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- Dillner, L, et al.
(författare)
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Association of serum antibodies against defined epitopes of human papillomavirus L1, E2, and E7 antigens and of HPV DNA with incident cervical cancer.
- 1995
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Ingår i: Cancer Detection and Prevention. - 0361-090X .- 1873-443X. ; 19:5, s. 381-93
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Tidskriftsartikel (refereegranskat)abstract
- In order to provide a large-scale evaluation of the association with cervical cancer of antibodies against human papillomavirus (HPV) antigens, sera from 233 patients with primary, untreated cervical cancer and from 157 healthy age- and sex-matched blood donors were analyzed for IgG and IgA antibodies against HPV-derived peptide antigens and against bovine papillomavirus. Several serological responses were strongly associated with cervical cancer, notably the IgG response against the HPV 16 epitopes L1:13 (Relative risk [RR]: 5.3), E2:9 (RR: 2.9), and E7:5 (RR: 4.3), and the IgA response against an HPV 18 E2-derived antigen (245:18, RR: 3.1). HPV DNA in corresponding cervical tumors was analyzed by Southern blotting (SB) and polymerase chain reaction (PCR) in 47 patients. Sixty-six percent of the patients carried HPV DNA as determined by SB, 91% of patients analyzed by PCR. Neither the antibody responses, nor the presence of HPV DNA were significantly associated with the biological properties of the tumors.
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- Grandien, A, et al.
(författare)
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An example of idiotypic mimicry
- 1997
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Ingår i: European journal of immunology. - 0014-2980. ; 27:7, s. 1808-1815
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Tidskriftsartikel (refereegranskat)
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- Mahani, A, et al.
(författare)
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Differential Transcriptional Reprogramming by Wild Type and Lymphoma-Associated Mutant MYC Proteins as B-Cells Convert to a Lymphoma Phenotype
- 2021
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Ingår i: Cancers. - : MDPI AG. - 2072-6694. ; 13:23
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Tidskriftsartikel (refereegranskat)abstract
- The MYC transcription factor regulates a vast number of genes and is implicated in many human malignancies. In some hematological malignancies, MYC is frequently subject to missense mutations that enhance its transformation activity. Here, we use a novel murine cell system to (i) characterize the transcriptional effects of progressively increasing MYC levels as normal primary B-cells transform to lymphoma cells and (ii) determine how this gene regulation program is modified by lymphoma-associated MYC mutations (T58A and T58I) that enhance its transformation activity. Unlike many previous studies, the cell system exploits primary B-cells that are transduced to allow regulated MYC expression under circumstances where apoptosis and senescence pathways are abrogated by the over-expression of the Bcl-xL and BMI1 proteins. In such cells, transition from a normal to a lymphoma phenotype is directly dependent on the MYC expression level, without a requirement for secondary events that are normally required during MYC-driven oncogenic transformation. A generalized linear model approach allowed an integrated analysis of RNA sequencing data to identify regulated genes in relation to both progressively increasing MYC level and wild type or mutant status. Using this design, a total of 7569 regulated genes were identified, of which the majority (n = 7263) were regulated in response to progressively increased levels of wild type MYC, while a smaller number of genes (n = 917) were differentially regulated, compared to wild type MYC, in T58A MYC- and/or T58I MYC-expressing cells. Unlike most genes that are similarly regulated by both wild type and mutant MYC genes, the set of 917 genes did not significantly overlap with known lipopolysaccharide regulated genes, which represent genes regulated by MYC in normal B cells. The genes that were differently regulated in cells expressing mutant MYC proteins were significantly enriched in DNA replication and G2 phase to mitosis transition genes. Thus, mutants affecting MYC proteins may augment quantitative oncogenic effects on the expression of normal MYC-target genes with qualitative oncogenic effects, by which sets of cell cycle genes are abnormally targeted by MYC as B cells transition into lymphoma cells. The T58A and T58I mutations augment MYC-driven transformation by distinct mechanisms.
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- Djerbi, M., et al.
(författare)
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Participation of FLIP, RIP and Bcl-x(L) in fas-mediated T-cell death
- 2007
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Ingår i: Scandinavian Journal of Immunology. - : Wiley. - 0300-9475 .- 1365-3083. ; 66:4, s. 410-421
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Tidskriftsartikel (refereegranskat)abstract
- Apart from the conventional Fas signalling pathway, alternative pathways including the mitochondrial caspase-dependent and RIP-mediated cell death routes have been proposed to operate during Fas-mediated cell death. To evaluate the contribution of different Fas signalling pathways, mice overexpressing FLIPL, Bcl-x(L), a kinase-deficient form of RIP (RIP Delta kin) or combinations thereof were generated by retroviral gene transfer of haematopoietic stem cells. Such mice did not show overt abnormalities in haematopoietic development, defects in thymic deletion, accumulation of double-negative T cells or signs of autoimmunity. Fas-mediated death of mitogen-activated T cells was caspase dependent and could be blocked by FLIPL overexpression only with the minor involvement of Bcl-x(L) or RIP Delta kin inhibitable pathways. Fas-mediated death of resting CD4(+) and CD8(+) T cells was mainly caspase dependent but could only partly be blocked by FLIPL overexpression. Both Bcl-x(L) or RIP Delta kin expression resulted in partial protection of CD8(+) T cells against Fas-mediated cell death. These results indicate that yet uncharacterized signalling pathways from the Fas receptor are critically involved in lymphoproliferative and autoimmune disease observed in lpr mice and autoimmune lymphoproliferative syndrome patients.
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| 29. |
- Djerbi, M, et al.
(författare)
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The inhibitor of death receptor signaling, FLICE-inhibitory protein defines a new class of tumor progression factors
- 1999
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Ingår i: The Journal of experimental medicine. - : Rockefeller University Press. - 0022-1007 .- 1540-9538. ; 190:7, s. 1025-1031
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Tidskriftsartikel (refereegranskat)abstract
- Death receptor–mediated apoptosis can be modulated by several antiapoptotic proteins, such as the FLICE (FADD [Fas-associated death domain]-like IL-1β–converting enzyme)-inhibitory proteins (FLIPs). The FLIP family includes both cellular and viral members. The Kaposi's sarcoma–associated herpesvirus protein (KSHV)-FLIP is expressed by human herpesvirus 8 (HHV-8), which is associated with malignancies such as Kaposi's sarcoma and certain lymphomas. In this paper, we demonstrate that KSHV-FLIP protects cells from Fas-mediated apoptosis by inhibiting caspase activation and permits clonal growth in the presence of death stimuli in vitro. Furthermore, we show that KSHV-FLIP can act as a tumor progression factor by promoting tumor establishment and growth in vivo. When injected into immunocompetent recipient mouse strains, murine B lymphoma cells (A20) transduced with KSHV-FLIP rapidly develop into aggressive tumors showing a high rate of survival and growth. The tumor-progressive activity of KSHV-FLIP is mediated by prevention of death receptor–induced apoptosis triggered by conventional T cells. Consequently, inhibitors of death receptor signaling can be regarded as a new class of tumor progression factors, and HHV-8–associated tumors may represent naturally occurring examples of the tumorigenic effect of such inhibitors.
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- Lord, M, et al.
(författare)
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Impact of Sox11 over-expression in Ba/F3 cells
- 2018
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Ingår i: Haematologica. - : Ferrata Storti Foundation (Haematologica). - 1592-8721 .- 0390-6078. ; 103:12, s. E594-E597
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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