Disease relevance of Tumor Escape

• We found that radiation up-regulates alpha(v)beta3 expression in endothelial cells and consecutively phosphorylates Akt, which may provide a tumor escape mechanism from radiation injury mediated by integrin survival signaling [1].
• CONCLUSIONS: Although tumor antigen-specific TAL were detected in ascites fluid, these cells were producing immunosuppressive cytokines which may contribute to tumor escape from recognition and/or destruction by the immune system [2].
• CONCLUSIONS: The antidendropoietic effect of PSA in vitro suggests a new mechanism of prostate cancer induced immunosuppression and tumor escape, and provides novel evidence of the immunoregulatory properties of PSA [3].
• We propose that in breast cancer, tumor escape from immunological surveillance results from the induction of apoptosis of Fas-bearing activated lymphocytes by FasL-bearing breast cancer cells [4].

High impact information on Tumor Escape

• Our findings demonstrate that although even advanced stages of epithelial malignancy remain dependent upon continued Wnt signaling for maintenance and growth, loss of p53 facilitates tumor escape and the acquisition of oncogene independence [5].
• The FAS receptor-ligand system plays a key role in regulating apoptotic cell death, and corruption of this signaling pathway has been shown to participate in tumor-immune escape and carcinogenesis [6].
• Therefore, our data indicate that CD95-dependent apoptosis constitutes a more prominent mechanism for tumor clearance than has so far been anticipated and that blockade of this pathway can result in tumor escape even when the perforin pathway is operational [7].
• Thus, expansion of peripheral immune repertoire to Melan-A/Mart-1 takes place in some metastatic patients and leads to enhanced CTL induction after antigen-presenting cell-mediated selection, but, in most metastatic lesions, it does not overcome tumor escape from immune surveillance [8].
• A tumor escape variant that has lost one major histocompatibility complex class I restriction element induces specific CD8+ T cells to an antigen that no longer serves as a target [9].

Biological context of Tumor Escape

• This suggests that tumor escape from immune surveillance may have occurred in vivo as a sequential result of (a) antigen loss, and (b) downregulation of the peptide-transporter protein TAP-1 expression by this patient's tumor over a 6-yr period from 1987 to 1993 [10].
• These altered HLA class I phenotypes and non-ubiquitous expression of NK receptor ligands constitute the major tumor escape mechanism facing tumor-specific CTL and/or NK cell mediated responses [11].
• The presented results suggest that RCAS1 might play an important role in tumor escape from host immunological surveillance and carry weight in the down regulation of the maternal immune response, thereby maintaining pregnancy [12].

Anatomical context of Tumor Escape

• The interaction between FasL on tumor cells and Fas on lymphocytes may represent a tumor immune escape mechanism [13].
• In the present review, we will focus on how the expression of killer Ig receptors (KIR) on tumor infiltrating lymphocytes can compromise their function and how tumors evade apoptotic death - two additional mechanisms of tumor escape [14].
• It is possible that the tumor escape mechanisms from T and natural killer cells select variants that express a particular MHC class I altered phenotype [15].

Associations of Tumor Escape with chemical compounds

• Thus modulation of TL antigenicity on tumor cells in vivo, but not tumor escape, required cell-bound C3 [16].
• Such patients could benefit from a combination of androgen deprivation and antiangiogenic therapy in order to minimize the induction of such tumor escape [17].
• In our opinion, the selection of ER-negative CBCs, which has previously been implicated to be the pivotal mechanism of tumor escape of CBCs evolving in tamoxifen-treated patients, is only one mechanism of tumor escape in patients receiving antiestrogen treatment [18].
• As a single drug therapy, thalidomide might not have good therapeutic effect for all cases, but a small ratio of patients had exciting response, the resistance or tumor escape would develop after long-term use [19].
• Indoleamine 2,3-dioxygenase (IDO), a catabolizing enzyme of tryptophan, is supposed to play a role in tumor immune escape [20].

Gene context of Tumor Escape

• These findings identify mucin secretion as a novel mechanism of tumor escape from immune surveillance and provide the basis for the generation of potentially tolerogenic DC [21].
• The identification of T cell epitopes presented by alternative HLA-B and -C alleles may provide a means to counteract the tumor escape mechanism based on the selection of tumor cells no longer susceptible to HLA-A-restricted T cell recognition [22].
• On the basis of numerous studies, HLA-G is also expressed in malignant tumors and involved in tumor immune escape [23].
• The selection of tumor variants with altered expression of classical and nonclassical MHC class I molecules: implications for tumor immune escape [24].
• AIM: To explore the role and significance of costimulatory molecules B7H1,B7H2 and ICOS within tissues of human gastric carcinoma and the possible mechanisms in tumor escape [25].

Analytical, diagnostic and therapeutic context of Tumor Escape

• Transforming growth factor B (TGF-beta) is a potent immunosuppressive cytokine that is frequently associated with mechanisms of tumor escape from immunosurveillance [26].

References