the p arm of chromosome 6. Microsatellite analysis of nine other T2-4 tumors and 13 Ta tumors showed that allelic imbalance was more frequent in T2-4 tumors than in Ta tumors (P<.001). We detected 8.5 allelic imbalances (median) in 348 informative loci in T1 tumors and 28 allelic imbalances (median) in 329 informative loci in T2-4 tumors. When pairs of T1 and T2-4 tumors were analyzed from eight patients, 68% of imbalances detected in T1 tumors (146 imbalances) occurred in the subsequent T2-4 tumors (99 imbalances). Homozygous TP53 mutations were more often associated (P =.005) with high allelic imbalance than with low allelic imbalance. CONCLUSION: SNP arrays are feasible for high-throughput, genome-wide scanning for allelic imbalances in bladder cancer.