@article{BatzkeBuechelHansenetal.2018,
  author    = {Batzke, Katharina and B{\"u}chel, Gabriele and Hansen, Wiebke and Schramm, Alexander},
  title     = {TrkB-target Galectin-1 impairs immune activation and radiation responses in neuroblastoma: implications for tumour therapy},
  series = {International Journal of Molecular Sciences},
  volume    = {19},
  journal   = {International Journal of Molecular Sciences},
  number    = {3},
  issn      = {1422-0067},
  doi       = {10.3390/ijms19030718},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-285097},
  year      = {2018},
  abstract  = {Galectin-1 (Gal-1) has been described to promote tumour growth by inducing angiogenesis and to contribute to the tumour immune escape. We had previously identified up-regulation of Gal-1 in preclinical models of aggressive neuroblastoma (NB), the most common extracranial tumour of childhood. While Gal-1 did not confer a survival advantage in the absence of exogenous stressors, Gal-1 contributed to enhanced cell migratory and invasive properties. Here, we review these findings and extend them by analyzing Gal-1 mediated effects on immune cell regulation and radiation resistance. In line with previous results, cell autonomous effects as well as paracrine functions contribute to Gal-1 mediated pro-tumourigenic functions. Interfering with Gal-1 functions in vivo will add to a better understanding of the role of the Gal-1 axis in the complex tumour-host interaction during immune-, chemo- and radiotherapy of neuroblastoma.},
  language  = {en}
}
@article{WernerHiguchiPomperetal.2021,
  author    = {Werner, Rudolf A. and Higuchi, Takahiro and Pomper, Martin G. and Rowe, Steven P.},
  title     = {Theranostics in oncology — thriving, now more than ever},
  series = {Diagnostics},
  volume    = {11},
  journal   = {Diagnostics},
  number    = {5},
  issn      = {2075-4418},
  doi       = {10.3390/diagnostics11050805},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-236662},
  year      = {2021},
  abstract  = {Tracing its roots back to the 1940s, theranostics in nuclear oncology has proved successful mainly due to the beneficial effects of image-guided therapeutic concepts for patients afflicted with a variety of different cancers. The majority of these treatments are not only characterized by substantial prolongation of progression-free and overall survival, but are also generally safe, rendering theranostic agents as an attractive treatment option in various clinical scenarios in oncology. In this Special Issue Novel Theranostic Agents, nine original articles from around the globe provide further evidence on the use of the theranostic concept for neuroendocrine neoplasm (NEN), prostate cancer (PC), meningioma, and neuroblastoma. The investigated diagnostic and therapeutic radiotracers target not only established structures, such as somatostatin receptor, prostate-specific membrane antigen or norepinephrine transporter, but also recently emerging targets such as the C-X-C motif chemokine receptor 4. Moreover, the presented original articles also combine the concept of theranostics with in-depth read-out techniques such as radiomics or novel reconstruction algorithms on pretherapeutic scans, e.g., for outcome prediction. Even 80 years after its initial clinical introduction, theranostics in oncology continues to thrive, now more than ever.},
  language  = {en}
}
@article{PelosiFioreDiMatteoetal.2021,
  author    = {Pelosi, Andrea and Fiore, Piera Filomena and Di Matteo, Sabina and Veneziani, Irene and Caruana, Ignazio and Ebert, Stefan and Munari, Enrico and Moretta, Lorenzo and Maggi, Enrico and Azzarone, Bruno},
  title     = {Pediatric tumors-mediated inhibitory effect on NK cells: the case of neuroblastoma and Wilms' tumors},
  series = {Cancers},
  volume    = {13},
  journal   = {Cancers},
  number    = {10},
  issn      = {2072-6694},
  doi       = {10.3390/cancers13102374},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-239615},
  year      = {2021},
  abstract  = {Natural killer (NK) cells play a key role in the control of cancer development, progression and metastatic dissemination. However, tumor cells develop an array of strategies capable of impairing the activation and function of the immune system, including NK cells. In this context, a major event is represented by the establishment of an immunosuppressive tumor microenvironment (TME) composed of stromal cells, myeloid-derived suppressor cells, tumor-associated macrophages, regulatory T cells and cancer cells themselves. The different immunoregulatory cells infiltrating the TME, through the release of several immunosuppressive molecules or by cell-to-cell interactions, cause an impairment of the recruitment of NK cells and other lymphocytes with effector functions. The different mechanisms by which stromal and tumor cells impair NK cell function have been particularly explored in adult solid tumors and, in less depth, investigated and discussed in a pediatric setting. In this review, we will compare pediatric and adult solid malignancies concerning the respective mechanisms of NK cell inhibition, highlighting novel key data in neuroblastoma and Wilms' tumor, two of the most frequent pediatric extracranial solid tumors. Indeed, both tumors are characterized by the presence of stromal cells acting through the release of immunosuppressive molecules. In addition, specific tumor cell subsets inhibit NK cell cytotoxic function by cell-to-cell contact mechanisms likely controlled by the transcriptional coactivator TAZ. These findings could lead to a more performant diagnostic approach and to the development of novel immunotherapeutic strategies targeting the identified cellular and molecular targets.},
  language  = {en}
}