20 Years Experience of TNF-Based Isolated Limb Perfusion for In-Transit Melanoma Metastases: TNF Dose Matters

Deroose, Jan P.; Eggermont, Alexander M.M.; Geel, Albertus N. van; Wilt, Johannes H. W. de; Burger, Jacobus W. A.; Verhoef, Cornelis

doi:10.1245/s10434-011-2030-7

Cited by 68 publications

(72 citation statements)

References 43 publications

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“…For multiple lesions on a limb, isolated limb perfusion with melphalan þ/e tumour necrosis factor has palliative value [88,89]. In stage III patients with satellite/in-transit metastases the procedure can be curative, as indicated by the reported 5 and 10 years survival rates of 40 and 30%, respectively.…”

Section: Skin Metastasesmentioning

confidence: 99%

Diagnosis and treatment of melanoma. European consensus-based interdisciplinary guideline – Update 2016

Garbe¹,

Peris²,

Hauschild

et al. 2016

European Journal of Cancer

364

259

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Section: Skin Metastasesmentioning

confidence: 99%

Diagnosis and treatment of melanoma. European consensus-based interdisciplinary guideline – Update 2016

Garbe¹,

Peris²,

Hauschild

et al. 2016

European Journal of Cancer

364

259

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“…However, these molecules are not employed to boost tumor-targeting immune responses, but rather as immunoreconstituting (G-CSF, GM-CSF) [36][37][38][39][40][41][42][43] or oncotoxic (TNF) factors. [44][45][46][47][48][49][50][51][52][53][54][55] Importantly, cytokines can cause relatively severe adverse effects (especially upon systemic administration), which de facto reflect their robust immunostimulatory activity and/or their biological pleiotropism. In particular, cytokines can (1) trigger an acute, potentially lethal systemic response that involves the release of pyrogenic and cytotoxic mediators (including additional cytokines) into the bloodstream; 56-60 (2) establish or perpetuate foci of chronic inflammation that may sustain oncogenesis or tumor progression; [61][62][63] or (3) promote proliferation among otherwise non-proliferating cells, thereby promoting the fixation of potentially oncogenic genetic or epigenetic defects.…”

Section: Introductionmentioning

confidence: 99%

Trial Watch—Immunostimulation with cytokines in cancer therapy

Vacchelli¹,

Aranda

Bloy³

et al. 2015

OncoImmunology

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During the past decade, great efforts have been dedicated to the development of clinically relevant interventions that would trigger potent (and hence potentially curative) anticancer immune responses. Indeed, developing neoplasms normally establish local and systemic immunosuppressive networks that inhibit tumor-targeting immune effector cells, be them natural or elicited by (immuno)therapy. One possible approach to boost anticancer immunity consists in the (generally systemic) administration of recombinant immunostimulatory cytokines. In a limited number of oncological indications, immunostimulatory cytokines mediate clinical activity as standalone immunotherapeutic interventions. Most often, however, immunostimulatory cytokines are employed as immunological adjuvants, i.e., to unleash the immunogenic potential of other immunotherapeutic agents, like tumor-targeting vaccines and checkpoint blockers. Here, we discuss recent preclinical and clinical advances in the use of some cytokines as immunostimulatory agents in oncological indications.

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“…In this setting, TNF-␣ has demonstrated potent antitumor activity with an acceptable safety profile. [19][20][21] In the sections to follow, we discuss the signaling events mediated by members of TNF superfamily and receptors with a particular emphasis on TNF-␣. We describe the role of this superfamily in normal physiology and disease.…”

mentioning

confidence: 99%

Historical perspectives on tumor necrosis factor and its superfamily: 25 years later, a golden journey

Aggarwal

Gupta

Kim

2012

Blood

705

604

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Although activity that induced tumor regression was observed and termed tumor necrosis factor (TNF) as early as the 1960s, the true identity of TNF was not clear until 1984, when Aggarwal and coworkers reported, for the first time, the isolation of 2 cytotoxic factors: one, derived from macrophages (molecular mass 17 kDa), was named TNF, and the second, derived from lymphocytes (20 kDa), was named lymphotoxin. Because the 2 cytotoxic factors exhibited 50% amino acid sequence homology and bound to the same receptor, they came to be called TNF-␣ and TNF-␤. Identification of the protein sequences led to cloning of their cDNA. Based on sequence homology to TNF-␣, now a total of 19 members of the TNF superfamily have been identified, along with 29 interacting receptors, and several molecules that interact with the cytoplasmic domain of these receptors. The roles of the TNF superfamily in inflammation, apoptosis, proliferation, invasion, angiogenesis, metastasis, and morphogenesis have been documented. Their roles in immunologic, cardiovascular, neurologic, pulmonary, and metabolic diseases are becoming apparent. TNF superfamily members are active targets for drug development, as indicated by the recent approval and expanding market of TNF blockers used to treat rheumatoid arthritis, psoriasis, Crohns disease, and osteoporosis, with a total market of more than US $20 billion. As we learn more about this family, more therapeutics will probably emerge. In this review, we summarize the initial discovery of TNF-␣, and the insights gained regarding the roles of this molecule and its related family members in normal physiology and disease. IntroductionThe tumor necrosis factor (TNF) superfamily, composed of 19 ligands and 29 receptors, plays highly diversified roles in the body. The interest in TNF research has increased dramatically over the years as indicated by more than 113 000 citations on TNF-␣ alone, 27 000 on anti-TNF-␣, 25 000 on TNF-␣ inhibitors, 55 000 on TNF receptors, 12 000 on TNF-mediated apoptosis, 40 000 on TNF-␣-induced signals, and 9610 reviews. All members of the TNF superfamily, without exception, exhibit pro-inflammatory activity, in part through activation of the transcription factor NF-B. Several members of the TNF superfamily exhibit proliferative activity on hematopoietic cells, in part through activation of various mitogen-activated kinases, and some members of this family play a role in apoptosis (Figure 1). 1,2 Some members of the TNF superfamily have also been reported to play a role in morphogenetic changes and differentiation. Most members of the TNF superfamily have both beneficial and potentially harmful effects. 3 Although TNF-␣, for example, has been linked with physiologic proliferation and differentiation of B cells under steady-state conditions, it also has been linked with a wide variety of diseases, including cancer, cardiovascular, neurologic, pulmonary, autoimmune, and metabolic disorders.Although the fascinating history of TNF could be traced back more than one century, the name ...

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20 Years Experience of TNF-Based Isolated Limb Perfusion for In-Transit Melanoma Metastases: TNF Dose Matters

Cited by 68 publications

References 43 publications

Diagnosis and treatment of melanoma. European consensus-based interdisciplinary guideline – Update 2016

Diagnosis and treatment of melanoma. European consensus-based interdisciplinary guideline – Update 2016

Trial Watch—Immunostimulation with cytokines in cancer therapy

Historical perspectives on tumor necrosis factor and its superfamily: 25 years later, a golden journey

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