|
Primary malignant neoplasm
|
0.040 |
Biomarker
|
group |
BEFREE |
PH-20 was abundant in all three extracts of all stages of cancer.
|
20849597 |
2010 |
|
Neoplasms
|
0.090 |
Biomarker
|
group |
BEFREE |
Tumor stage (P = .019) and HYAL-1 (P = .046) transcript levels were also associated with disease-specific mortality.
|
20960509 |
2011 |
|
Neoplasm Metastasis
|
0.040 |
AlteredExpression
|
phenotype |
BEFREE |
In univariate and multivariate analyses, tumor stage (P = .003), lymph node invasion (P = .033), HYAL-1 (P = .019), and HAS1 (P = .027) transcript levels, and HYAL-1 staining (P = .021) were independently associated with metastasis.
|
20960509 |
2011 |
|
Tumor Cell Invasion
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
In univariate and multivariate analyses, tumor stage (P = .003), lymph node invasion (P = .033), HYAL-1 (P = .019), and HAS1 (P = .027) transcript levels, and HYAL-1 staining (P = .021) were independently associated with metastasis.
|
20960509 |
2011 |
|
Malignant neoplasm of urinary bladder
|
0.020 |
Biomarker
|
disease |
BEFREE |
Among the HA family members, transcript levels of the HA synthases, HYAL-1, CD44v, and RHAMM were 4- to 16-fold higher in BCa tissues than in normal tissues (P < .0001); however, CD44s levels were lower.
|
20960509 |
2011 |
|
Bladder Neoplasm
|
0.020 |
Biomarker
|
disease |
BEFREE |
Among the HA family members, transcript levels of the HA synthases, HYAL-1, CD44v, and RHAMM were 4- to 16-fold higher in BCa tissues than in normal tissues (P < .0001); however, CD44s levels were lower.
|
20960509 |
2011 |
|
Carcinoma of bladder
|
0.020 |
Biomarker
|
disease |
BEFREE |
Among the HA family members, transcript levels of the HA synthases, HYAL-1, CD44v, and RHAMM were 4- to 16-fold higher in BCa tissues than in normal tissues (P < .0001); however, CD44s levels were lower.
|
20960509 |
2011 |
|
Neoplasms
|
0.090 |
Biomarker
|
group |
BEFREE |
The tumor cell-derived hyaluronidase (HAase) HYAL-1 degrades hyaluronic acid (HA) into proangiogenic fragments that support tumor progression.
|
21555367 |
2011 |
|
Malignant Neoplasms
|
0.060 |
Biomarker
|
group |
BEFREE |
Although HYAL-1 is a critical determinant of tumor progression and a marker for cancer diagnosis and metastasis prediction, it has not been evaluated as a target for cancer therapy.
|
21555367 |
2011 |
|
Neoplasm Metastasis
|
0.040 |
Biomarker
|
phenotype |
BEFREE |
Although HYAL-1 is a critical determinant of tumor progression and a marker for cancer diagnosis and metastasis prediction, it has not been evaluated as a target for cancer therapy.
|
21555367 |
2011 |
|
Primary malignant neoplasm
|
0.040 |
Biomarker
|
group |
BEFREE |
Although HYAL-1 is a critical determinant of tumor progression and a marker for cancer diagnosis and metastasis prediction, it has not been evaluated as a target for cancer therapy.
|
21555367 |
2011 |
|
Tumor Progression
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
Although HYAL-1 is a critical determinant of tumor progression and a marker for cancer diagnosis and metastasis prediction, it has not been evaluated as a target for cancer therapy.
|
21555367 |
2011 |
|
Epithelial ovarian cancer
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
HYAL-1 enzyme activity was measured in EOC cell lines and in plasma samples from patients.
|
21695196 |
2011 |
|
Carcinoma, Ovarian Epithelial
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
HYAL-1 enzyme activity was measured in EOC cell lines and in plasma samples from patients.
|
21695196 |
2011 |
|
Nasal Polyps
|
0.010 |
Biomarker
|
disease |
BEFREE |
On mRNA level, it was found that hyal-1-wt was decreased in NPs compared to NM and hyal-1-v3, -v4 and -v5 were substantially increased.
|
26661071 |
2016 |
|
Neoplasms
|
0.090 |
Biomarker
|
group |
BEFREE |
Tumor cell-derived hyaluronidase HYAL-1 degrades hyaluronic acid (HA) into angiogenic fragments (AGF: 10-12 disaccharides).
|
27419371 |
2017 |
|
Neoplasm Metastasis
|
0.040 |
AlteredExpression
|
phenotype |
BEFREE |
Urine and tissue HAase/HYAL-1 levels are sensitive markers for high-grade bladder cancer (BCa) and its metastasis.
|
27419371 |
2017 |
|
Tumor Cell Invasion
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
At IC50 for HAase activity inhibition (5-20 μg/ml [0.4-1.7 μM]), sHA-F significantly inhibited proliferation, motility and invasion of HYAL-1 expressing BCa cells (253J-Lung, HT1376, UMUC-3), P<0.001. sHA-F did not affect the growth of HYAL-1 non-expressing BCa (5637, RT4, T24, TCCSUP) and normal urothelial (Urotsa, SV-HUC1) cells. sHA-F treatment induced apoptosis by death receptor pathway. sHA-F downregulated transcript and/or protein levels of HA receptors (CD44, RHAMM), p-AKT, β-catenin, pβ-Catenin(S552), Snail and Twist but increased levels of pβ-Catenin(T41/S45), pGSK-3α/β(S21/S9) and E-cadherin. sHA-F also inhibited CD44/Phosphoinositide 3-kinase (PI-3K) complex formation and PI-3K activity.
|
27419371 |
2017 |
|
Malignant neoplasm of urinary bladder
|
0.020 |
Biomarker
|
disease |
BEFREE |
At IC50 for HAase activity inhibition (5-20 μg/ml [0.4-1.7 μM]), sHA-F significantly inhibited proliferation, motility and invasion of HYAL-1 expressing BCa cells (253J-Lung, HT1376, UMUC-3), P<0.001. sHA-F did not affect the growth of HYAL-1 non-expressing BCa (5637, RT4, T24, TCCSUP) and normal urothelial (Urotsa, SV-HUC1) cells. sHA-F treatment induced apoptosis by death receptor pathway. sHA-F downregulated transcript and/or protein levels of HA receptors (CD44, RHAMM), p-AKT, β-catenin, pβ-Catenin(S552), Snail and Twist but increased levels of pβ-Catenin(T41/S45), pGSK-3α/β(S21/S9) and E-cadherin. sHA-F also inhibited CD44/Phosphoinositide 3-kinase (PI-3K) complex formation and PI-3K activity.
|
27419371 |
2017 |
|
Bladder Neoplasm
|
0.020 |
Biomarker
|
disease |
BEFREE |
At IC50 for HAase activity inhibition (5-20 μg/ml [0.4-1.7 μM]), sHA-F significantly inhibited proliferation, motility and invasion of HYAL-1 expressing BCa cells (253J-Lung, HT1376, UMUC-3), P<0.001. sHA-F did not affect the growth of HYAL-1 non-expressing BCa (5637, RT4, T24, TCCSUP) and normal urothelial (Urotsa, SV-HUC1) cells. sHA-F treatment induced apoptosis by death receptor pathway. sHA-F downregulated transcript and/or protein levels of HA receptors (CD44, RHAMM), p-AKT, β-catenin, pβ-Catenin(S552), Snail and Twist but increased levels of pβ-Catenin(T41/S45), pGSK-3α/β(S21/S9) and E-cadherin. sHA-F also inhibited CD44/Phosphoinositide 3-kinase (PI-3K) complex formation and PI-3K activity.
|
27419371 |
2017 |
|
Carcinoma of bladder
|
0.020 |
Biomarker
|
disease |
BEFREE |
At IC50 for HAase activity inhibition (5-20 μg/ml [0.4-1.7 μM]), sHA-F significantly inhibited proliferation, motility and invasion of HYAL-1 expressing BCa cells (253J-Lung, HT1376, UMUC-3), P<0.001. sHA-F did not affect the growth of HYAL-1 non-expressing BCa (5637, RT4, T24, TCCSUP) and normal urothelial (Urotsa, SV-HUC1) cells. sHA-F treatment induced apoptosis by death receptor pathway. sHA-F downregulated transcript and/or protein levels of HA receptors (CD44, RHAMM), p-AKT, β-catenin, pβ-Catenin(S552), Snail and Twist but increased levels of pβ-Catenin(T41/S45), pGSK-3α/β(S21/S9) and E-cadherin. sHA-F also inhibited CD44/Phosphoinositide 3-kinase (PI-3K) complex formation and PI-3K activity.
|
27419371 |
2017 |
|
Neoplasms
|
0.090 |
AlteredExpression
|
group |
BEFREE |
To minimize the premature release, hyaluronic acid (HA) was further coating on the outer surface of pSiO<sub>2</sub>, which would be degraded by over-expressed hyaluronidase (Hyal-1) in the tumor microenvironment.
|
28888002 |
2017 |
|
Neoplasms
|
0.090 |
Biomarker
|
group |
BEFREE |
Phase 1 trials of PEGylated recombinant human hyaluronidase PH20 in patients with advanced solid tumours.
|
28949957 |
2018 |
|
Chronic Obstructive Airway Disease
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
HYAL-1 enzymatic activity at stable state was inversely correlated with FEV<sub>1</sub> % pred (p=0.034) and survival time (p=0.017).Serum HA is associated with COPD severity and predicts overall survival.
|
30705130 |
2019 |
|
Thromboangiitis Obliterans
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Both PH20 and HMW-HA upregulated CD44 expression and inhibited SMAD2/3 expression in the TAO group, and the inhibitory effects were partially reversed by CD44 blockage.
|
30947333 |
2019 |