Pub Date : 2005-01-01DOI: 10.1016/s0921-4410(04)22037-3
Mark R Albertini, Jacquelyn A Hank, Paul M Sondel
{"title":"Native and genetically engineered anti-disialoganglioside monoclonal antibody treatment of melanoma.","authors":"Mark R Albertini, Jacquelyn A Hank, Paul M Sondel","doi":"10.1016/s0921-4410(04)22037-3","DOIUrl":"https://doi.org/10.1016/s0921-4410(04)22037-3","url":null,"abstract":"","PeriodicalId":72508,"journal":{"name":"Cancer chemotherapy and biological response modifiers","volume":" ","pages":"789-97"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25258167","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Chemotherapy, cytokines, and biochemotherapy for melanoma.","authors":"Omar Eton","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":72508,"journal":{"name":"Cancer chemotherapy and biological response modifiers","volume":" ","pages":"739-48"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25258163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2005-01-01DOI: 10.1016/s0921-4410(04)22033-6
O. Eton
{"title":"Chemotherapy, cytokines, and biochemotherapy for melanoma.","authors":"O. Eton","doi":"10.1016/s0921-4410(04)22033-6","DOIUrl":"https://doi.org/10.1016/s0921-4410(04)22033-6","url":null,"abstract":"","PeriodicalId":72508,"journal":{"name":"Cancer chemotherapy and biological response modifiers","volume":"22 1","pages":"739-48"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"56279885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2005-01-01DOI: 10.1016/s0921-4410(04)22013-0
Lawrence G Lum, Pamela A Davol
The development of BiAbs for therapeutic applications in cancer shows promise. As our understanding of effector cell receptor biology for triggering of cytotoxic functions improves and the behavior of TAA and the targeting antibody engagement is elucidated, customized BiAb reagents can be engineered to optimize in vivo or ex vivo arming of T cells for targeting tumors. Additionally, other variables that require consideration in the equation for successful T cell immunotherapy include: the type of effector cells, their state of activation, the type of effector receptor being activated or tareeted. the presence of Tregs, the affinity of the anti-effector cell antibody and the anti-TAA antibody, the type of BiAb (mouse, humanized, or human), the number of binding sites for the T cells or TAA, the presence or absence of decoy antigen, whether the TAA modulates after being engaged by antibody, the type of tumor, the tumor burden, and last, but not least, the amount of 'immunologic' space available for the adoptively transferred cells to expand and function.
{"title":"Retargeting T cells and immune effector cells with bispecific antibodies.","authors":"Lawrence G Lum, Pamela A Davol","doi":"10.1016/s0921-4410(04)22013-0","DOIUrl":"https://doi.org/10.1016/s0921-4410(04)22013-0","url":null,"abstract":"<p><p>The development of BiAbs for therapeutic applications in cancer shows promise. As our understanding of effector cell receptor biology for triggering of cytotoxic functions improves and the behavior of TAA and the targeting antibody engagement is elucidated, customized BiAb reagents can be engineered to optimize in vivo or ex vivo arming of T cells for targeting tumors. Additionally, other variables that require consideration in the equation for successful T cell immunotherapy include: the type of effector cells, their state of activation, the type of effector receptor being activated or tareeted. the presence of Tregs, the affinity of the anti-effector cell antibody and the anti-TAA antibody, the type of BiAb (mouse, humanized, or human), the number of binding sites for the T cells or TAA, the presence or absence of decoy antigen, whether the TAA modulates after being engaged by antibody, the type of tumor, the tumor burden, and last, but not least, the amount of 'immunologic' space available for the adoptively transferred cells to expand and function.</p>","PeriodicalId":72508,"journal":{"name":"Cancer chemotherapy and biological response modifiers","volume":" ","pages":"273-91"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25258143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2003-01-01DOI: 10.1016/s0921-4410(03)21012-7
Michael S Turner, John R McKolanis, Ramesh K Ramanathan, David C Whitcomb, Olivera J Finn
The mucin family has been under study by molecular biologists, biochemists, pathologists and immunologists interested in cancer because of the role these molecules can play in the diagnosis and treatment of cancer. Immense knowledge has been accumulated, but the high speed of progress in the laboratory has not been matched by the progress towards applying this knowledge in the clinic. For example, specific knowledge of cancer-associated changes in the expression and glycosylation of various mucins, which can aid in the diagnosis as well as prognosis of GI cancers, has not yet led to the use of a panel of anti-mucin antibodies as a standard diagnostic tool. Similarly, many more opportunities exist for using mucin-based therapies than are currently being considered in the clinic. This chapter aimed to highlight some of these opportunities and to interest clinician scientists in exploring them in the near future.
{"title":"Mucins in gastrointestinal cancers.","authors":"Michael S Turner, John R McKolanis, Ramesh K Ramanathan, David C Whitcomb, Olivera J Finn","doi":"10.1016/s0921-4410(03)21012-7","DOIUrl":"https://doi.org/10.1016/s0921-4410(03)21012-7","url":null,"abstract":"<p><p>The mucin family has been under study by molecular biologists, biochemists, pathologists and immunologists interested in cancer because of the role these molecules can play in the diagnosis and treatment of cancer. Immense knowledge has been accumulated, but the high speed of progress in the laboratory has not been matched by the progress towards applying this knowledge in the clinic. For example, specific knowledge of cancer-associated changes in the expression and glycosylation of various mucins, which can aid in the diagnosis as well as prognosis of GI cancers, has not yet led to the use of a panel of anti-mucin antibodies as a standard diagnostic tool. Similarly, many more opportunities exist for using mucin-based therapies than are currently being considered in the clinic. This chapter aimed to highlight some of these opportunities and to interest clinician scientists in exploring them in the near future.</p>","PeriodicalId":72508,"journal":{"name":"Cancer chemotherapy and biological response modifiers","volume":"21 ","pages":"259-74"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24660523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2003-01-01DOI: 10.1016/s0921-4410(03)21018-8
Paulo C Rodríguez, Arnold H Zea, Augusto C Ochoa
The results from in vitro immunological experiments, murine tumor models and patients with cancer clearly demonstrate that tumors have multiple mechanisms to evade the immune response. During the early stages of tumor development malignant cells can be poor stimulators, present poor targets or become resistant to the innate immune response, while at later stages, progressively growing tumors impair the adaptive immune response by blocking the maturation and function of APCs and causing alterations in T-cell signal transduction and function. Preliminary results also suggest a correlation between some of these changes and an increased metastatic potential of the tumor cells, a diminished response to immunotherapy, and poor prognosis. Carefully coordinated basic research studies and clinical immunotherapy trials will be required to fully determine the impact of these mechanisms of tumor evasion on the outcome of the disease and the response to treatment. However, understanding the mechanisms used by tumor cells to evade the immune system could result in new therapeutic approaches for preventing and/or reversing these immune alterations and could have the potential of improving the current results of immunotherapy trials.
{"title":"Mechanisms of tumor evasion from the immune response.","authors":"Paulo C Rodríguez, Arnold H Zea, Augusto C Ochoa","doi":"10.1016/s0921-4410(03)21018-8","DOIUrl":"https://doi.org/10.1016/s0921-4410(03)21018-8","url":null,"abstract":"<p><p>The results from in vitro immunological experiments, murine tumor models and patients with cancer clearly demonstrate that tumors have multiple mechanisms to evade the immune response. During the early stages of tumor development malignant cells can be poor stimulators, present poor targets or become resistant to the innate immune response, while at later stages, progressively growing tumors impair the adaptive immune response by blocking the maturation and function of APCs and causing alterations in T-cell signal transduction and function. Preliminary results also suggest a correlation between some of these changes and an increased metastatic potential of the tumor cells, a diminished response to immunotherapy, and poor prognosis. Carefully coordinated basic research studies and clinical immunotherapy trials will be required to fully determine the impact of these mechanisms of tumor evasion on the outcome of the disease and the response to treatment. However, understanding the mechanisms used by tumor cells to evade the immune system could result in new therapeutic approaches for preventing and/or reversing these immune alterations and could have the potential of improving the current results of immunotherapy trials.</p>","PeriodicalId":72508,"journal":{"name":"Cancer chemotherapy and biological response modifiers","volume":"21 ","pages":"351-64"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24660529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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