% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Rdel:301328,
      author       = {F. Rödel$^*$ and M. Fleischmann$^*$ and M. Diefenhardt$^*$
                      and H. Dapper and A. Hoffmann and C. Rödel$^*$ and D.
                      Martin$^*$ and E. Fokas},
      title        = {{E}merging advances and future opportunities in the
                      molecular and therapeutic landscape of anal cancer.},
      journal      = {Nature reviews / Clinical oncology},
      volume       = {22},
      issn         = {1759-4774},
      address      = {New York, NY},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2025-01000},
      pages        = {483–498},
      year         = {2025},
      note         = {22, pages 483–498 (2025)},
      abstract     = {Anal squamous cell carcinoma (ASCC) is a rare malignancy
                      with an increasing incidence. Primary chemoradiotherapy
                      (CRT) is the standard-of-care treatment for patients with
                      localized ASCC. In the metastatic setting, trials testing
                      immune-checkpoint inhibitor monotherapy have demonstrated
                      outcomes similar to those of patients receiving
                      chemotherapy. Conversely, adding the anti-PD-1 antibody
                      retifanlimab to chemotherapy in patients with recurrent or
                      metastatic ASCC has been shown to significantly improve
                      outcomes. Despite considerable efforts to develop
                      personalized therapy, treatment guidance and prognosis
                      remain reliant on baseline clinical characteristics. An
                      improved understanding of the molecular characteristics of
                      ASCC has provided insights into the mechanisms that mediate
                      tumour progression and response to CRT. For example, human
                      papillomavirus (HPV) infection is known to have an
                      aetiological role in most ASCCs and can modulate cellular
                      responses to CRT via several distinct mechanisms. In this
                      Review, we summarize emerging advances in the molecular and
                      therapeutic landscape of ASCC, including the implementation
                      of biomarkers for treatment guidance and translation into
                      new therapeutic approaches, with HPV infection constituting
                      a global determinant of both tumour biology and clinical
                      outcome. We also discuss the rationale for combining
                      immune-checkpoint inhibitors with CRT in patients with HPV+
                      tumours.},
      subtyp        = {Review Article},
      cin          = {FM01},
      ddc          = {610},
      cid          = {I:(DE-He78)FM01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40360682},
      doi          = {10.1038/s41571-025-01025-x},
      url          = {https://inrepo02.dkfz.de/record/301328},
}