D Rouillard

Unité Inserm U1077, Caen, Lower Normandy, France

Are you D Rouillard?

Claim your profile

Publications (28)136.59 Total impact

  • [show abstract] [hide abstract]
    ABSTRACT: Ewing sarcoma cells are resistant to TNFα-induced cell death and this resistance results from the activation of the transcription factor NF-κB. Here, we investigated whether NF-κB activation interferes with 2-Me-induced cell death signaling in Ewing sarcoma cells and we examined the effect of treatment of these cells with 2-Me either alone or in combination with TNFα. Our results show that TNFa cooperates with 2-Me to induce apoptosis in Ewing tumor cells through mitochondrial cell death signaling. These results suggest that the use of TNFα in combination with 2-Me may be beneficial for Ewing tumor treatment.
    Annals of the New York Academy of Sciences 01/2006; 1010(1):159 - 162. · 4.38 Impact Factor
  • [show abstract] [hide abstract]
    ABSTRACT: Ewing sarcoma cells are resistant to TNFalpha-induced cell death and this resistance results from the activation of the transcription factor NF-kappaB. Here, we investigated whether NF-kappaB activation interferes with 2-Me-induced cell death signaling in Ewing sarcoma cells and we examined the effect of treatment of these cells with 2-Me either alone or in combination with TNFalpha. Our results show that TNFa cooperates with 2-Me to induce apoptosis in Ewing tumor cells through mitochondrial cell death signaling. These results suggest that the use of TNFalpha in combination with 2-Me may be beneficial for Ewing tumor treatment.
    Annals of the New York Academy of Sciences 01/2004; 1010:159-62. · 4.38 Impact Factor
  • Source
    [show abstract] [hide abstract]
    ABSTRACT: Xenopus p53 has biological and biochemical properties similar to those of human p53, except for optimal temperature. The frog protein is fully active at 30 degrees C and inactive at 37 degrees C, leading to a temperature-sensitive behavior similar to that of the human mutant p53Ala(143) and the murine mutant p53Val(135). Using hybrid proteins between human and Xenopus expressed from artificial p53 minigenes, we have been able to demonstrate that change of conformation of the DNA-binding domain is the major determinant of this heat sensitivity. It has been reported that some human tumor-derived p53 mutants can engage in a physical association with p73, thus inhibiting its transactivating properties. The mechanism of this association remains to be elucidated. The nature of the mutant p53 that can engage in this association also remains controversial. Using the unique opportunity of the temperature sensitivity of Xenopus p53, we demonstrate that binding of and interference with p73 require a change of conformation in the p53 protein. This interaction occurs through the DNA-binding domain of p53 only when it is in a denatured state. These results reinforce the notion that mutant p53 with a conformational change can act as a down-regulator of the p73 pathway in human cancer and could confer a selective advantage to the tumor.
    Journal of Biological Chemistry 04/2003; 278(12):10546-55. · 4.65 Impact Factor
  • Brigitte Surin, Dany Rouillard, Brigitte Bauvois
    [show abstract] [hide abstract]
    ABSTRACT: Modulation of the adhesive responses of monocytic cells may reflect their motility at sites of diseased tissues (inflammation, tumors). Integrins alpha5beta1 mediate fibronectin (Fn)-dependent adhesion of human monocytes and their precursors. The effect of type I IFNs (alpha, beta) and type II IFN (gamma) was assessed on the adhesive capacities of promonocytic U937 cells and monocytes. IFN-beta and IFN-gamma abrogated monocytic cell adhesion to Fn, but such impaired cell attachment was not due to altered levels of alpha5beta1 integrins. In contrast, IFN-alpha did not affect cell adhesion to Fn. Participation of cytoskeleton assembly in IFN-mediated cell detachment was evaluated. Activation of RhoA activity with lysophosphatidic acid (LPA) increased 2-fold the adhesion of monocytic cells to Fn in a alpha5beta1-mediated fashion, and IFN-gamma treatment reversed the enhancing effect of LPA. Moreover, U937 cells and monocytes dominantly expressed the 44-46 kDa paxillin forms and IFN-beta and IFN-gamma led to the accumulation of 66-70 kDa paxillin forms. These results indicate that IFN-mediated loss of monocyte adhesion to Fn is associated with changes in the cytoskeleton associated proteins paxillin and Rho.
    International Journal of Molecular Medicine 08/2002; 10(1):25-31. · 1.96 Impact Factor
  • Source
    [show abstract] [hide abstract]
    ABSTRACT: Ras oncoproteins are mutated in about 50% of human colorectal cancers, but their precise role in tumor initiation or progression is still unclear. This study presents transgenic mice that express K-ras(V12G), the most frequent oncogenic mutation in human tumors, under control of the murine villin promoter in epithelial cells of the large and small intestine. More than 80% of the transgenic animals displayed single or multiple intestinal lesions, ranging from aberrant crypt foci (ACF) to invasive adenocarcinomas. Expression of K-ras(V12G) caused activation of the MAP kinase cascade, and the tumors were frequently characterized by deregulated cellular proliferation. Unexpectedly, we obtained no evidence of inactivating mutations of the tumor suppressor gene Apc, the "gatekeeper" in colonic epithelial proliferation. However, spontaneous mutation of the tumor-suppressor gene p53, a frequent feature in the human disease, was found in 3 of 7 tumors that were tested. This animal model recapitulates the stages of tumor progression as well as a part of the genetic alterations found in human colorectal cancer. Furthermore, it indicates that activation of K-ras in concert with mutations in p53 may constitute a route to digestive tumor formation and growth, underlining the fact that the pathway to intestinal cancer is not necessarily a single road.
    Gastroenterology 08/2002; 123(2):492-504. · 12.82 Impact Factor
  • Source
    [show abstract] [hide abstract]
    ABSTRACT: The genetic hallmark of Ewing's sarcoma family of tumours (ET) is the presence of the translocation t(11;22)(q24;q12), which creates the ET fusion gene, leading to cellular transformation. Five human gamma-glutamyl transpeptidase (gamma-GT) genes are located near the chromosomal translocation in ET. gamma-GT is a major enzyme involved in glutathione homoeostasis. Five human cell lines representative of primary or metastatic tumours were investigated to study whether gamma-GT alterations could occur at the chromosomal breaks and rearrangements in ET. As shown by enzymic assays and FACS analyses, all ET cell lines consistently expressed a functional gamma-GT which however did not discriminate steps of ET progression. As shown previously [Sancéau, Hiscott, Delattre and Wietzerbin (2000) Oncogene 19, 3372-3383], ET cells respond to the antiproliferative effects of interferons (IFNs) type I (alpha and beta) and to a much less degree to IFN type II (gamma). IFN-alpha and -beta arrested cells in the S-phase of the cell cycle. We found an enhancement of gamma-GT mRNA species with IFN-alpha and -beta by reverse transcriptase-PCR analyses. This is reflected by up-regulation of gamma-GT protein, which coincides with the increase in gamma-GT-specific enzymic activity. Similarly, IFNs up-regulate the levels of gamma-GT in another IFN-responsive B cell line. Whether this up-regulation of gamma-GT by IFNs is of physiological relevance to cell behaviour remains to be studied.
    Biochemical Journal 07/2002; 364(Pt 3):719-24. · 4.65 Impact Factor
  • [show abstract] [hide abstract]
    ABSTRACT: Gamma-glutamyl transpeptidase (GGT) is a key enzyme in the catabolism of glutathione (GSH). Recently, it has been reported that the extracellular cleavage of GSH by GGT induced the production of reactive oxygen species (ROS), suggesting that GGT plays a pro-oxidant role. In the present study, we investigated the nature of the oxidative stress generate by glutathione and GGT and the possibility that this stress affects the activity of NF-kappaB a prototypical oxidant-stress-responsive transcription factor. We found that, in the presence of iron, a natural substrate of GGT, glutathione induces lipid peroxidation in U937 cells. This induction depends on GGT activity as it is prevented by the Serine/Borate complex, a GGT inhibitor. We found that y-glutamyl transpeptidase activity induces NF-kappaB DNA binding activity, an effect which is significantly reduced by the addition of GGT inhibitors (Serine/Borate complex and Acivicin). Moreover, we show that lipid peroxidation is involved in GGT-dependent NF-kappaB activation since vitamin E, which completely inhibits GGT-induced generation of lipid peroxides, prevents the GGT-dependent NF-kappaB activation. Finally, inhibition of GGT by either the Serine/Borate complex or by Acivicin resulted in cell apoptosis. This finding suggests that GGT-mediated NF-kappaB activation plays a role in the control of apoptosis in U937 cells.
    Molecular and Cellular Biochemistry 04/2002; 232(1-2):103-11. · 2.33 Impact Factor
  • [show abstract] [hide abstract]
    ABSTRACT: Gamma-glutamyl transpeptidase (GGT) is a key enzyme in the catabolism of glutathione (GSH). Recently, it has been reported that the extracellular cleavage of GSH by GGT induced the production of reactive oxygen species (ROS), suggesting that GGT plays a pro-oxidant role. In the present study, we investigated the nature of the oxidative stress generate by glutathione and GGT and the possibility that this stress affects the activity of NF-κB a prototypical oxidant-stress-responsive transcription factor. We found that, in the presence of iron, a natural substrate of GGT, glutathione induces lipid peroxidation in U937 cells. This induction depends on GGT activity as it is prevented by the Serine/Borate complex, a GGT inhibitor. We found that γ-glutamyl transpeptidase activity induces NF-κB DNA binding activity, an effect which is significantly reduced by the addition of GGT inhibitors (Serine/Borate complex and Acivicin). Moreover, we show that lipid peroxidation is involved in GGT-dependent NF-κB activation since vitamin E, which completely inhibits GGT-induced generation of lipid peroxides, prevents the GGT-dependent NF-κB activation. Finally, inhibition of GGT by either the Serine/Borate complex or by Acivicin resulted in cell apoptosis. This finding suggests that GGT-mediated NF-κB activation plays a role in the control of apoptosis in U937 cells.
    Molecular and Cellular Biochemistry 01/2002; 232(1):103-111. · 2.33 Impact Factor
  • Source
    [show abstract] [hide abstract]
    ABSTRACT: Although interferon (IFN)-beta has shown a significant clinical benefit in multiple sclerosis (MS), its mechanism of action remains unclear. We found that IFN-beta treatment of patients with MS resulted in a significant increase in apoptotic cell death (measured by annexin V staining and nuclear fragmentation) of monocyte-derived macrophages, as compared with cells derived from patients before treatment. Stimulation of the cells with IFN-beta in vitro resulted in an even further increase of annexin V binding, as well as increased Fas (CD 95, APO-1) expression. However, no increased Fas expression, apoptotic monocytes, or monocytopenia were observed upon in vivo treatment. This indicates that IFN-beta does not deliver a death signal to monocytes but rather primes for subsequent macrophage apoptosis upon activation or differentiation.
    Journal of Leukocyte Biology 12/2001; 70(5):745-8. · 4.57 Impact Factor
  • Source
    K Bensaad, D Rouillard, T Soussi
    [show abstract] [hide abstract]
    ABSTRACT: In mammalian cells, the p53 protein is a key regulator of the cell cycle following DNA damage. In the present study, we investigated the function of p53 in the A6 amphibian cell line. Using various specific Xenopus p53 monoclonal antibodies, we showed that Xenopus p53 accumulates after DNA damage, including gamma and UV irradiation or treatment with adriamycin. Such accumulation is accompanied by an increase in the apparent molecular weight of the protein. This change was shown to be the result of a phosphorylation event that occurs after DNA damage. Accumulation of Xenopus p53 is parallel to a drastic change in the cell cycle distribution. Brief exposure to adriamycin or gamma irradiation induces reversible growth arrest, whereas long-term exposure to adriamycin leads to apoptosis. Taken together, these results indicate that p53 has a similar behaviour in frog cells and mammalian cells, and that it conserves two activities, cell cycle arrest and apoptosis.
    Oncogene 07/2001; 20(29):3766-75. · 7.36 Impact Factor
  • [show abstract] [hide abstract]
    ABSTRACT: The effects of vitamin E supplementation were evaluated in cultured human normal fibroblasts exposed to ultraviolet A radiation (320-380 nm) (UVA). Cells were incubated in medium containing alpha-tocopherol, alpha-tocopherol acetate or the synthetic analog Trolox for 24 h prior to UVA exposure. DNA damage in the form of frank breaks and alkali-labile sites, collectively termed single-strand breaks (SSB), was assayed by the technique of single cell gel electrophoresis (comet assay), immediately following irradiation or after different repair periods. The generation of hydrogen peroxide (H2O2) and superoxide ion (O2.-) was measured by flow cytometry through the oxidation of indicators into fluorescent dyes. It was observed that pretreatment of cells with any form of vitamin E resulted in an increased susceptibility to the photoinduction of DNA SSB and in a longer persistence of damage, whereas no significant change was observed in the production of H2O2 and O2.- reactive oxygen species, compared to untreated controls. These findings indicate that in human normal fibroblasts, exogenously added vitamin E exerts a promoting activity on DNA damage upon UVA irradiation and might lead to increased cytotoxic and mutagenic risks.
    Photochemistry and Photobiology 05/2001; 73(4):370-7. · 2.29 Impact Factor
  • [show abstract] [hide abstract]
    ABSTRACT: B cell chronic lymphocytic leukaemia (B-CLL) is characterised by defective apoptosis that cannot be explained solely on the basis of the known chromosomal abnormalities. We and other have now reported that the leukemic cells spontaneously display the inducible isoform of nitric oxide synthase, iNOS. Inhibition of the iNOS pathway leads to increased apoptosis of the tumoral cells in vitro, indicating that the endogenous release of NO contributes to their resistance to the normal apoptotic process. The factors that induce the expression of iNOS in vivo in the leukemic cells are not yet identified. Yet, as interaction of B-CLL leukemic cells with bone marrow stromal cells promotes their survival, the involvement of adhesion molecules and integrins may be suspected. The engagement of CD23 stimulates iNOS activation in the tumoral cells, suggesting that in vivo interaction of CD23 with one of its recognised ligands may contribute to iNOS induction. A role for CD40-CD40 ligand interaction may also be hypothesised. The mechanisms involved in the anti-apoptotic role of NO are not fully understood, but may implicate the inhibition of caspase activity, hence the impairment of the Fas pathway. In addition, the mitochondrial membrane potential disruption appears to be a NO-sensitive step in the apoptosis cascade. The presence of a NOS displaying anti-apoptotic properties has now been recognised in different cell types, including various leukaemia. A better knowledge of the mechanisms governing the ultimate fate of NO, anti- versus pro-apoptotic would allow the development of new therapeutic approaches for the treatment of these diseases.
    Leukemia and Lymphoma 02/2001; 40(3-4):243-57. · 2.30 Impact Factor
  • Source
    [show abstract] [hide abstract]
    ABSTRACT: Interferons (IFNs alpha, beta and gamma) and all trans retinoic acid (RA) have the ability to activate genes with GAS sites. We have found that the promoter of CD26/dipeptidylpeptidase IV (DPPIV) contains a consensus GAS site TTCnnnGAA located at bp-35 to -27, and computer analysis confirmed this sequence to be a putative Stat binding site. Consistent with this finding, we show that IFNs and RA rapidly enhanced CD26 gene and protein expression in chronic B lymphocytic leukemia (B-CLL) cells. Immunoblot analyses revealed that unstimulated B-CLL cells expressed detectable levels of serine/tyrosine-phosphorylated Stat1alpha, and RA and IFN-gamma treatment led to increased levels of tyrosine phosphorylation of Stat1alpha and its nuclear accumulation. As shown by electrophoretic mobility shift assay, RA and IFN-gamma increased the binding of a nuclear protein to the GAS-CD26 element. Shift-Western blotting identified Stat1alpha as the GAS-CD26 binding factor. Augmented levels of CD26 protein in malignant B cells cultured with IFNs or RA coincided with the enhancement of DPPIV activity. Taken together, our results are in favor of the IFN-/RA-mediated upregulation of CD26/DPPIV in B-CLL through the signaling pathway involving Stat1alpha and the GAS response element of CD26 promoter.
    Oncogene 02/2000; 19(2):265-72. · 7.36 Impact Factor
  • Source
    B Surin, D Rouillard, B Bauvois
    [show abstract] [hide abstract]
    ABSTRACT: Modulation of the adhesive responses of monocytic cells may reflect their motility within the bone marrow and at sites of inflammation. Monocyte alpha5beta1 integrins mediate fibronectin-dependent adhesion. We previously showed that type II IFN-gamma reduces adhesiveness to fibronectin (Fn) whereas TGF-beta1 enhances cell attachment. Here, we investigate the role of type I IFNs (alpha, beta) on the adhesive capacity of monocytic cells. The influence of IFNs on the human U937 cell line adhesion to fibronectin-coated surfaces was determined. The expression of integrins and cytoskeleton proteins was analyzed by FACS, Western blotting and/or fluorescence microscopy analyses. IFN-alpha did not affect cell adhesion to fibronectin. In contrast, IFN-beta, like IFN-gamma, abrogated U937 adhesion to fibronectin and antagonized TGF-beta1-mediated cell attachment to Fn. The impaired binding of IFN-beta- and IFN-gamma-treated cells to fibronectin was not due to reduced levels of alpha5beta1 integrins. IFN-beta and IFN-gamma re-organized filamentous actin, and such rearrangement differed from that observed in TGF-beta1-adhesive cells. U937 cells dominantly expressed 44 to 46 kDa paxillin forms and treatment with IFNs enhanced the number of 66 to 70 kDa forms of paxillin. Our data show that IFN-beta and IFN-gamma induced loss of monocytic adhesion to fibronectin associated with changes in actin and paxillin cytoskeleton, thereby pointing to a possible effect of these cytokines in monocyte trafficking.
    The Hematology Journal 02/2000; 1(3):172-80. · 1.86 Impact Factor
  • [show abstract] [hide abstract]
    ABSTRACT: Only half of colorectal-cancer patients elicit serum antibodies in response to intratumoral p53-gene mutations. Our study was designed to compare cellular events (p53-protein accumulation and gene mutations) with the presence of circulating anti-p53 antibodies (p53-Ab). Thirty-five colorectal-cancer patients were studied for their intratumoral p53-protein accumulation and circulating p53-Ab. Tumour DNA was analyzed for genomic mutations in a sub-set of 28 patients. In all, 18 tumours (51.4%) were positive by immunohistochemistry, and 17 tumour extracts were shown to contain “mutant” conformation p53 protein, 16 of them being were concordant by both methods. Of the 28 tumours tested by DGGE, 16 contained alterations in p53 exons 5 to 8 (57.1%). Of 12 tumours without detectable mutations, 10 were “mutant”-conformation-negative by immunohistochemistry and ELISA. Paradiploid tumors presented more frequently wild-type p53 genes and were significantly less frequently immunohistochemistry- or p53-Ab-positive than polyploid tumors. Circulating p53-Ab were detected in the serum of 11 patients (31%). In 9/11 cases, a gene mutation was found in the corresponding tumour. Three of four mutations in exon 8 and 3/3 mutations in exons 5-6 were associated with p53-Ab, in contrast with only 3/9 mutations in exon 7. We found good agreement in the detection of p53-gene alterations by different methods. However, our data suggest that all gene mutations may not be equivalent in term of immunogenicity. Int. J. Cancer 81:712–718, 1999. © 1999 Wiley-Liss, Inc.
    International Journal of Cancer 11/1999; 81(5):712 - 718. · 6.20 Impact Factor
  • [show abstract] [hide abstract]
    ABSTRACT: The activation antigen CD38, which has NAD+ glycohydrolase activity in its extracellular domain, is expressed by a large variety of cell types. Few investigations into the regulation of CD38 expression by physiologic stimuli have been reported. As the CD38 promoter contains potential binding sites for interferon (IFN) regulatory factor-1 (IRF-1), we investigated the influence of IFN type I (alpha and beta) and type II (gamma) on CD38 gene expression of leukemic B cells. Using the IFN-responsive B cell line Eskol, we found by RT-PCR analysis a rapid time-dependent induction in CD38 mRNA (starting at 6 h) with each type of IFN. This induction was independent of protein synthesis, suggesting that CD38 gene activation does not require IRF-1 but is merely under direct transcriptional regulation by latent IFN-inducible factors. mRNA stimulation was followed within 24 h by induction of membrane CD38, which coincided with rises of CD38-specific ectoenzymatic activities, that is, NAD+ glycohydrolase, (A/G)DP-ribosyl cyclase, and cyclic ADP ribose hydrolase activities. IFN failed to induce or upregulate the other CD38-related ectoenzymes analyzed, that is, CD39, CD73, CD157, and PC-1. Similarly, treatment of leukemic cells of patients with B chronic lymphocytic leukemia (B-CLL) with IFN resulted in an increase in CD38 mRNA mirrored by plasma membrane upregulation of CD38 and NAD+ glycohydrolase activity. Further investigation in relation to CD38 gene activation and B-CLL behavior remains to be defined.
    Journal of Interferon & Cytokine Research 10/1999; 19(9):1059-66. · 3.30 Impact Factor
  • Source
    [show abstract] [hide abstract]
    ABSTRACT: We report here a systematic analysis of the effects of different p53 mutations on both spontaneous and radiation-stimulated homologous recombination in mouse L cells. In order to monitor different recombination pathways, we used both direct and inverted repeat recombination substrates. In each line bearing one of these substrates, we expressed p53 proteins mutated at positions: 175, 248 or 273. p53 mutations leading to an increased spontaneous recombination rate also stimulate radiation-induced recombination. The effect on recombination may be partially related to the conformation of the p53 protein. Moreover, p53 mutations act on recombination between direct repeats as well as between inverted repeats indicating that strand invasion mechanisms are stimulated. Although all of the p53 mutations affect the p53 transactivation activity measured on the WAF1 and MDM2 gene promoters, no correlation between the transactivation activity and the extent of homologous recombination can be drawn. Finally, some p53 mutations do not affect the G1 arrest after radiation but stimulate radiation-induced recombination. These results show that the role of p53 on transactivation and G1 cell cycle checkpoint is separable from its involvement in homologous recombination. A direct participation of p53 in the recombination mechanism itself is discussed.
    Oncogene 07/1999; 18(24):3553-63. · 7.36 Impact Factor
  • [show abstract] [hide abstract]
    ABSTRACT: Only half of colorectal-cancer patients elicit serum antibodies in response to intratumoral p53-gene mutations. Our study was designed to compare cellular events (p53-protein accumulation and gene mutations) with the presence of circulating anti-p53 antibodies (p53-Ab). Thirty-five colorectal-cancer patients were studied for their intratumoral p53-protein accumulation and circulating p53-Ab. Tumour DNA was analyzed for genomic mutations in a sub-set of 28 patients. In all, 18 tumours (51.4%) were positive by immunohistochemistry, and 17 tumour extracts were shown to contain "mutant" conformation p53 protein, 16 of them being were concordant by both methods. Of the 28 tumours tested by DGGE, 16 contained alterations in p53 exons 5 to 8 (57.1%). Of 12 tumours without detectable mutations, 10 were "mutant"-conformation-negative by immunohistochemistry and ELISA. Paradiploid tumors presented more frequently wild-type p53 genes and were significantly less frequently immunohistochemistry- or p53-Ab-positive than polyploid tumors. Circulating p53-Ab were detected in the serum of 11 patients (31%). In 9/11 cases, a gene mutation was found in the corresponding tumour. Three of four mutations in exon 8 and 3/3 mutations in exons 5-6 were associated with p53-Ab, in contrast with only 3/9 mutations in exon 7. We found good agreement in the detection of p53-gene alterations by different methods. However, our data suggest that all gene mutations may not be equivalent in term of immunogenicity.
    International Journal of Cancer 06/1999; 81(5):712-8. · 6.20 Impact Factor
  • Source
    [show abstract] [hide abstract]
    ABSTRACT: We have investigated the expression of the ectoenzyme dipeptidylpeptidase IV (DPP IV)/CD26 on lymphocytes obtained from patients with B chronic lymphocytic leukaemia (B-CLL) and compared it with healthy subjects. Using two-colour immunofluorescence analysis with CD26 and CD20 or CD23 monoclonal antibodies, CD26 was found undetectable on peripheral resting B-cells (CD20+ CD23-) from normal donors whereas it was expressed on B-cells activated in vitro with interleukin (IL)-4 and Staphylococcus aureus strain cowan I (CD20+ CD23+). The expression of CD26 on leukaemic B-cells (CD20+ CD23+) was clearly induced in 22 out of 25 patients examined. Consequently, induced levels of CD26 cell surface expression on either normal activated and malignant B-cells coincided with the enhancement of DPP IV activity detected on the surface of these cells. Reverse transcription polymerase chain reaction analyses showed that the transcript levels of the CD26 gene was higher in normal activated B-cells and B-CLL cells than in resting B-cells, suggesting that CD26 was expressed at the level of transcriptional activation. These observations provide evidence of the abnormal expression of DPPIV/CD26 in B-CLL which, therefore, may be considered as a novel marker for B-CLL. Further investigation in relation to CD26 expression and other B malignancies needs to be defined.
    British Journal of Cancer 04/1999; 79(7-8):1042-8. · 5.08 Impact Factor
  • Biology of The Cell - BIO CELL. 01/1998; 90(1):110-110.