Capacity of B‐lymphocytic lines of diverse tumor origin to produce and respond to B‐cell growth factors: A progression model for B‐cell lymphomagenesis

Gordon, John; Åman, Pierre; Rosén, Anders; Ernberg, Ingemar; Ehlin‐Henriksson, Barbro; Klein, George

doi:10.1002/ijc.2910350218

Cited by 49 publications

(7 citation statements)

References 33 publications

(6 reference statements)

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“…Furthermore, they still responded to T BCGF by an enhancement of proliferation but their growth was not dependent on the presence of this factor. These results support a progression model of lymphomagenesis, as suggested by Gordon et al (1985), based upon the utilization, production and emancipation of the tumor from growth-promoting soluble factors.…”

Section: Discussionsupporting

confidence: 84%

“…However, the expression of the growth factor receptors could be modulated from the onset of the disease to the stage of clinical presentation; expression could even be different on the fresh tumor and the cell line established from it, as we observed for cell line BL93. Gordon et al (1985), using a panel of BL lines, including some used in this study (Raji, BL67, Ramos, B b , and BJAB) showed that they were able to secrete their own autologous BCGF but lost the property to respond to it (except for B b ) . Furthermore, they still responded to T BCGF by an enhancement of proliferation but their growth was not dependent on the presence of this factor.…”

Section: Discussionmentioning

confidence: 71%

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EBV‐negative and ‐positive burkitt cell lines variably express receptors for B‐cell activation and differentiation

Favrot

Suzuki

et al. 1986

Intl Journal of Cancer

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The expression of receptors for proliferation and differentiation factors was analyzed by indirect immunofluorescence on 29 Burkitt lymphoma (BL) cell lines previously classified into 3 groups on the basis of their reactivity with 8 monoclonal antibodies (MAbs), including anti-CALLA, BL13 and TU1. BL13 and HB5 antibodies recognize different epitopes of the EBV/CR2 receptors. The determinant recognized by BL13 has been previously shown to be expressed only on cell lines of the first two groups, supposed to derive from the germinal center and to be negative on a third group of lines of putative BM origin and established from sporadic cases of BL. In contrast, and as expected from its reactivity on normal B cells in the BM or in the lymph nodes, HB5 antibody reacts with all BL lines except one. The receptor for transferrin is expressed on the 29 lines. Two new MAbs, Bac-1 and B1H5, could recognize respectively receptors for BCGF1 and BCGF2. Bac-1 reacts with 15 of 17 BL lines belonging to the first two groups and 7 of 12 BL lines of the third group; 14 of 15 EBV + lines express Bac-1. No BL line expresses B1H5. The IL2 receptor is weakly expressed on 5 EBV + cell lines and one EBV (-) line. All delta are BCGF1-positive. The almost constant expression of BCGF1 receptor on EBV + cell lines is the only strict relation between the expression of receptors for growth factors and their characteristics (i.e. EBV association, translocation, ethnic origin and clinical presentation). The maturation stage or the origin of BL cell lines in relation to the expression of growth factor receptors and the functional significance of these receptors will be discussed.

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Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 71%

EBV‐negative and ‐positive burkitt cell lines variably express receptors for B‐cell activation and differentiation

Favrot

Suzuki

et al. 1986

Intl Journal of Cancer

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“…The Bac-1 mAb, which recognizes an antigen expressed on B95-8-converted Burkitt cells, was shown to inhibit the BCGF-induced enhancement of DNA synthesis in B cells activated with anti-IgM antibody (12), suggesting that Bac-1 is a receptor for a BCGF. Autocrine production of BCGF is believed to play an important role in EBV-induced proliferation (35,36). CR2 is defined as the EBV/C3d receptor on lymphocytes and was characterized as a 140-kDa glycoprotein recognized by OKB7 mAb (7,37).…”

Section: Resultsmentioning

confidence: 99%

Epstein-Barr virus (EBV) induces expression of B-cell activation markers on in vitro infection of EBV-negative B-lymphoma cells.

Calender

Billaud

Aubry

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

224

158

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A set of B-cell activation markers, including the EBV/C3d receptor [complement receptor type 2 (CR2) (CD21)], the 45-kDa lymphoblastoid cell-associated (Blast-2)antigen (CD23), and the B-cell restricted activation (Bac-l) antigen (which was recently identified as a potential B-cell growth factor receptor) can be turned on by infecting lymphoma cells that are genome negative for Epstein-Barr virus (EBV) with the B95-8 immortalizing strain of the virus. The nonimmortalizing EBV variant, strain P3HR-1, which possesses a deletion within the BamHI WYH region of the genome containing the coding sequence for the EBV-determined nuclear antigen 2, does not induce expression of these markers. Other lymphoblastoid cell-associated antigen markers can be activated by infection with either immortalizing or nonimmortalizing viruses. These results suggest that the immortalizing potential of EBV is correlated with its ability to induce expression of B-cell activation markers, which are suspected to play a major role in the physiological pathway leading to lymphoid cell proliferation. The viral genomic region deleted in the nonimmortalizing strain of EBV seems to be required for activation of some of these markers. Human lymphoma cell lines, such as those used in this study, can thus help identify the specific EBV genes involved in lymphoid B-cell proliferation and the mechanism of action of these genes.

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“…Not surprisingly, the expression of the activation antigen CD23 parallels that ofEBNA 2 )-indicating that this possible growth factor receptor, which could be critical to the transformation of B lymphocytes, may not be involved in the pathogenesis of Burkitt's lymphoma. Perhaps this is because Burkitt's lymphoma cells can proliferate independently of the growth factors required by EBV -transformed lymphoblastoid cell lines-as has been shown by in vitro experiments Gordon et al 1985). One explanation for this is that the deregulation of c-myc eliminates, or markedly reduces, the requirement for growth factor binding to surface receptors, but alternatively, Burkitt's cells may synthesize adequate quantities of their own growth factor.…”

Section: Molecular Genetics Of Ebv Infectionmentioning

confidence: 97%

Infectious Mononucleosis

1989

Clinical Topics in Infectious Disease

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Infectious mononucleosis is a clinical entity characterized by pharyngitis, cervical lymph node enlargement, fatigue and fever, which results most often from a primary Epstein-Barr virus (EBV) infection. EBV, a lymphocrytovirus and a member of the γ-herpesvirus family, infects at least 90% of the population worldwide, the majority of whom have no recognizable illness. The virus is spread by intimate oral contact among adolescents, but how preadolescents acquire the virus is not known. During the incubation period of approximately 6 weeks, viral replication first occurs in the oropharynx followed by viremia as early as 2 weeks before onset of illness. The acute illness is marked by high viral loads in both the oral cavity and blood accompanied by the production of immunoglobulin M antibodies against EBV viral capsid antigen and an extraordinary expansion of CD8 + T lymphocytes directed against EBV-infected B cells. During convalescence, CD8 + T cells return to normal levels and antibodies develop against EBV nuclear antigen-1. A typical clinical picture in an adolescent or young adult with a positive heterophile test is usually sufficient to make the diagnosis of infectious mononucleosis, but heterophile antibodies are not specific and do not develop in some patients especially young children. EBV-specific antibody profiles are the best choice for staging EBV infection. In addition to causing acute illness, long-term consequences are linked to infectious mononucleosis, especially Hodgkin lymphoma and multiple sclerosis. There is no licensed vaccine for prevention and no specific approved treatment. Future research goals are development of an EBV vaccine, understanding the risk factors for severity of the acute illness and likelihood of developing cancer or autoimmune diseases, and discovering anti-EBV drugs to treat infectious mononucleosis and other EBV-spurred diseases.

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Capacity of B‐lymphocytic lines of diverse tumor origin to produce and respond to B‐cell growth factors: A progression model for B‐cell lymphomagenesis

Cited by 49 publications

References 33 publications

EBV‐negative and ‐positive burkitt cell lines variably express receptors for B‐cell activation and differentiation

EBV‐negative and ‐positive burkitt cell lines variably express receptors for B‐cell activation and differentiation

Epstein-Barr virus (EBV) induces expression of B-cell activation markers on in vitro infection of EBV-negative B-lymphoma cells.

Infectious Mononucleosis

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