Disease relevance of Stag1

• In contrast, normal T cells, or T cells from donor mice bearing a YAC-1 lymphoma, failed to provide TXB recipients with the ability to cause regression of their SA-1 sarcoma in response to IL-1 treatment [1].
• To determine whether electropermeabilization can potentiate antitumor effectiveness of cis-diamminedichloroplatinum(II) (CDDP), electrochemotherapy with CDDP was tested in vitro and in vivo on s.c. SA-1, EAT, and melanoma B16 tumors in mice [2].
• These macrophages possess nonspecific tumoricidal activity in vivo as immune distinct MCA207 tumor cells inoculated i.p., but not s.c., in mice bearing regressing Sa1 ascites tumors after Cy + IL-12 therapy are rejected [3].
• The effect of electric pulses on tumour blood flow was investigated in the murine fibrosarcoma SA-1 [4].
• The immunological requirements for endotoxin-induced regression of an established subcutaneous tumour (SA 1 sarcoma) were investigated by employing tumour-bearing T-cell deficient mice as test recipients, and mice generating concomitant immunity, or Corynebacterium parvum-augmented concomitant immunity, as donors of sensitized T cells [5].

Psychiatry related information on Stag1

• SLE was induced in BALB/c mice only when immunized with SA-1, TB-68, and 4B4, namely antibodies with diverse binding capacities albeit having the 16/6 Id [6].

High impact information on Stag1

• The F19 cell surface glycoprotein of reactive fibroblasts is a prototypic stromal antigen since it is found in the stroma of > 90% of common epithelial cancers but is absent or expressed at low levels in normal tissues and benign epithelial tumors [7].
• In the present study, we define an additional tumor stromal antigen, FB5, that is selectively expressed in vascular endothelial cells of malignant tumors [7].
• Study of cyclophosphamide plus IL-12 (Cy + IL-12)-induced rejection of ascites Sa1 tumor demonstrates that macrophages are the predominant immune cell infiltration in the ascites [3].
• Furthermore, Cy + IL-12-treated Sa1 ascites cells or macrophages, but not spleen macrophages from the same mouse or inflammatory macrophages induced by thioglycollate, are able to suppress the development of immune-irrelevant s.c. tumors in a Winn assay [3].
• We measured changes in tumor perfusion by Patent blue staining, tumor blood volume and microvascular permeability by contrast-enhanced magnetic resonance imaging, and tumor oxygenation by EPR in s.c. SA-1 murine tumors [8].

Chemical compound and disease context of Stag1

• Mice bearing the syngeneic SA-1 sarcoma or treated with live Mycobacterium bovis BCG or Formalin-killed Corynebacterium parvum acquired a greatly increased susceptibility to the lethal effects of endotoxin [9].
• In this work basic principles of the method will be described as well as some examples of tumor oxygenation changes after application of chemotherapeutic drugs (vinblastine, cisplatin, bleomycin) or electric pulses in combination with cisplatin or bleomycin to fibrosarcoma SA-1 tumors in mice [10].

Biological context of Stag1

• The human SA-1 gene was cloned by homology from a thymus cDNA library and the sequence of the predicted protein was found to be highly homologous to the murine SA-1 (>98.9%) [11].
• RESULTS: In naïve recipient mice, studies in major histocompatibility complex (MHC)-I-deficient mice and with depleting anti-CD8 monoclonal antibody (mAb) demonstrate that CD8 T cells are important for Sa1 rejection [12].
• Modification of TNF-alpha pharmacokinetics in SA-1 tumor-bearing mice [13].
• We evaluated the ability of surface antigen-1 (SA-1), defined as those antigens recognized by neutralizing mAb 17.41, to elicit a protective antibody response when used as an immunogen [14].
• The results of this study indicate that VLB affects cell membrane by increasing the membrane fluidity of SA-1 tumor cells in vivo in a dose-and time-dependent manner [15].

Anatomical context of Stag1

• Mice were challenged subcutaneously with the allogeneic murine tumor cell line, Sa1, or with the xenogenic human tumor, MDA435 [12].
• Effects of vinblastine on cell membrane fluidity and the growth of SA-1 tumor in mice [15].
• Effect of surface antigen-1 (SA-1) immune lymphocyte subsets and naive cell subsets in protecting scid mice from initial and persistent infection with Cryptosporidium parvum [16].
• SA-1 cells were spin labeled with the methylester of 5-doxylpalmitate, which primarily dissolves in the membranes [17].
• Cryptosporidium parvum-specific antibody was detected on day 12 post engraftment in mice receiving SA-1 immune CD4 T and B lymphocytes but was not detectable in mice receiving naive cell subsets [16].

Associations of Stag1 with chemical compounds

• After only one application of this treatment combination in the LPB tumor model, specific tumor growth delay was prolonged in the combined treatment group compared to electrogene therapy with p53 or electrochemotherapy with cisplatin alone, whereas in SA-1 tumors this treatment combination resulted in 31.6% of cured animals [18].
• Inhibition studies with ssDNA, dsDNA and cardiolipin revealed that all 3 antigens decreased the serum levels of the SA1 idiotype despite absence of detectable anti-DNA antibodies by other methods [19].
• Electrochemotherapy with bleomycin in SA-1 tumor-bearing mice--natural resistance and immune responsiveness [20].
• Cytotoxicity of bioreductive drug tirapazamine is increased by application of electric pulses in SA-1 tumours in mice [21].
• Two optical methods were used simultaneously to evaluate the effect of a vasoactive drug hydralazine on oxygenation and blood flow in SA-1 tumors in A/J mice [22].

Analytical, diagnostic and therapeutic context of Stag1

• The identification of SA-1 protein in tissues and cells required combined immunoprecipitation and Western blotting using a polyclonal antiserum raised against a predicted peptide of SA-1 and the B92 mAb [11].
• SA-1, a nuclear protein encoded by one member of a novel gene family: molecular cloning and detection in hemopoietic organs [11].
• Northern blot and PCR analysis indicated that on the mRNA level the SA-1 gene is expressed in all tissues analyzed and probably encodes a single transcript [11].
• This study shows that it is not possible to cause regression of the immunogenic SA-1 sarcoma by adoptive immunotherapy with tumor-sensitized T-cells, unless the tumor-bearing recipient is exposed to a sublethal dose of gamma-irradiation to remove a barrier that prevents adoptive immunity from being expressed [23].
• BACKGROUND: A quantitative model of immunosuppression was previously developed based on the rejection of the allogeneic A/J murine tumor sarcoma 1 (Sa1) in immunocompetent mice [12].

References