% 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{Koukourakis:284766,
      author       = {I. M. Koukourakis and K. Platoni and V. Kouloulias and S.
                      Arelaki$^*$ and A. Zygogianni},
      title        = {{P}rostate {C}ancer {S}tem {C}ells: {B}iology and
                      {T}reatment {I}mplications.},
      journal      = {International journal of molecular sciences},
      volume       = {24},
      number       = {19},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {DKFZ-2023-02077},
      pages        = {14890},
      year         = {2023},
      abstract     = {Stem cells differentiate into mature organ/tissue-specific
                      cells at a steady pace under normal conditions, but their
                      growth can be accelerated during the process of tissue
                      healing or in the context of certain diseases. It is
                      postulated that the proliferation and growth of carcinomas
                      are sustained by the presence of a vital cellular
                      compartment resembling stem cells residing in normal
                      tissues: 'stem-like cancer cells' or cancer stem cells
                      (CSCs). Mutations in prostate stem cells can lead to the
                      formation of prostate cancer. Prostate CSCs (PCSCs) have
                      been identified and partially characterized. These express
                      surface markers include CD44, CD133, integrin α2β1, and
                      pluripotency factors like OCT4, NANOG, and SOX2. Several
                      signaling pathways are also over-activated, including Notch,
                      PTEN/Akt/PI3K, RAS-RAF-MEK-ERK and HH. Moreover, PCSCs
                      appear to induce resistance to radiotherapy and
                      chemotherapy, while their presence has been linked to
                      aggressive cancer behavior and higher relapse rates. The
                      development of treatment policies to target PCSCs in tumors
                      is appealing as radiotherapy and chemotherapy, through
                      cancer cell killing, trigger tumor repopulation via
                      activated stem cells. Thus, blocking this reactive stem cell
                      mobilization may facilitate a positive outcome through
                      cytotoxic treatment.},
      subtyp        = {Review Article},
      keywords     = {chemotherapy (Other) / prostate cancer (Other) /
                      radiotherapy (Other) / stem cells (Other)},
      cin          = {B280},
      ddc          = {540},
      cid          = {I:(DE-He78)B280-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37834336},
      pmc          = {pmc:PMC10573523},
      doi          = {10.3390/ijms241914890},
      url          = {https://inrepo02.dkfz.de/record/284766},
}