50 research outputs found
Anti-Tyrosinase Antibodies participate in the immune-response to vaccination with antiidiotypic antibodies mimicking the the High-Molecular-Weight-Melanoma-Associated-Antigen
No full textSeven patients with metastatic melanoma were vaccinated with anti-idiotypic monoclonal antibody (mAb) MK2-23 which mimics the high-molecular-weight melanoma-associated antigen (HMW MAA), Sera samples were assayed for anti-anti-idiotypic antibodies, by Ab1-Ab2 complex inhibition test, for anti-Bls epitope antibodies, which are a heterogeneous group against various antigens presented on B16 melanoma cells and for anti-tyrosinase antibodies, which are specific against tyrosinase. Our results pointed to the participation of anti-tyrosinase antibodies in the immune response to vaccination by antiidiotypic antibodies mimicking the HMW MAA. The antityrosinase antibody kinetic curves presented an initial increase in titres in five cases followed by decreasing titres; in two cases a constant decrease was noted. The inhibition assay demonstrated an increasing percentage of inhibition (range 17-100%) within 100-400 days of treatment, The titre of the anti-tyrosinase antibodies increased following the vaccination, then decreased - probably due to absorption of the antibodies to melanoma cells and normal melanocytes. A positive slope in the percentage of inhibition was roughly associated with a negative slope of anti-tyrosinase antibodies. In one case, a long-standing complete clinical response was accompanied by development of melanoma-associated hypopigmentation. Anti-ale epitope antibodies had no role in the response to vaccination, The development of anti-tyrosinase antibodies in response to vaccination by anti-idiotypic antibodies mimicking another antigen may be explained by induction of non-specific polyclonal B lymphocytes activation, a well-recognized phenomenon in autoimmune disorders, While in autoimmune diseases the production of a second autoantibody may aggravate the course, in melanoma it may contribute to the regression of the disease in some patients
Melanoma-associated hypopigmentation: Where are the antibodies?
No full textAntibodies to the B16 melanoma cell line and to tyrosinase have been recently defined in our laboratory in sera of patients with vitiligo, melanoma, melanoma-associated hypopigmentation (MAH), and in healthy subjects. The antibody titers in each subject were measured by enzyme-linked immunosorbent assay, were compared with the mean optical density (OD) of the control group, and were expressed as relative OD. The titers of anti-B16 antibodies (relative OD � standard error) were 1.000 (0.058) in the controls, 1.025 (0.077) in patients with metastatic melanoma, 0.5862 (0.15) in MAH, 1.377 in surgery-induced MAH, 1.087 in vaccination with anti-idiotypic antibodies, and 2.098 (0.15) in autoimmune vitiligo. The titers in vitiligo were significantly higher (p < 0.0001) than in MAH or in healthy controls. Antityrosinase antibodies were found in titers of 1.000 (0.1024) in the controls, 1.516 (0.225) in metastatic melanoma, 1.027 (0.180) in MAH, 1.075 in surgery-induced MAH, 2.308 in vaccination-induced MAH, and 4.536 in vitiligo. Differences were found between vitiligo and MAH (p = 0.008), surgery-induced MAH (p = 0.009), vaccination-induced MAH (p = 0.059), and healthy subjects (p < 0.0001). The results of this study point to the cross-antigenicity between melanocytes and melanoma cells, and to participation of antibodies against melanoma-associated membrane antigens in the mechanism leading to the development of MAH in patients with melanoma
Ductal carcinoma in situ (DCIS) of the breast in Israeli women treated by radiation therapy following breast-conserving surgery
No full text
Soft tissue and visceral sarcomas: ESMO-EURACAN Clinical Practice Guidelines for diagnosis, treatment and follow-up
No full textAnn Oncol 2018; 29: iv51-iv67 (doi:10.1093/annonc/mdy096) The following corrections have been made under authorship: The author R.L. Haas has been added with the corresponding affiliation and author disclosure statement. The author name P. Rutkovski has been replaced with: P. Rutkowski Under authorship, the author name: A. Hannu has been replaced with: H.T. Aro. Under authorship, A. A. Safwat s affiliation: Finland has been replaced with: Denmark. Under authorship, the author name: W. Van der Graaf has been replaced with: W.T.A. van der Graaf. W.T.A. van der Graaf s institution: 30 has been replaced with: 30, 33, 51
Corrections to “Gastrointestinal stromal tumours: ESMO–EURACAN Clinical Practice Guidelines for diagnosis, treatment and follow-up” (Annals of Oncology (2018) 29(S4) (iv68–iv78), (S0923753419316916), (10.1093/annonc/mdy095))
No full textAnn Oncol 2018; 29: iv68–iv78 (doi:10.1093/annonc/mdy095) The following corrections have been made under authorship: The author R.L. Haas has been added with the corresponding affiliation and author disclosure statement. The author name P. Rutkovski has been replaced with: P. Rutkowski Under authorship, the author name: A. Hannu has been replaced with: H.T. Aro. Under authorship, A. A. Safwat's affiliation: Finland has been replaced with: Denmark. Under authorship, the author name: W. Van der Graaf has been replaced with: W.T.A. van der Graaf. W.T.A. van der Graaf's institution: 30 has been replaced with: 30, 33, 51
