Cancer-testis and melanocyte-differentiation antigen expression in malignant glioma and meningioma.
New York City, United States. In J Clin Neurosci, 2012
The following primers were analyzed for CTA: LAGE-1, NY-ESO-1, MAGE-1, MAGE-3, MAGE-4, MAGE-10, CT-7, CT-10, HOM-MEL 40, BAGE, and SCP-1; and for MDA: tyrosinase, gp100, MELAN-A/MART-1, and TRP-2.
Cancer/testis antigens and urological malignancies.
Baltimore, United States. In Nat Rev Urol, 2012
There has been an explosion in CTA-based research since CTAs were first identified in 1991 and MAGE-1 was shown to elicit an autologous cytotoxic T-lymphocyte (CTL) response in a patient with melanoma.
Evaluation of MAGE A1 in oral squamous cell carcinoma.
Belo Horizonte, Brazil. In Oncol Rep, 2012
results show the absence and/or low expression of MAGE A1 transcripts in oral squamous cell carcinoma; presence of hypomethylation at a small level at the promoter site of MAGE A1 was detected in both oral squamous cell carcinoma and normal oral mucosa
[Antitumor vaccines: conception, development and evaluation in humans].
France. In Ann Pharm Fr, 2002
A series of phase I/II clinical studies evaluating ALVAC recombinants carrying either the CEA, p53, MAGE1 or MAGE3 genes, administered through the subcutaneous, intradermal or intravenous routes, has shown that this approach is safe and can induce tumor-specific antibody or T cell responses in at least some of the patients.
The immunology and immunotherapy of breast cancer: an update.
Tampa, United States. In Int J Immunopharmacol, 1999
CMI and humoral immune reactivity have been demonstrated to autologous tumor and a variety of tumor-associated antigens (TAA) have been implicated including CEA, HER-2/neu, MAGE-1, p53, T/Tn and MUC-1.
Breast cancer-associated antigen, DF3/MUC1, induces apoptosis of activated human T cells.
Boston, United States. In Nat Med, 1996
Given the plethora of well-documented breast carcinoma-associated antigens in humans including MAGE-1, -2 and -3, mutated p53, p21ras, HER-2/neu and DF3/MUC-1, coupled with evidence that humoral and cytotoxic T-cell responses against these antigens exist, the central dilemma facing tumor immunologists is why the host immune response is so inefficient.