|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Unexpectedly, we found that treatment of tumor-bearing mice with an ABL allosteric inhibitor promoted differentiation of lung adenocarcinomas from poorly differentiated tumors expressing basal cell markers to tumors expressing terminal differentiation markers <i>in vivo</i>, which rendered lung adenocarcinomas susceptible to chemotherapy.
|
30956771 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Correction: ABL kinase inhibition sensitizes primary lung adenocarcinomas to chemotherapy by promoting tumor cell differentiation.
|
31666936 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Using a mouse xenograft model we demonstrate that, while primary tumor size is not affected by ABL kinase inhibitors, the <i>in vivo</i> matrix metalloproteinase (MMP) activity, tumor cell invasion, and consequent spontaneous metastasis to lungs are significantly impaired in inhibitor-treated mice.
|
29774130 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Administration of 5-MTP to a murine xenograft tumor model reduced vimentin protein expression in the tumor tissues compared to vehicle control which was correlated with reduction of metastasis in the 5-MTP treated mice.
|
27145282 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
5-MTP blocks cancer cell migration and invasion in vitro and inhibits tumor growth and cancer metastasis in a xenograft model.
|
24589238 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Similarly, the treatment of primary MALT lymphoma cells with the ABL inhibitors imatinib and dasatinib prevented tumor cell growth.
|
21454413 |
2011 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These results indicate that Bcl11b and H2AX function as tumor suppressor and that haploinsufficiency and acquired loss of these gene products cooperate with p210BCR/ABL to develop CML BC.
|
19432895 |
2009 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Virus infection induced acute lymphoblastic leukemia (ALL) in p210BCR/ABL Tg with a higher frequency and in a shorter latency than wild-type littermates, and inverse PCR detected two retrovirus common integration sites (CISs) in p210BCR/ABL Tg tumors.
|
18193087 |
2008 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
ABL KD mutations were detected by direct sequencing in 15 of 17 patients (88%) who had recurrent Ph-positive ALL and received prior imatinib (n = 16) or dasatinib (n = 1) treatment and in 6 of 7 patients (86%) who had resistant/recurrent tumors treated with >or=2 KIs compared with 0 of 12 patients with recurrent Ph-positive ALL who never received KIs.
|
18615627 |
2008 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We also show that RIN1 acts as a negative regulator of tumor cell invasive growth and that this requires the ABL kinase-signaling function of RIN1, suggesting a mechanism through which RIN1 silencing may contribute to breast cancer progression.
|
18089779 |
2007 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Although the ABL kinase inhibitor imatinib mesylate (Gleevec) provides highly effective treatment for BCR-ABL-positive chronic myelogenous leukemia, it has proven far less efficacious in the treatment of BCR-ABL-positive acute lymphoblastic leukemias (ALLs), many of which sustain deletions of the INK4A-ARF (CDKN2A) tumor suppressor locus.
|
16618932 |
2006 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
There was no difference in tumor latency in young mice infected; however, following ABL-MYC infection, aged Bcl-X(L) mice demonstrated a median survival of 9 weeks, while littermate control mice demonstrated a median survival of 19 weeks.
|
15725478 |
2005 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
This is the first report of an ALL case with ABL amplification, and the authors speculate that both ABL proto-oncogene amplification and the p16(INK4a) tumor suppressor gene deletion have been implicated in leukemogenesis in the present case, although whether the ABL amplification truly contributes to the leukemogenesis or merely an epiphenomenon representing underlying genomic instability remains to be determined.
|
15282669 |
2004 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The ABL oncoprotein-p53 paradigm represents the relationship between an oncogenic tyrosine kinase and a tumor suppressor gene.
|
15492510 |
2004 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We have developed a sensitive, competitive, nested reverse transcription polymerase chain reaction (RT-PCR) titration assay that quantifies the number of Wilm's tumour (WT1) gene transcripts in bone marrow (BM) and peripheral blood (PB), coupled with a competitive RT-PCR protocol for the ABL gene as control.
|
14510942 |
2003 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The phenotype depends both on expression of BCR/ABL and NUP98/HOXA9, but tumors retain sensitivity to the ABL inhibitor STI571 in vitro and in vivo.
|
12032333 |
2002 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Alterations in the tumor suppressor gene p53 are associated with the pathogenesis of blastic transformation of chronic myeloid leukemia (CML), but their exact role, particularly their relationship with the chimeric protein p210BCR/ABL, is poorly defined.
|
8282066 |
1994 |