Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C1658953 (
tumor vasculature
)
2,390
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Systemic chemotherapies for advanced or metastatic thyroid carcinomas have been of only limited effectiveness. For patients with differentiated or medullary carcinomas unresponsive to conventional treatments, novel therapies are needed to improve disease outcomes. Multiple novel therapies primarily targeting angiogenesis have entered clinical trials for metastatic thyroid carcinoma. Partial response rates up to 30% have been reported in single agent studies, but prolonged disease stabilization is more commonly seen. The most successful agents target the vascular endothelial growth factor receptors, with potential targets including the mutant kinases associated with papillary and medullary oncogenesis. Two drugs approved for other malignancies, sorafenib and sunitinib, have had promising preliminary results reported, and are being used selectively for patients who do not qualify for clinical trials. Additional agents targeting
tumor vasculature
, nuclear receptors, epigenetic abnormalities, and the immune response to neoplasia have also been investigated. Randomized trials for several agents are underway that may lead to eventual drug approval for
thyroid cancer
. Treatment for patients with metastatic or advanced thyroid carcinoma now emphasizes clinical trial opportunities for novel agents with considerable promise. Alternative options now exist for use of tyrosine kinase inhibitors that are well tolerated and may prove worthy of regulatory approval for this disease.
...
PMID:Targeted therapy of thyroid cancer. 2047 74
The incidence of papillary thyroid carcinoma (PTC) has steadily increased over the recent years, making this cancer a common malignant tumor world-wide. We tested the hypothesis that
N
uclear
E
nriched
A
bundant sh-NEAT1 knock-down ranscript 1 (NEAT1) is involved in the pathogenesis of PTC
in vitro
and
in vivo
. We show that NEAT1 is highly expressed in
P
apillary
T
hyroid
C
arcinoma cell line (PTC-1) and anaplastic thyroid cancer cell line (SW1736) as compared with the human thyroid follicular epithelial cell line (Nthy-ori 3-1). shRNA knockdown of NEAT1 led to the inhibition of cell growth, invasion, migration and
E
pithelial to
M
esenchymal
T
ransition (EMT) of
thyroid cancer
cells. This treatment increased the rate of apoptosis in SW1736 cells. Silencing of NEAT1 increased the level of its regulator, miRNA-126 and down-regulated VEGFA that sets the density of
tumor vasculature
. Administrtation of sh-NEAT1 also inhibited tumor growth
in vivo
, increased the miRNA-126 level and down-regulated VEGFA. Taken together, these results indicate that silencing NEAT1 suppresses thyroid carcinoma via miR-126/NEAT1/VEGFA axis.
...
PMID:Silencing NEAT1 suppresses thyroid carcinoma via miR-126/NEAT1/VEGFA axis. 3158 4
