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J H Van Krieken

Publications and source records attributed to J H Van Krieken.

At least 19 recordsLinked to original sources
PubMed2001

Rhinovirus-induced airway inflammation in asthma: effect of treatment with inhaled corticosteroids before and during experimental infection.

Asthma exacerbations are frequently linked to rhinovirus infections. However, the associated inflammatory pathways are poorly understood, and treatment of exacerbations is often unsatisfactory. In the present study we investigated whether antiinflammatory treatment with inhaled corticosteroids prevents any rhinovirus-induced worsening of lower airway inflammation. To that end, we selected 25 atopic patients with mild asthma who underwent experimental rhinovirus 16 (RV16) infection, while receiving double-blind, placebo-controlled treatment with the inhaled corticosteroid budesonide (800 microg twice a day) throughout the study period, starting 2 wk before infection. We assessed inflammatory cell numbers in the bronchial mucosa as obtained by bronchial biopsies 2 d before and 6 d after RV16 infection, and analyzed those in relation to cold symptoms, changes in blood leukocyte counts, airway obstruction, and airway hyperresponsiveness. RV16 colds induced an increase in CD3(+) cells in the lamina propria (p = 0.03) and tended to decrease the numbers of epithelial eosinophils (p = 0.06) in both groups analyzed as a whole. The T cell accumulation was positively associated with cold symptoms. Budesonide pretreatment improved airway hyperresponsiveness (p = 0.02) and eosinophilic airways inflammation (p = 0.04). Yet it did not significantly affect the RV16-associated changes in the numbers of any of the inflammatory cell types. We conclude that RV16 infection by itself induces only subtle worsening of airway inflammation in asthma, which is not improved (or worsened) by inhaled corticosteroids. The latter finding is in keeping with the limited protection of inhaled corticosteroids against acute asthma exacerbations.

Administration, Inhalation↗
PubMed2001

Image analysis and quantification in lung tissue.

On 9-10 September 1999, an international workshop on image analysis and quantification in lung tissue was held at the Leiden University Medical Center, Leiden, The Netherlands. Participants with expertise in pulmonary and/or pathology research discussed the validity and applicability of techniques used for quantitative examination of inflammatory cell patterns and gene expression in bronchial or parenchymal tissue in studies focusing on asthma and chronic obstructive pulmonary disease (COPD). Differences in techniques for tissue sampling and processing, immunohistochemistry, cell counting and densitometry are hampering the comparison of data between various laboratories. The main goals of the workshop were to make an inventory of the techniques that are currently available for each of these aspects, and in particular to address the validity and unresolved problems of using digital image analysis (DIA) as opposed to manual scoring methods for cell counting and assessment of gene and protein expression. Obviously, tissue sampling and handling, fixation and (immunohistochemical) staining, and microscope settings, are having a large impact on any quantitative analysis. In addition, careful choices will have to be made of the commercially available optical and recording systems as well as the application software in order to optimize quantitative DIA. Finally, it appears to be of equal importance to reach consensus on which histological areas are to be analysed. The current proceedings highlight recent advances and state of the art knowledge on digital image analysis for lung tissue, and summarize the established issues and remaining questions raised during the course of the workshop.

Animals↗
PubMed2000

Vaccination of melanoma patients with an allogeneic, genetically modified interleukin 2-producing melanoma cell line.

Thirty-three metastatic melanoma patients were vaccinated according to a phase I-II study with an allogeneic melanoma cell line that was genetically modified by transfection with a plasmid containing the gene encoding human interleukin 2 (IL-2). The cell line expresses the major melanoma-associated antigens and the HLA class I alleles HLA-A1, -A2, -B8, and Cw7. All patients shared one or more HLA class I alleles with this cell line vaccine. Patients were immunized by three vaccinations, each consisting of 60 x 106 irradiated (100 Gy) melanoma cells (secreting 120 ng of IL-2/10(6) cells/24 hr) administered subcutaneously at weekly intervals for 3 consecutive weeks. Side effects of treatment consisted of swelling of locoregional lymph nodes and induration at the site of injection, i.e., a delayed-type hypersensitivity (DTH) reaction. In three patients, vaccination induced inflammatory responses in distant metastases containing necrosis or apoptosis along with T cell infiltration. Apoptosis occurred only in Bcl-2-negative areas, not in Bcl-2-expressing parts of the metastases. Two other patients experienced complete or partial regression of subcutaneous metastases. Seven patients had protracted stabilization (4 to >46 months) of soft tissue metastases, including one patient who developed vitiligo after vaccination. Immune responses to the vaccine could be detected in 67% of the 27 patients measured. Vaccination was shown to induce a variable change in the number of anti-vaccine cytotoxic T lymphocytes (CTLs) in peripheral blood, which did not correlate with response to treatment. However, in two of five patients the frequency of anti-autologous tumor CTLs measured was significantly higher than before vaccination. This study demonstrates the feasibility, safety, and therapeutic potential of vaccination of humans with allogeneic, gene-modified tumor cells, and that frequencies of vaccine-specific CTLs among patient lymphocytes can be determined by using a modified limited dilution analysis (LDA).

Adult↗
PubMed2000

Epidemiological and prognostic aspects of gastric MALT-lymphoma.

Since mucosa-associated lymphoid tissue (MALT) lymphoma was defined in the mid-1980s as a clinicopathologic entity, many sets of data on pathological, biological and clinical aspects have been generated. In particular, the finding that this process was responding well to antibiotic treatment fueled interest in it and has led to several clinical trials. This overview deals with epidemiological and prognostic aspects and identifies important questions which need to be answered before data from different sources can be compared. Incidence figures of gastric MALT lymphoma vary between countries and parallel the numbers of all non-Hodgkin's lymphoma. The incidence does not parallel the occurrence data of Helicobacter pylori infection. Incidence figures are highly dependent on the definition used for MALT-type primary gastric lymphomas. Several studies show that some prognostic factors are relevant, for instance stage and grade, whereas other factors such as the International Prognostic Index or treatment are not. These studies do not include the recently introduced antibiotic therapy. The inclusion of recent insights in biology and the treatment of gastric MALT lymphomas in prospective clinical studies will soon answer some of the main questions posed.

Aged↗
PubMed2000

Experimental rhinovirus 16 infection increases intercellular adhesion molecule-1 expression in bronchial epithelium of asthmatics regardless of inhaled steroid treatment.

BACKGROUND: Rhinovirus infections in airway epithelial cells in vitro have been shown to upregulate intercellular adhesion molecule-1 (ICAM-1) expression. Epithelial ICAM-1, in its dual role as the major rhinovirus receptor and as adhesion molecule for inflammatory cells may be involved in the pathogenesis of rhinovirus-induced exacerbations of asthma. OBJECTIVE: We aimed to investigate the effect of experimental rhinovirus 16 (RV16) infection on ICAM-1 expression in bronchial mucosal biopsies in asthma. In addition, the effect of 2 weeks pretreatment with inhaled budesonide (800 microg b.d.) on RV16-associated changes in ICAM-1 expression was studied. METHODS: The study had a parallel, placebo-controlled design in 25 steroid-naive nonsmoking atopic asthmatic subjects. After 2 weeks budesonide (BUD) or placebo (PLAC) pretreatment bronchoscopy was performed 2 days before (day -2) and 6 days after (day 6) RV16 inoculation (on days 0 and 1). Immunohistochemical staining for ICAM-1 was performed on snap-frozen bronchial biopsies. ICAM-1 staining intensity on the basal epithelial cells was scored semiquantitatively from 1 (weak) to 3 (intense). Similarly, epithelial intactness was noted (1 = basal cells only, 2 = basal and parabasal cells, 3 = intact epithelium). RESULTS: ICAM-1 scores were not significantly different between the groups at day -2 (P > or = 0.08). Subsequent RV16 infection was associated with a trend towards an increase in ICAM-1 expression in the BUD-group (P = 0.07), whereas the increase was significant in the PLAC-group (P = 0.03). However, the increase was not significantly different between the groups (P = 0.74). Epithelial intactness score was not different between the groups before RV16 infection (P > or = 0.07), and no significant changes were observed in either group (P > or = 0.59). Moreover, ICAM-1 score did not correlate significantly with epithelium score in either group, at any time-point (P > or = 0.27). CONCLUSION: We conclude that an RV16 common cold in atopic asthmatic subjects is associated with increased ICAM-1 expression in the bronchial epithelium, which is not related to epithelial intactness. Glucocorticoid treatment does not appear to prevent the RV16-associated increased ICAM-1 expression. This suggests that other treatment modalities are required to protect against the spreading of infection during rhinovirus-induced exacerbations in asthma.

Administration, Inhalation↗
PubMed1999

Mesalazine-induced apoptosis of colorectal cancer: on the verge of a new chemopreventive era?

BACKGROUND: It is an accepted fact that non-steroidal anti-inflammatory drugs (NSAIDs) are potent inhibitors of colorectal carcinogenesis. However, the major disadvantages of NSAIDs are gastrointestinal and renal toxicity. We conducted a prospective pilot study on the effects of the safe salicylic acid derivative, mesalazine, on apoptosis and proliferation of tumour cells and on normal tissue in colorectal cancer patients. METHODS: Patients with colorectal cancer were asked to take mesalazine enemas for 14 days. Biopsies from malignant and normal tissue were taken prior to and after this treatment. Apoptosis was scored on haematoxylin/eosin-stained tissue sections, and cell proliferation was assessed by the proliferation marker Ki-67. RESULTS: Ten out of 14 patients completed the study. The apoptotic score increased significantly in the tumour samples (pre-treatment 14.6 +/- 1.3 vs. post-treatment 19.4 +/- 0.8; P < 0.03). The apoptotic index in the normal mucosa was unchanged (pre-treatment 3.1 +/- 0.4 vs. post-treatment 2.9 +/- 0.3; N.S.). The cell proliferation in malignant tissue, according to the Ki-67 score, was hardly affected by mesalazine (pre-treatment 522 +/- 38 vs. post-treatment 493 +/- 39; N.S.). There was no effect on the Ki-67 index of normal mucosa (pre-treatment 24.2 +/- 2.0 vs. post-treatment 28.3 +/- 2.0; N.S.). CONCLUSIONS: This pilot study conducted in patients with colorectal cancer clearly shows that mesalazine selectively induces apoptosis of tumour cells. On the basis of these findings, which need to be confirmed in larger studies, it may be speculated that 5-ASA could be useful in the chemoprevention of colorectal cancer.

Aged↗
PubMed1997

Effective treatment of experimental lupus nephritis by combined administration of anti-CD11a and anti-CD54 antibodies.

Mice with chronic graft-versus-host disease (GVHD), induced by injection of DBA/2 lymphocytes in (C57BL10*DBA/2) F1 hybrids, develop a syndrome resembling systemic lupus erythematosus (SLE) with immune complex glomerulonephritis. In this model we evaluated the role of interactions between CD11a (LFA-1alpha) and CD54 (intercellular adhesion molecule-1 (ICAM-1)) molecules on leucocytes in the development of renal disease in systemic autoimmunity. Two weeks after induction of GVHD, when anti-nuclear autoantibodies were detected in the circulation and immune complexes had formed in the glomeruli, mice were injected twice per week with rat anti-CD11a and anti-CD54 MoAbs, or with their vehicle PBS, or with control rat IgG. MoAb treatment significantly lowered albuminuria and increased survival compared with control mice with GVHD. In the glomeruli of MoAb-treated mice there was markedly less binding of immunoglobulin and C3, while anti-renal tubular epithelium autoantibodies, but not anti-glomerular basement membrane autoantibodies, were significantly lowered in the circulation 4 weeks after disease induction. In addition, MoAb treatment inhibited the glomerular influx of CD11a+ cells and decreased development of histological abnormalities in the kidneys. Both rat IgG- and MoAb-treated mice developed anti-rat immunoglobulin antibodies. Furthermore, a marked splenomegaly with an increase of the T cell compartment was observed in MoAb-treated mice with GVHD. These results show that CD11a/CD54 interactions are crucial for the full-blown development of lupus nephritis in this model. Treatment aimed at blocking the activity of these molecules profoundly attenuated the development of renal disease in chronic GVHD even if started when first symptoms of SLE (i.e. anti-nuclear autoantibodies in sera and glomerular binding of immunoglobulins) were already detectable.

Albuminuria↗
PubMed1997

Comparison of inflammatory cell counts in asthma: induced sputum vs bronchoalveolar lavage and bronchial biopsies.

BACKGROUND: Induced sputum potentially allows monitoring of airway inflammation in patients with asthma in a non-invasive way. However, the relationship between the cellular content in sputum and airway tissue has not been fully clarified. OBJECTIVE: We compared the cellular compositions of hypertonic saline-induced sputum, bronchoalveolar lavage fluid (BAL) and bronchial biopsies in 18 clinically stable patients with mild to moderate atopic asthma (baseline FEV1: range 61-114%pred, PC20 methacholine: 0.04-4.7 mg/mL). They were treated with inhaled short-acting bronchodilators on demand, with (n = 8) or without (n = 10) regular inhaled steroids. METHODS: Each patient underwent sputum induction and fiberoptic bronchoscopy on separate days in random order. Differential cell counts of induced sputum, bronchoalveolar lavage and bronchial wash were determined on May-Grünwald-Giemsa stained cytospins. Flow cytometry was performed on sputum and BAL samples. Immunohistochemical techniques were used to stain inflammatory cells in 6 microm cryostat sections of bronchial biopsies. RESULTS: Sputum cell differentials were not different between the patients with and without inhaled steroids, and showed a median value of 19.4% squamous cells, with 1.0% eosinophils, 3.3% lymphocytes, 28.7% neutrophils, 49.4% macrophages and 6.9% cylindric epithelial cells (in percentage non-squamous cells). The percentage eosinophils in sputum was significantly correlated with their percentage in bronchial wash (Rs = 0.52, P = 0.03) and in BAL (Rs = 0.55, P= 0.02), whilst there was a trend towards such a correlation between the number of eosinophils/mL sputum and the number of EG2+ eosinophils/mm2 lamina propria in bronchial biopsies (Rs = 0.44, P = 0.07). In addition, the percentage of CD4+ lymphocytes correlated between sputum and BAL (Rs = 0.55, P = 0.03). CONCLUSION: We conclude that the eosinophil counts in hypertonic saline-induced sputum from patients with asthma are related to those in bronchial wash and BAL and, to a lesser extent, with the counts in bronchial biopsies. This suggests that induced sputum can be used to monitor the presence and severity of airway inflammation in asthma.

Adolescent↗
PubMed1996

Prognostic factors in resected non-small cell lung cancer: an immunohistochemical study of 39 cases.

Non-small cell lung carcinoma (NSCLC) is a histologically heterogeneous collection of tumours with variable clinical behaviour. Performance status, tumour stage and histological type have important prognostic implications, but the clinical outcome in an individual patient remains unpredictable. In search of other prognostic factors we studied the expression of several immunohistochemical markers in NSCLC, resected with curative intent. Tumour samples of 19 patients with a postoperative disease-free survival of at least 5 years and those of 20 patients who died of tumour recurrence within 2 years after resection were selected for this study. The populations were matched for age, sex and tumour stage. We investigated the expression of markers for neuroendocrine differentiation, cell adhesion and cell cycle regulation in both populations. None of the investigated immunohistochemical markers distinguished between long- and short-term survivors of resected NSCLC. In stage 1 tumours expression of embryonal NCAM was observed more often in the short survival group (P = 0.026) and in stage 3a EGF-r expression was associated with the long survival group (P = 0.047). However, these findings remained to be confirmed. Expression of Rb, NCAM and embryonal NCAM was not detected in adenocarcinomas, whereas T-Ag and chromogranin A immunoreactivity was absent from squamous cell carcinomas.

Aged↗
PubMed1996

Mantle-cell lymphoma: a population-based clinical study.

PURPOSE: From a population-based non-Hodgkin's lymphoma (NHL) registry, 41 patients with mantle cell lymphoma (MCL) -- a recently defined distinct B-cell NHL -- were selected and compared with patients with low- or intermediate-grade NHL from the same registry. PATIENTS AND METHODS: The incidence and behavior of MCL in the area of the Comprehensive Cancer Center West (CCCW) from 1981 to 1989 were analyzed. Age, performance, tumor bulk, extranodal localization, stage, response to therapy, and survival were registered. Expression of cyclin D1 protein and Ki-67 were measured in 29 patients. RESULTS: MCL made up 3.7% of NHLs. The median age was 68 years, and the male-to-female ratio was 1.6:1. Seventy-eight percent presented with stage IV, with the majority having bone marrow involvement. The complete response (CR) rate was 32% (13 of 41), with a median duration of 25 months. The median overall survival time was 31.5 months. The International Prognostic Index identified five patients with a low-risk score and a median survival time of 93+ months. In 23 of 29 patients, cyclin D1 overexpression was present, without any relation to overall or disease-free survival. In contrast, a proliferative index less than 10% was significantly related to a better overall survival time (50 v 24 months). CONCLUSION: MCL is a disease of the elderly, who present with widespread disease and with a poor response to therapy. Although it harbors features of an indolent NHL, it behaves clinically as an aggressive NHL with a short overall survival time.

Aged↗
PubMed1993

Urogenital malacoplakia treated with fluoroquinolones.

We report 2 cases of urogenital malacoplakia and discuss the problems associated with diagnosing and treating this rare disease. In 1 case extensive pelvic disease was successfully controlled with ciprofloxacin. In the other case the malacoplakia was localized in the distal ureter and was initially mistaken for urothelial carcinoma. Nephrectomy was performed due to persistent ureteral obstruction and renal dysfunction. In the management of urogenital malacoplakia it seems essential that urinary tract infections be effectively treated. The new fluoroquinolones appear to be potentially successful in managing this disorder due to their high uptake of macrophages.

Ciprofloxacin↗
PubMed1993

Differences in clinical behaviour and immunophenotype between primary cutaneous and primary nodal anaplastic large cell lymphoma of T-cell or null cell phenotype.

The histological, immunophenotypic and clinical features of 19 primary cutaneous anaplastic large cell lymphomas (cutaneous ALCL) were compared with those of 18 primary nodal anaplastic large cell lymphomas (nodal ALCL) of T-cell or null cell type. Although cutaneous ALCL and nodal ALCL had identical morphological features, differences in surface marker expression and clinical behaviour were found. Immunophenotypical differences concerned the expression of epithelial membrane antigen (82% of the nodal ALCL were positive v. none of the cutaneous ALCL) and the cutaneous lymphocyte antigen (HECA-452), a possible skin-homing receptor on cutaneous T-lymphocytes (most tumour cells in 44% of cutaneous ALCL cases were positive, whereas nodal ALCL showed expression of HECA-452 on only few tumour cells (< 25%) in 18% of cases tested). Loss of T-cell markers was more pronounced for nodal ALCL. Patients with cutaneous ALCL were generally older (median 61 years) than patients with nodal ALCL (median 24 years) and, in contrast to the latter group, did not show bimodal age distribution. Survival after 4 years, using lymphoma-related death as an end-point, differed significantly between cutaneous ALCL and nodal ALCL; 92% for cutaneous ALCL and 65% for nodal ALCL (P = 0.04). The better survival of cutaneous ALCL patients could not be ascribed to differences in age, stage or initial mode of treatment. These data indicate that differences in immunophenotype and clinical behaviour exist between morphologically identical primary cutaneous and primary node-based ALCL. They indicate that the primary site is an important prognostic factor in predicting the clinical outcome of ALCL.

Adolescent↗
PubMed1992

Diffuse aggressive B-cell lymphomas of the gastrointestinal tract. An immunophenotypic and gene rearrangement analysis of 22 cases.

Twenty-two diffuse aggressive B-cell lymphomas of the gastrointestinal tract were studied using light microscopic examination, immunohistochemical methods, and Southern blot analysis. The results suggest that diffuse aggressive B-cell gastrointestinal tract lymphomas may be divided into two groups: large cell lymphomas and small noncleaved cell lymphomas. Large cell lymphomas often involve the stomach; commonly express the lymphocyte adhesion molecules CD44, LFA-1 (CD11a and CD18), and CD54; and may express monotypic cytoplasmic immunoglobulin in approximately one third of cases. Southern blot analysis demonstrates rearrangements of the c-myc gene that do not co-migrate with rearrangements of the immunoglobulin heavy chain gene, as detected with a JH probe in approximately one half of the cases. Small noncleaved cell lymphomas typically involve the ileocecal region. In these lesions, monotypic cytoplasmic immunoglobulin is not detected, and the CD44 and LFA-1 molecules usually are not expressed, particularly in small noncleaved cell lymphomas of the Burkitt type. The CD54 antigen is positive in fewer than one half of cases. Southern blot studies often demonstrate rearrangements of the c-myc gene that co-migrate with immunoglobulin heavy chain gene rearrangements indicative of the t(8;14) chromosomal translocation, with the c-myc region translocated into the immunoglobulin heavy chain gene joining region. Thus, immunohistochemical and genotypic results, in accordance with the site of involvement and histologic findings, suggest a different pathogenesis for large cell lymphomas and small noncleaved cell lymphomas. The findings in large cell immunoblastic lymphomas are more akin to those of the large cell group. In addition, immunophenotypic and molecular data may be helpful in improving histologic classification when the morphologic findings are equivocal.

Adult↗
PubMed1992

The association of c-myc rearrangements with specific types of human non-Hodgkin's lymphomas.

The function of c-myc in physiology is only partially known. Its product has DNA binding properties and plays a role in the control of proliferation and differentiation. In general, increased c-myc expression leads to proliferation and abolishment of differentiation. The involvement of c-myc in mouse plasmacytomas and human Burkitt's lymphoma is well known: due to chromosomal translocation c-myc comes under the influence of regulatory elements of immunoglobulin genes, leading to increased expression of the gene and proliferation of the cells. In man, the chromosomal translocations may occur within the increased pool of (pre) B-cells due to Epstein Barr virus (EBV) and malaria infection with subsequent immunosuppression. Apart from these early (primary?) events in lymphomagenesis, c-myc is also often involved in tumour progression, probably by a similar mechanism. Different types of c-myc involvement are associated with specific types of lymphoma: there are differences between endemic, sporadic and ileocecal Burkitt's lymphoma as well as between those and primary extranodal large cell lymphoma and large cell lymphoma which has progressed. These differences are associated with the differentiation of the involved lymphoid cells and may point to the stage of differentiation in which the oncogenic event occurred.

Burkitt Lymphoma↗
PubMed1990

Association of bcl-1 rearrangements with lymphocytic lymphoma of intermediate differentiation.

Previous studies using classical cytogenetics have demonstrated the presence of the t(11;14) (q13;q32) chromosomal translocation in some cases of lymphocytic lymphoma of intermediate differentiation (IDL), a distinct type of low grade B-cell lymphoma. This finding suggested that the bcl-1 region (located at band q13 of chromosome 11) might be involved in this neoplasm. Using a genomic probe from the major breakpoint area of the bcl-1 locus, we identified rearrangements of the bcl-1 region in 10 of 19 cases, 2 of which comigrated with a rearranged allele of the immunoglobulin heavy chain gene joining region. In contrast, bcl-1 rearrangements were not found in other types of low grade B-cell lymphoma, specifically in 36 cases of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) and 27 cases of follicular lymphoma (FL). To further assess the molecular pathology of IDL, we analyzed these cases for rearrangements of the bcl-2 proto-oncogene, which is associated primarily with follicular lymphomas. None of the 19 cases of IDL had rearrangements. Furthermore, none of the 36 cases of CLL/SLL showed bcl-2 rearrangements, whereas, as expected, 21 of 27 cases of FL had rearrangements of the bcl-2 locus. Our findings demonstrate an association between a rearranged bcl-1 region with approximately 50% of IDLs and suggest that abnormalities of this locus may be important in the pathogenesis of IDL.

Adult↗
PubMed1990

Adhesion molecules in the prognosis of diffuse large-cell lymphoma: expression of a lymphocyte homing receptor (CD44), LFA-1 (CD11a/18), and ICAM-1 (CD54).

Adhesive interactions between lymphocyte cell-surface receptors and components of the vascular endothelium and the extracellular matrix play an important role in the control of lymphocyte migration and homing. To investigate whether lymphocyte adhesion molecules involved in the migration of normal lymphocytes, i.e., CD44 homing receptor, LFA-1 (CD11a/18), and ICAM-1 (CD54), also play a role in the spread and hence in the disease course of non-Hodgkin's lymphomas (NHL), expression of these molecules was examined in 78 cases of diffuse large-cell lymphoma. Other potential risk factors considered in this study were sex, age, primary tumor localization, lineage (T cell vs. B cell), and histopathological subtype. 27 of 53 (51%) patients with a lymphoma having a high CD44 antigen expression showed tumor spread beyond stage II at diagnosis while this was the case in only three of 25 (12%) patients with lymphomas that were CD44 low/negative (chi-square 25.4, p less than 0.001). Similarly, poor response to treatment, i.e., absence of remission or relapse, and or death from lymphoma, was more common among patients with lymphomas expressing high levels of CD44; actuarial survival among patients with CD44 high and low lymphomas was 47% and 91%, respectively (Mantel-Cox 6.1, p = 0.02). Neither LFA-1 nor ICAM-1 expression showed a significant correlation to lymphoma dissemination or disease course. Of the other factors considered, T cell phenotype was associated with an unfavorable prognosis while nodal localization was a risk factor for dissemination. Taken together, our findings suggest that CD44 antigen expression plays an important role in the dissemination of NHL and via this mechanism exerts an unfavorable prognostic influence.

Antigens, CD↗