Fig 1.
Haematoxylin and eosin (H&E) staining of human nasal conchae (A) and PaCa 5061 xenograft tumour (B).
Fig 2.
Hyaluronan (HA) deposition in human nasal conchae as determined by anti-HA antibody staining (A) and after hyaluronidase pretreatment (B). Changes in staining patterns and intensity were not seen, unlike when detecting HA by hyaluronic acid binding protein (HABP) ligand histochemistry (C), which showed a complete absence of HA after pretreatment (D).
Fig 3.
PaCa 5061 primary human pancreatic adenocarcinoma xenograft immunohistochemically stained with an anti-hyaluronan polyclonal antibody.
Note the staining of the cancer cells themselves, which were more intensively stained than the surrounding extracellular matrix (A). If hyaluronan was detected by hyaluronic acid binding protein, it was present in the extracellular matrix and not in the cancer cells themselves (C). If the section was pre-treated with hyaluronidase, the hyaluronan immunoreactivity did not vanish after antibody IHC (B); in contrast, hyaluronidase pre-treatment abolished its reactivity completely according to HABP staining (D). Collectively these results indicate that the anti-hyaluronan antibody binding is not caused by hyaluronan and that this approach is therefore unsuitable for its detection.
Table 1.
Clinico-pathological data of patients with pancreatic adenocarcinoma correlated with hyaluronan (HA) expression levels (n.a. not available).
Fig 4.
Hyaluronan deposition in pancreatic ductal adenocarcinoma as determined by hyaluronic acid binding protein (HABP) ligand histochemistry.
Some tumours showed no extracellular HA (A) deposition while other tumours showed moderate (B) or high amounts of HA (C).
Fig 5.
Kaplan-Meier survival analysis for overall survival (A) and disease-free survival (B) in patients with PDAC after surgical tumour resection.