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PMID |
Sentence |
1 |
15647767
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Sarcomas represent a rational target for this approach given the high frequency of p53 mutations (40-75%) and MDM-2 amplification (10-30%).
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2 |
15647767
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Immunohistochemistry of the metastatic lesions prior to treatment showed that five out of six patients were positive for p53, while two patients also had mdm-2 overexpression.
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3 |
15647767
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One patient with p53 mutation and MDM-2 amplification achieved a partial response to treatment that lasted 11 months.
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4 |
15647767
|
Sarcomas represent a rational target for this approach given the high frequency of p53 mutations (40-75%) and MDM-2 amplification (10-30%).
|
5 |
15647767
|
Immunohistochemistry of the metastatic lesions prior to treatment showed that five out of six patients were positive for p53, while two patients also had mdm-2 overexpression.
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6 |
15647767
|
One patient with p53 mutation and MDM-2 amplification achieved a partial response to treatment that lasted 11 months.
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7 |
15647767
|
Sarcomas represent a rational target for this approach given the high frequency of p53 mutations (40-75%) and MDM-2 amplification (10-30%).
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8 |
15647767
|
Immunohistochemistry of the metastatic lesions prior to treatment showed that five out of six patients were positive for p53, while two patients also had mdm-2 overexpression.
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9 |
15647767
|
One patient with p53 mutation and MDM-2 amplification achieved a partial response to treatment that lasted 11 months.
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10 |
17071473
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Several antigens have been characterized as tumor/leukemia associated antigens (T/LAAs) in B-CLL with the potential to elicit specific anti-tumor response encompassing idiotype immunoglobulin, oncofetal antigen-immature laminin receptor protein (OFAiLRP), survivin, as well as fibromodulin, the receptor for hyaluronic acid mediated motility (RHAMM/CD168) and the murine double-minute 2 oncoprotein (MDM2).
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11 |
17101070
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A variety of new monoclonal antibody (MoAb) agents, such as humanized anti-CD20, alemtuzumab, anti-HLA-DR, anti-CD22 (as an immunotoxin carrier), anti-CD40, as well as MoAb-targeting TRAIL-R1 and TRAIL-R2 are being tested.
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12 |
17101070
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Other targets include gene transcription through histone regulation; nuclear factor-ķB pathway; protein kinase C inhibitors; small-molecules targeting apoptosis, such as antisense Bcl-2, pan-Bcl-2 family member inhibitors; MoAb agonists of cell death receptors; caspases regulators (inhibitors of apoptosis proteins, survivin); and MDM2 antagonist regulators of p53.
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13 |
18779747
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We demonstrate that DCs pulsed with the modified tumor cells efficiently activate T lymphocytes against CLL and that overexpressed Ags related to leukemogenesis, such as BCL-2, MDM2, and ETV5, serve as targets for those T cells.
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14 |
20463003
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Other biologic approaches include the development of oncolytic viruses designed to replicate and kill only p53 defective cells and also the development of siRNA and antisense RNA's that activate p53 by inhibiting the function of the negative regulators Mdm2, MdmX, and HPV E6.
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15 |
21444629
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Synergistic suppression of prostatic cancer cells by coexpression of both murine double minute 2 small interfering RNA and wild-type p53 gene in vitro and in vivo.
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16 |
21444629
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Our objective was to evaluate cell growth and death effects by inhibiting Murine Double Minute 2 (MDM2) expression in human prostate cancer cells overexpressing the wild-type (WT) p53 gene.
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17 |
21444629
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We demonstrated that human prostate tumors had increased expression of MDM2 and mutant p53 proteins.
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18 |
21444629
|
Synergistic suppression of prostatic cancer cells by coexpression of both murine double minute 2 small interfering RNA and wild-type p53 gene in vitro and in vivo.
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19 |
21444629
|
Our objective was to evaluate cell growth and death effects by inhibiting Murine Double Minute 2 (MDM2) expression in human prostate cancer cells overexpressing the wild-type (WT) p53 gene.
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20 |
21444629
|
We demonstrated that human prostate tumors had increased expression of MDM2 and mutant p53 proteins.
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21 |
21444629
|
Synergistic suppression of prostatic cancer cells by coexpression of both murine double minute 2 small interfering RNA and wild-type p53 gene in vitro and in vivo.
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22 |
21444629
|
Our objective was to evaluate cell growth and death effects by inhibiting Murine Double Minute 2 (MDM2) expression in human prostate cancer cells overexpressing the wild-type (WT) p53 gene.
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23 |
21444629
|
We demonstrated that human prostate tumors had increased expression of MDM2 and mutant p53 proteins.
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24 |
23687157
|
The CEL-im cell line has negative telomerase activity, and when compared with the primary passage 2 CEL cell counterpart, mRNA expression of tumor suppressor protein p53, mouse double minute 2 (Mdm2), cyclin dependent kinase (CDK) inhibitor p21 (p21(WAF)), and CDK inhibitor p16 (p16(INK4)) were downregulated in the CEL-im cell line, whereas retinoblastoma (Rb), transcription factor E2F, member 1 (E2F-1), and alternative reading frame of p16(INK4) (ARF) were upregulated.
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25 |
26451325
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In this study, a chimeric antigen receptor (CAR) specific for HERV-K env protein (K-CAR) was generated using anti-HERV-K mAb.
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26 |
26451325
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Furthermore, downregulation of HERV-K expression in tumors of mice treated with K-CAR correlated with upregulation of p53 and downregulation of MDM2 and p-ERK.
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27 |
26451325
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Our results indicate that HERV-K env protein is an oncoprotein and may play an important role in tumorigenesis related to p53 and Ras signaling pathways.
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