HP-NAP inhibits the growth of bladder cancer in mice by activating a cytotoxic Th1 response
Cytotoxicity, Immunologic
0301 basic medicine
Cytotoxicity
Bacterial Protein
Inbred C57BL
Cell Line
Mice
03 medical and health sciences
Bacterial Proteins
Immunologic
Cell Line, Tumor
Animals
Humans
Tumor
Bladder cancer; HP-NAP; Immunotherapy; Th1 response; Administration, Intravesical; Animals; BCG Vaccine; Bacterial Proteins; Cell Line, Tumor; Cytotoxicity, Immunologic; Female; Helicobacter pylori; Humans; Immunotherapy; Mice; Mice, Inbred C57BL; Th1 Cells; Urinary Bladder Neoplasms
Helicobacter pylori
Intravesical
Animal
Bladder cancer
Th1 Cells
hp-nap
3. Good health
HP-NAP
Mice, Inbred C57BL
Th1 Cell
Administration, Intravesical
Urinary Bladder Neoplasms
Th1 response
Administration
HP-NAP inhibits the growth of bladder cancer in mice by activating a cytotoxic Th1 response.
BCG Vaccine
Female
Immunotherapy
Human
DOI:
10.1007/s00262-011-1087-2
Publication Date:
2011-08-10T11:44:31Z
AUTHORS (9)
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.
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