Showing papers on "Large cell published in 2005"

Primary non-Hodgkin's lymphoma of the liver.

Abstract: We review the literature on primary hepatic lymphoma (PHL). PHL is a rare malignancy, and constitutes about 0.016% of all cases of non-Hodgkin's lymphoma. It has been reported to occur with increased frequency in patients with chronic hepatitis C infection. Most patients with PHL present with abdominal pain, constitutional symptoms and have hepatomegaly on examination. Imaging studies reveal solitary, or less often, multiple masses in the liver. The predominant histology is B-cell lymphoma, most commonly diffuse large cell type. Most patients are treated with chemotherapy, with some physicians employing a multimodality approach incorporating surgery and radiotherapy with chemotherapy. The prognosis is variable, with good response to early aggressive combination chemotherapy.

A case and review of bowel perforation secondary to metastatic lung cancer.

Abstract: Gastrointestinal tract perforation (GITP) secondary to metastatic lung cancer is extremely rare. We present a case of small bowel perforation secondary to metastatic lung cancer. The objective of this study was to review the current literature and further characterize the incidence, histology, and risk of GITP secondary to lung cancer metastasis. A Medline search was done to identify all the cases of GITP attributed to metastatic lung cancer reported in the literature. Data was collected and analyzed from a collection of cases in the medical literature since 1960. We identified 98 cases of perforated lung cancer metastasis to the small intestine. Four gastric perforations, three colonic perforations, and one appendiceal perforation were also identified but not analyzed. The mean age was 64.5 years. There was a male predominance of 89 per cent versus 11 per cent female. Perforations occurred most often in the jejunum (53%) followed by ileum (28%). Combined jejunum-ileum lesions accounted for 4 per cent of perforations. No duodenal perforations were reported, though a specific site was not determined in 13 per cent of cases. Small bowel perforations were most often caused by adenocarcinoma (23.7%), squamous cell carcinoma (22.7%), large cell carcinoma (20.6%), and small cell carcinoma (19.6%). The prevalence of small bowel perforation secondary to a given primary lung cancer histology varied by region. The mean survival was 66 days with 50 per cent of patients not surviving past 30 days. Despite a high incidence of lung cancer, small bowel perforation secondary to lung cancer metastasis remains relatively rare. Perforated metastases occur more often in men and are found more commonly in the jejunum. Small bowel perforations are caused most often by adenocarcinoma; however, squamous cell and large cell carcinoma metastases are more likely to result in perforation. Small bowel perforation in this setting has a significant impact on mortality, decreasing 1-year survival to less than 3 per cent.

Large B-cell lymphoma with Hodgkin's features

Abstract: Aims: To describe the features of a series of nine cases of diffuse large B-cell lymphoma (DLBCL) showing morphological and immunophenotypic features that are intermediate with Hodgkin's lymphoma (HL). Methods and results: Most cases (6/9) presented as mediastinal tumours affecting young males, while the other three cases arose in extramediastinal locations. Histopathologically, tumours showed diffuse large cell areas in a polymorphous background, with pleomorphic cytology and the common presence of Hodgkin's and Reed-Sternberg cells. Immunophenotypically, tumours shared features of DLBCL and classical HL, with expression of CD30, CD15 (6/9), and a full B-cell profile including CD45RB, CD20, CD79a and OCT2. Epstein-Barr virus-latent membrane protein expression was found in 2/9 cases. The majority of tumours had immunohistochemical features consistent with activation of the NF-κB pathway, including nuclear location of the c-REL/p65 subunit, overexpression of phosphorylated IκBα, and overexpression of NF-κB targets. Finally, 2/9 cases showed 3q27 (BCL6) rearrangement, and 1/9 had p53 gene mutations, both of which are rarely detected in classical HL. Conclusions: These findings suggest that DLBCLs with HL features constitute a distinctive subgroup of aggressive lymphomas whose neoplastic growth and peculiar characteristics could be facilitated by a particular microenvironment found in the mediastinum. © 2005 Blackwell Publishing Limited.

CDX2 immunostaining as a gastrointestinal marker: expression in lung carcinomas is a potential pitfall.

Abstract: Paraffin-embedded sections of various adenocarcinomas (13 colonic, 11 mucinous ovarian, 5 serous ovarian, 8 pancreatic, 6 ampullary, 12 gastric, 5 esophageal, 10 endometrial, 29 breast, and 55 lung) and 29 additional lung carcinomas (nonadenocarcinomas) were immunostained with antibodies to CDX2 protein, cytokeratin 7 (CK7), and cytokeratin 20 (CK20). The 84 lung carcinomas were also stained with antibody to thyroid transcription factor-1 (TTF-1). All colorectal and most ovarian mucinous carcinomas were strongly and diffusely immunoreactive for CDX2. Esophageal, gastric, and ampullary adenocarcinomas showed variable immunoreactivity for CDX2. All breast, nonmucinous ovarian, and most endometrial and pancreatic adenocarcinomas showed no immunoreactivity for CDX2. CK7 and CK20 expression was similar to previous reports. Ten of 84 primary lung carcinomas (12%) were immunoreactive for CDX2 expression. Of these, 5 (4 adenocarcinomas and 1 large cell carcinoma) were reactive for TTF-1. Gene expression profiling data--available for 32 of these 84 tumors--showed CDX2 gene expression in 7 of 8 (88%) CDX2 immunoreactive tumors whereas only 1 of 24 (4%) tumors negative for CDX2 immunoreactivity showed CDX2 gene expression. The authors conclude that CDX2 is a relatively specific marker for tumors with intestinal differentiation, with the caveat that its expression can be seen in primary large cell and adenocarcinomas of the lung and mucinous carcinomas of the ovary.

Deletions at chromosome 2q and 12p are early and frequent molecular alterations in bronchial epithelium and NSCLC of long-term smokers

Abstract: Most lung cancer is attributed to long-term smoking. In order to define chromosomal regions with an accumulation of smoking-related early molecular damage, we applied 15 microsatellite markers at 8 chromosomal regions (2q35-q36, 3p21.3, 3p14.2, 3p25, 10q11.2, 11p14-15, 12p13.1-p12.3 and 12q14) in an allelotyping study. We studied samples of 42 patients with primary non-small cell lung cancer (NSCLC) (25 squamous cell carcinomas, 13 adenocarcinomas, 2 large cell and 2 bronchioalveolar carcinomas) to compare the frequency of allelic loss in cancer tissue of smokers with matched bronchial epithelium. As a control group we used 11 samples of non-smokers. In NSCLC we found significantly higher frequencies of loss of heterozygosity (LOH) than in matched tumor free bronchial epithelium (p = 0.007). Most frequently, allelic loss was detected in NSCLC at chromosome 3p [3p25 (46%), 3p21.3 (45%), 3p14 (40%)], at 2q35 (24%), 12p12 (29%) and 12q14 (13%), but infrequently at 10q11 (7%) and 11p14-15 (5%). In corresponding histological normal bronchial epithelium, the highest percentage of LOH was found at chromosome 3p [3p21 (17%), 3p25 (12%), 3p14 (9%)] and chromosome 2q (2q35-q36) (17%) and 12p (12p12-p13) (12%). LOH in histologically normal bronchial epithelium was significantly associated with long-term smoking (p = 0.048), especially at chromosome 12p12 (p = 0.018). Our results demonstrate two further deletion hot spots at the chromosomal region 2q35-q36 and 12p12-p13 in tumor tissue of NSCLC and matched histological normal bronchial epithelium of long-term smokers, reflecting a phenomenon referred to as 'field cancerization'. These chromosomal regions represent interesting loci for potential NSCLC associated tumor suppressor genes and could be useful as screening markers for molecular risk assessment of smokers.

Array-based comparative genomic hybridization analysis of high-grade neuroendocrine tumors of the lung

Abstract: We examined a large number of primary high-grade neuroendocrine tumors of the lung (10 small cell lung carcinomas and 31 large cell neuroendocrine carcinomas) by using array-based comparative genomic hybridization using microarrays spotted with 800 bacterial artificial chromosome clones containing tumor-related genes from throughout the human genome. We identified the genome-wide copy number alteration profiles of these tumors, including recurrent amplifications located at 2q21.2, 3q21-27, 3q26, 3q27-29, 5p14.2, 5p13, 7q21.1, 8q21, and 8q24 and homozygous deletions at 1p36, 4p16, 4p16.3, 9p21.3, 9p21, 19p13.3, and 20q13. Our results revealed that small cell lung carcinomas and large cell neuroendocrine carcinomas have multiple characteristic chromosomal alterations in common, but that distinctive alterations also exist between the two subtypes. Moreover, we found that the two subtypes undergo different processes of accumulating these genetic alterations during tumor development. By comparing the genetic profiles with the clinicopathological features, we discovered many chromosomal loci whose alterations were significantly associated with clinical stage and patient prognosis. These results will be valuable for evaluating clinical status, including patient prognosis, and for identifying novel molecular targets for effective therapies.

Alteration of the E-cadherin/β-catenin cell adhesion system is common in pulmonary neuroendocrine tumors and is an independent predictor of lymph node metastasis in atypical carcinoids

Abstract: BACKGROUND To the authors' knowledge, little is known regarding the role of E-cadherin/β-catenin system dysregulation in pulmonary neuroendocrine tumors. METHODS E-cadherin and β-catenin immunoreactivity was evaluated in 10 hyperplastic neuroendocrine tumorlets and 210 neuroendocrine tumors, including 96 typical carcinoids (CTs), 35 atypical carcinoids (ACTs), 49 large cell neuroendocrine carcinomas (LCNECs), and 30 small cell lung carcinomas (SCLCs). RESULTS Normal and hyperplastic bronchial neuroendocrine cells expressed E-cadherin/β-catenin with an orderly distribution along the cell membrane. Neuroendocrine tumors retained β-catenin expression in all tumors and E-cadherin in most tumors, with the exception of 2% of LCNECs, 3% of SCLCs and 9% of ACTs. E-cadherin showed a prevalent membrane-associated, linear immunoreactivity in CTs, whereas membrane-disarrayed and cytoplasmic staining was seen in most ACTs, LCNECs, and SCLCs (P < 0.001). β-Catenin exhibited similar immunoreactivity patterns according to tumor type and a close association with E-cadherin subcellular distribution (P < 0.001). Nuclear accumulation of β-catenin was found only in seven LCNECs and in two SCLCs. In ACTs, disarrayed immunoreactivity for E-cadherin and/or β-catenin was associated with a nontrabecular growth pattern, altered expression of the cell-motility marker fascin, and lymph node metastases. Furthermore, a disarrayed E-cadherin distribution pattern was associated with the pathologic lymph node classification and the number of involved lymph nodes. Multivariate analysis confirmed that a disarrayed E-cadherin or β-catenin pattern was an independent predictor of lymph node metastases in patients with ACT. CONCLUSIONS The subcellular compartmentalization of the E-cadherin/β-catenin complex was altered in pulmonary neuroendocrine tumors. This likely affects the tumor growth pattern and cell motility of ACT and was correlated with the occurrence of lymph node metastases. Cancer 2005. © 2005 American Cancer Society.

CT Findings of Surgically Resected Pleomorphic Carcinoma of the Lung in 30 Patients

Abstract: OBJECTIVE. The objective of our study was to assess the CT features of surgically resected pleomorphic carcinoma of the lung.CONCLUSION. The CT features of pleomorphic carcinoma of the lung appear to be dictated by the epithelial component of the tumor. Among the various subtypes of pleomorphic carcinoma, the large cell and giant cell subtype showed constant CT features including subpleural location, peritumoral areas of ground-glass attenuation, and extensive central low-attenuation areas.

The utility of interphase fluorescence in situ hybridization for the detection of the translocation t(11;14)(q13;q32) in the diagnosis of mantle cell lymphoma on fine-needle aspiration specimens.

Abstract: BACKGROUND Mantle cell lymphoma can be difficult to differentiate cytologically from other small cell non-Hodgkin lymphomas. Nevertheless, the distinction is important, because mantle cell lymphoma is more aggressive than other small cell non-Hodgkin lymphomas. The purpose of this study was to determine whether fluorescence in situ hybridization (FISH) is helpful in diagnosing mantle cell lymphoma on fine-needle aspiration (FNA) specimens by detecting the t(11;14)(q13;q32) translocation that is characteristic of this tumor. METHODS Fifty-five lymph node FNA specimens from 53 patients were analyzed using FISH. A 2-color FISH assay that employed probes at the 14q32 (immunoglobulin H) and 11q13 (dual-colored, directly labeled cyclin D1) loci was used. The number of single-fusion and double-fusion signals in 200 cells was counted. If ≥ 14% single-fusion signals or ≥ 1.5% double-fusion signals or both were present, then the sample was considered FISH positive. The findings were correlated with the cytologic, histologic, and immunophenotypic findings in each specimen. RESULTS Of the 55 cytology specimens, 17 were mantle cell lymphomas, and 38 were nonmantle cell lymphomas, including 16 small lymphocytic lymphomas (9 of 16 in an accelerated phase), 5 large cell lymphomas, 5 follicular lymphomas, 7 transformed large cell lymphomas (Richter syndrome), 3 atypical lymphoid proliferations, and 2 low-grade B-cell lymphomas. All 17 mantle cell lymphomas were positive by FISH. In addition, there were six small lymphocytic lymphomas (two in accelerated phase), one transformed large cell lymphoma, and one large cell lymphoma of follicular origin positive by FISH. The mean number of single-fusion and double-fusion signals, respectively, was 36 and 33 in mantle cell lymphoma specimens and 19 and 3 in positive nonmantle cell lymphoma specimens. CONCLUSIONS The detection of the t(11;14)(q13;q32) translocation by FISH analysis was helpful in diagnosing mantle cell lymphoma on FNA specimens. Double-fusion signals were more specific for mantle cell lymphoma than single-fusion signals. In rare instances, other non-Hodgkin lymphomas also showed increased numbers of single-fusion signals that were not necessarily indicative of the t(11;14)(q13;q32) translocation. Therefore, in an initial diagnosis of mantle cell lymphoma, significant numbers of double-fusion FISH signals should be identified and interpreted in conjunction with the cytologic and immunologic studies. Cancer (Cancer Cytopathol) 2005. © 2005 American Cancer Society.

Frequency, symptoms and outcome of intestinal metastases of bronchopulmonary cancer. Case report and review of the literature

Abstract: We report a new case of small bowel metastases from primary lung cancer Such metastases are not exceptional, but their clinical manifestations are rare The case involved a 56-year-old man with a squamous cell carcinoma of the lung (stage IV) that had been treated with chemotherapy He presented fourteen months after diagnosis with an acute abdominal pain Abdominal CT-scan demonstrated a perforated jejunum and he underwent emergency surgery Postoperative pathologic analysis confirmed the diagnosis of metastatic pulmonary carcinoma The patient was discharged after ten days, but died 8 weeks after surgery at home on tumor progression We were able to find 58 documented similar cases in the literature Most cases presented with bowel perforation or obstruction Squamous cell carcinoma was the most common histological cell type followed by large cell carcinoma Other metastases are often present, and the prognosis is mostly fatal at short term

Mice transgenic for NPM-ALK develop non-Hodgkin lymphomas.

Abstract: Background: The t(2;5)(p23;q35) translocation is associated with a high percentage of anaplastic large-cell lymphomas (ALCL) of T- or null-cell phenotype. The translocation produces an 80 kDa hyperphosphorylated chimeric protein (p80) derived from the fusion of the anaplastic lymphoma kinase (ALK) with nucleophosmin (NPM). The NPM-ALK chimeric protein is an activated tyrosine kinase that has been shown to be a potent oncogene and presumably plays a causative role in lymphomagenesis. Materials and Methods: A transgenic mouse line was generated, where the human NPM-ALK cDNA is driven by the lck promoter conferring transgene expression to early T- cells. Results: Mice rapidly developed large cell lymphoblastic lymphomas with a median latency of 8 weeks, primarily involving the thymus, with lymph node as well as histologically evident extranodal organ infiltration by large tumor cells. Conclusion: The transgenic approach described provides direct evidence for the strong transforming potential of NPM-ALK in T-cells and furthermore represents a system for the analysis of the oncogenic events mediated by NPM- ALK in vivo, which might be instrumental in the development of tyrosine kinase inhibitor therapies of potential clinical use. Anaplastic large-cell lymphoma (ALCL) is a form of T-cell lymphoma which is defined by CD30 positivity and anaplastic

Expression of p63 in reactive hyperplasias and malignant lymphomas.

Abstract: p63 is a recently described p53 homologue. It is involved in survival and differentiation of reserve/stem cells in epithelia. To obtain new insights into the role of p63 in malignant lymphomas (MLs), immunohistochemical staining for p63 and p53 was performed in 126 cases of MLs. p63 was expressed in 38 cases of MLs (30.2%) including 32/61 cases (52.5%) of diffuse large B-cell lymphoma (DLBCL), 1/8 cases (12.5%) of precursor T-lymphoblastic lymphoma (T-LBL), 4/14 cases (28.6%) of follicular lymphoma, 1/6 cases (16.7%) of T/NK cell lymphoma. Among p63 positive cases, p63 was strongly expressed in 15/32 cases of DLBCL and 1/1 case of T-LBL. p63 was not expressed in mantle cell lymphomas, peripheral T-cell lymphomas, marginal zone B-cell lymphomas, plasma cell myelomas and Hodgkin's lymphomas. p63 was coexpressed with p53 in 18/38 p63 positive cases in which only 4 cases were strongly coexpressed. All p63+/p53+ cases were DLBCL. p63 overexpression (above 30%) cases showed significant poor survival (p=0.0228) in DLBCL. However, there was no statistically significant correlation between p63 expression and IPI score on Multivariate analysis. We could speculate that p63 could act indirectly as an oncogene by inhibiting p53 functions. Stage of differentiation of neoplastic lymphocytes appears to have a correlation with p63 expression in MLs.

Primary lung cancer arising from the wall of a giant bulla.

Abstract: We report a 58-year-old man who underwent surgical treatment of primary lung cancer arising from the wall of a giant bulla. Chest roentgenography and computed tomography revealed multiple emphysematous bullae in the bilateral upper lobes, and a right upper giant bulla with a mass measuring 6 cm arising on the bulla wall. Right upper lobectomy was performed, the postoperative pathological diagnosis was large cell carcinoma arising from the wall of a giant bulla. Although the postoperative course was uneventful and he was discharged, he underwent partial resection of the jejunum for recurrence of carcinoma in the jejunum, and postoperative chemotherapy, and he was alive 20 months after that operation. In general, patients with both pulmonary bullous disease and primary lung cancer have a very poor prognosis, because they receive treatment when the tumor is at an advanced stage. On the basis of our review of the literature, we recommend that middle-age male patients with a giant bulla who smoke should have annual chest roentgenography and/or chest computed tomography to screen for lung cancer arising in or close to the bullous disease, and that a giant bulla should be resected in patients older than 50 years because of the high incidence of coexisting cancer and bulla, to improve the prognosis of this disease.

Cytologic features of plasmablastic lymphoma.

Abstract: BACKGROUND Plasmablastic lymphomas (PBLs) were originally described exclusively in human immunodeficiency virus (HIV)-positive patients who presented with jaw or oral mucosa involvement. Recent studies have reported this neoplasm also in patients without HIV infection and involving sites other than head and neck. This lymphoma has a heterogeneous morphologic presentation but distinct phenotype. METHODS Cytologic features from four cases of histologically confirmed PBL were evaluated. The cytology specimens were evaluated for criteria as follow: cellularity, cell size and shape, pleomorphism, cytoplasmic characteristics, chromatin pattern, nucleolar features, and mitotic figures. RESULTS Specimens evaluated were two head and neck fine needle aspiration specimens, one anal smear, and one cerebrospinal fluid specimen. Atypical lymphocytes ranged from intermediate to large in size and demonstrated slight nuclear pleomorphism. The cytoplasm varied from scant to moderate in the alcohol-fixed slides. Nuclei were round with vesicular chromatin. Nucleoli varied from a prominent one to multiple small ones. Multinucleated cells and mitotic figures were easily identified in three of four cases. Tingible-body histiocytes were seen in one case. Ancillary studies in two cases demonstrated expression of CD138 with lack of CD20 expression. CONCLUSION PBL is a variant of large cell lymphoma with heterogeneous cytologic findings but distinct immunophenotype. Knowledge of the cytomorphologic spectrum of PBLs and detection of CD138 expression by flow cytometry can be helpful in achieving a correct diagnosis. Cancer (Cancer Cytopathol) 2005. © 2005 American Cancer Society.

Composite glandular-endocrine cell carcinomas of the stomach: clinicopathologic and methylation study†

Abstract: Four cases of very rare composite glandular-endocrine cell carcinoma of the stomach are presented with methylation findings. All but one of the tumors arose in the antrum and two of them were at the early stage. Each composite carcinoma was accompanied by atrophic and metaplastic gastritis in the adjacent mucosa. Three cases showed lymph nodes metastasis, and one of them showed both glandular and neuroendocrine tumor components within the metastatic nodes. Mucin stains were positive in the adenocarcinoma areas while only the neuroendocrine markers were positive in neuroendocrine tumor components. Of all seven markers tested for, p16INK4A methylation was observed in both components of one composite carcinoma and hMLH1 was methylated in the neuroendocrine tumor component within the same tumor. An additional six gastric large cell neuroendocrine carcinomas showed no methylation. Follow up of patients indicated short survival in patients with poorly differentiated neuroendocrine carcinoma components and advanced stages of tumors, while patients with well-differentiated neuroendocrine tumor components and early stages showed long disease-free survival. Our results suggest that hypermethylation of tumor suppressor genes is rare in gastric composite and neuroendocrine carcinomas, and prognosis of gastric composite carcinomas appears to be related to the histopathology of neuroendocrine components and tumor stage.

Primary and isolated anaplastic large cell lymphoma of the bone marrow.

Abstract: Anaplastic large cell lymphoma (ALCL) is a T-cell lymphoma in which the majority of patients present with advanced stage III or IV disease. Here we report a case of ALCL where bone marrow was the only site of disease, in a 60-year-old man with pyrexia and pancytopenia. The diagnosis of ALCL was made on detection of CD30-positive anaplastic cells in the bone marrow, together with prominent hemophagocytosis. Genetics confirmed the clonal nature of the disease and showed it to be anaplastic lymphoma kinase (ALK) negative. Primary isolated bone marrow ALCL should be considered in the diagnosis of pancytopenia associated with hemophagocytosis.

Extended resection of T4 lung cancer with invasion of the aorta: is it justified?

Abstract: Background We report our 10-year experience of performing surgical resection of T4 lung cancer invading the thoracic aorta. Patients and methods From 1994 to 2004, sixteen patients with T4 primary lung cancer with local invasion of the thoracic aorta underwent tumor resection. Surgical resection included 8 pneumonectomies and 8 lobectomies. The histologic type was squamous cell carcinoma in 7 patients, adenocarcinoma in 7, large cell carcinoma in 1, and small cell carcinoma in 1. Complete resection of the tumor with mediastinal lymph node dissection was achieved in 8 patients (50 %), while the resection was incomplete in the other 8 cases. Results The overall cumulative survival of the 16 patients at 3 and 5 years was 34.7 % and 17.4 %, respectively. The survival of the patients in the complete resection group was found to be 36.5 % at 5 years, with 2 patients surviving more than 5 years without a recurrence, which was significantly better than that of the incomplete resection group ( p = 0.005). Conclusions Extended aortic resection with primary lung cancer is complex and possibly high risk, but can achieve long-term survival in selected patients. Surgical resection should be considered as a treatment option for T4 lung cancer for this T4 subcategory.