Six eligible PDA patients underwent multimodal therapy comprising dendritic cells (DCs) pulsed with Wilms' tumor 1 (WT1) peptide (DC/WT1-I) restricted by the human leukocyte antigen (HLA) class I (A*24:02 or A*02:06) allele, chemotherapy, radiation, and/or surgery.
Our previous study of congenital aniridia patients revealed a noticeable number of aniridia patients with WAGR-region deletions but without Wilms' tumor in their medical history.
Prolonged low levels of a granulocyte-related systemic inflammatory response after the early period of therapy and low cytoplasmic WT1 expression in PDA cells may be markers predictive of OS in PDA patients receiving WT1-targeting immunochemotherapy.
Wilms tumor 1 (WT1) and preferentially expressed antigen in melanoma (PRAME) are promising immunogenic antigen candidates for immunotherapy, and their clinical effects on patients with MDS with thrombocytopenia are still not well understood.
For the clinical development, we produced the B440 pharmaceutical formulation, which is lyophilized powder of inactivated <i>B. longum</i> 440 displaying the partially modified human WT1 protein.We confirmed that <i>B. longum</i> 440 could induce cellular immunity specific to multiple WT1 epitopes.
Immunohistochemistry showed that the tumor cells were positive for CD10, estrogen receptor (ER), progesterone receptor (PR), Wilms tumor-1 (WT-1) and smooth muscle actin (SMA).
Among the multilayered SECs, the superficial/luminal layer showed mucin 4 (MUC4), cytokeratin 5/6 (CK5/6), and CK7 expression in 5 cases (100%); MUC1, carcinoembryonic antigen (CEA), CA19-9, and thrombomodulin expression in 4 cases (80%); Wilms' tumor-1 (WT-1) and Hector Battifora mesothelial-1 (HBME-1) expression in 2 cases (40%), but it did not express p63 or D2-40.
Retinoic acid-dependent and -independent hallmark genes of GATA6<sup>+</sup> macrophages were induced by mesothelial and fibroblastic stromal cells that express the transcription factor Wilms' Tumor 1 (WT1), which drives the expression of two rate-limiting enzymes in retinol metabolism.
Few reports suggested a prognostic impact of Wilms'Tumor-1 (WT1)-mRNA overexpression in MDS, but translation into clinical routine was hampered by limited patients numbers, differing sample sources, non-standardized methods/cut-offs.
Wilms tumor 1 (WT1), Zonula occludens-1 (ZO-1), AMP activated protein kinase (AMPK), and NADPH oxidase-4 (NOX-4) expression were evaluated by immunohistochemistry and Western blot.
We expect that the procedure including IL-21 would improve the production rate of hTERT- and Wilms tumor 1 (WT1)-specific CD8<sup>+</sup> T cells for clinical trials.
We investigated pain sensitivity in humans with WAGR (Wilms tumor, aniridia, genitourinary anomaly, and range of intellectual disabilities) syndrome, who have variably sized heterozygous deletion of the 11p13 region.
The results indicated that PCE caused ultrastructural abnormalities on podocyte, and inhibited the expression of podocyte marker genes such as Nephrin, Wilms tumor 1 (WT1), the histone 3 lysine 9 acetylation (H3K9ac) level in the Kruppel-like factor 4 (KLF4) promoter and its expression in the male offspring from GD20 to PW28.
Here, we utilize the Wilms Tumor-1 (Wt1)-Cre to delete Mrtfs or Srf in the epicardium, which reduced the number of EPDCs in the adult cardiac interstitium.
Loss of function mutations in <i>GPC3</i> lead to Simpson-Golabi-Behmel Syndrome, an X-linked overgrowth condition with a predisposition to GPC3-expressing cancers including hepatoblastoma and Wilms tumor.