HP-NAP inhibits the growth of bladder cancer in mice by activating a cytotoxic Th1 response

Pierfrancesco Bassi, Andrea Volpe, Gaia Codolo, Matteo Fassan, Fabio Munari, Massimo Rugge, Francesco Pagano, Mario Milco D'Elios, Marina De Bernard

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Intravesical Bacillus Calmette-Guérin (BCG) is the gold standard treatment for intermediate and high-risk non-muscle-invasive bladder cancer. BCG therapy is the most successful example of immunotherapy in cancer. Unfortunately, the treatment-related side effects are still relevant. Furthermore, non-responder patients are candidate to radical cystectomy in the absence of valuable alternative options. These aspects have prompted the search for newer biological response modifiers (BRM) with a better benefit/side effects ratio. The toll-like receptor (TLR) 2 ligand, Helicobacter pylori protein HP-NAP, has been shown to deserve a potential role as BRM. HP-NAP is capable of driving the differentiation of T helper (Th) 1 cells, both in vitro and in vivo, because of its ability to create an IL-12-enriched milieu. Herein, we report that local administration of HP-NAP decreases tumour growth by triggering tumour necrosis in a mouse model of bladder cancer implant. The effect is accompanied by a significant accumulation of both CD4+ and CD8+ IFN-γ-secreting cells, within tumour and regional lymph nodes. Noteworthy, HP-NAP-treated tumours show also a reduced vascularization due to the anti-angiogenic activity of IFN-γ induced by HP-NAP. Our findings strongly indicate that HP-NAP might become a novel therapeutic "bullet" for the cure of bladder tumours
Original languageEnglish
Pages (from-to)31-40
Number of pages10
JournalCANCER IMMUNOLOGY, IMMUNOTHERAPY
DOIs
Publication statusPublished - 2012

Keywords

  • Bladder cancer
  • hp-nap

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