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Artikel: MTBP and MYC: A Dynamic Duo in Proliferation, Cancer, and Aging.

Grieb, Brian C / Eischen, Christine M

2022 Band 11, Heft 6

Abstract: The oncogenic transcription factor c-MYC (MYC) is highly conserved across species and is frequently overexpressed or dysregulated in human cancers. MYC regulates a wide range of critical cellular and oncogenic activities including proliferation, ... ...

Abstract	The oncogenic transcription factor c-MYC (MYC) is highly conserved across species and is frequently overexpressed or dysregulated in human cancers. MYC regulates a wide range of critical cellular and oncogenic activities including proliferation, metabolism, metastasis, apoptosis, and differentiation by transcriptionally activating or repressing the expression of a large number of genes. This activity of MYC is not carried out in isolation, instead relying on its association with a myriad of protein cofactors. We determined that MDM Two Binding Protein (MTBP) indirectly binds MYC and is a novel MYC transcriptional cofactor. MTBP promotes MYC-mediated transcriptional activity, proliferation, and cellular transformation by binding in a protein complex with MYC at MYC-bound promoters. This discovery provided critical context for data linking MTBP to aging as well as a rapidly expanding body of evidence demonstrating MTBP is overexpressed in many human malignancies, is often linked to poor patient outcomes, and is necessary for cancer cell survival. As such, MTBP represents a novel and potentially broad reaching oncologic drug target, particularly when MYC is dysregulated. Here we have reviewed the discovery of MTBP and the initial controversy with its function as well as its associations with proliferation, MYC, DNA replication, aging, and human cancer.
Sprache	Englisch
Erscheinungsdatum	2022-06-08
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article ; Review
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology11060881
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: HER2-Directed Therapy in Advanced Gastric and Gastroesophageal Adenocarcinoma: Triumphs and Troubles.

Grieb, Brian C / Agarwal, Rajiv

Current treatment options in oncology

2021 Band 22, Heft 10, Seite(n) 88

Abstract: Opinion statement: Gastric and gastroesophageal junction (GEJ) cancers represent the third leading cause of malignancy-associated death worldwide. Approximately 15-20% of these adenocarcinomas overexpress the human epidermal growth factor receptor 2 ( ... ...

Abstract	Opinion statement: Gastric and gastroesophageal junction (GEJ) cancers represent the third leading cause of malignancy-associated death worldwide. Approximately 15-20% of these adenocarcinomas overexpress the human epidermal growth factor receptor 2 (HER2), a pro-proliferative receptor tyrosine kinase that has been therapeutically exploited in other disease contexts. The landmark ToGA trial demonstrated that trastuzumab, an anti-HER2 antibody, could improve overall survival for patients with HER2 overexpressing advanced gastric and GEJ adenocarcinomas. In the ensuing decade, great effort has been made to refine and expand this therapeutic strategy through a variety of avenues including optimization of chemotherapy backbones, identifying potential synergy with immune checkpoint inhibition, deployment of alternative HER2-targeted antibodies, use of small molecule inhibitors, and development of HER2-directed antibody drug conjugates. While the results of these efforts have had variable success, they have led to a greater understanding of the mechanisms of both primary and acquired resistance to HER2-directed therapies, laying the groundwork for future investigations. Recently, KEYNOTE-811 and DESTINY-Gastric01 have led to the FDA approvals of pembrolizumab in combination with trastuzumab and chemotherapy in the 1st-line advanced setting and trastuzumab deruxtecan (fam-trastuzumab deruxtecan-nxki) in the 2nd-line setting, respectively. Herein, we review these significant works as well as discuss the ongoing investigations they have inspired, which aim to find and utilize additional means for targeting HER2 in gastric and GEJ cancers.
Mesh-Begriff(e)	Adenocarcinoma/drug therapy ; Adenocarcinoma/genetics ; Adenocarcinoma/metabolism ; Antibodies, Monoclonal, Humanized/administration & dosage ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Capecitabine/administration & dosage ; Cisplatin/administration & dosage ; Clinical Trials as Topic ; Drug Combinations ; Drug Resistance, Neoplasm ; Esophagogastric Junction ; Fluorouracil/administration & dosage ; Humans ; Irinotecan/administration & dosage ; Lapatinib/administration & dosage ; Oxaliplatin/administration & dosage ; Oxonic Acid/administration & dosage ; Paclitaxel/administration & dosage ; Receptor, ErbB-2/genetics ; Receptor, ErbB-2/metabolism ; Stomach Neoplasms/drug therapy ; Stomach Neoplasms/genetics ; Stomach Neoplasms/metabolism ; Tegafur/administration & dosage ; Trastuzumab/administration & dosage
Chemische Substanzen	Antibodies, Monoclonal, Humanized ; Drug Combinations ; Oxaliplatin (04ZR38536J) ; Lapatinib (0VUA21238F) ; S 1 (combination) (150863-82-4) ; Tegafur (1548R74NSZ) ; Oxonic Acid (5VT6420TIG) ; Capecitabine (6804DJ8Z9U) ; Irinotecan (7673326042) ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1) ; pertuzumab (K16AIQ8CTM) ; Trastuzumab (P188ANX8CK) ; Paclitaxel (P88XT4IS4D) ; Cisplatin (Q20Q21Q62J) ; Fluorouracil (U3P01618RT)
Sprache	Englisch
Erscheinungsdatum	2021-08-23
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2057351-0
ISSN	1534-6277 ; 1527-2729
ISSN (online)	1534-6277
ISSN	1527-2729
DOI	10.1007/s11864-021-00884-7
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: MTBP and MYC: A Dynamic Duo in Proliferation, Cancer, and Aging

Grieb, Brian C. / Eischen, Christine M.

Biology. 2022 June 08, v. 11, no. 6

2022

Abstract	The oncogenic transcription factor c-MYC (MYC) is highly conserved across species and is frequently overexpressed or dysregulated in human cancers. MYC regulates a wide range of critical cellular and oncogenic activities including proliferation, metabolism, metastasis, apoptosis, and differentiation by transcriptionally activating or repressing the expression of a large number of genes. This activity of MYC is not carried out in isolation, instead relying on its association with a myriad of protein cofactors. We determined that MDM Two Binding Protein (MTBP) indirectly binds MYC and is a novel MYC transcriptional cofactor. MTBP promotes MYC-mediated transcriptional activity, proliferation, and cellular transformation by binding in a protein complex with MYC at MYC-bound promoters. This discovery provided critical context for data linking MTBP to aging as well as a rapidly expanding body of evidence demonstrating MTBP is overexpressed in many human malignancies, is often linked to poor patient outcomes, and is necessary for cancer cell survival. As such, MTBP represents a novel and potentially broad reaching oncologic drug target, particularly when MYC is dysregulated. Here we have reviewed the discovery of MTBP and the initial controversy with its function as well as its associations with proliferation, MYC, DNA replication, aging, and human cancer.
Schlagwörter	DNA replication ; apoptosis ; cell viability ; drugs ; humans ; metabolism ; metastasis ; neoplasm cells ; patients ; transcription (genetics) ; transcription factors
Sprache	Englisch
Erscheinungsverlauf	2022-0608
Erscheinungsort	Multidisciplinary Digital Publishing Institute
Dokumenttyp	Artikel
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology11060881
Datenquelle	NAL Katalog (AGRICOLA)

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Artikel ; Online: New Opportunities for Minimizing Toxicity in Rectal Cancer Management.

Couwenberg, Alice M / Varvoglis, Dimitrios N / Grieb, Brian C / Marijnen, Corrie A M / Ciombor, Kristen K / Guillem, Jose G

American Society of Clinical Oncology educational book. American Society of Clinical Oncology. Annual Meeting

2023 Band 43, Seite(n) e389558

Abstract: Advances in multimodal management of locally advanced rectal cancer (LARC), consisting of preoperative chemotherapy and/or radiotherapy followed by surgery with or without adjuvant chemotherapy, have improved local disease control and patient survival ... ...

Abstract	Advances in multimodal management of locally advanced rectal cancer (LARC), consisting of preoperative chemotherapy and/or radiotherapy followed by surgery with or without adjuvant chemotherapy, have improved local disease control and patient survival but are associated with significant risk for acute and long-term morbidity. Recently published trials, evaluating treatment dose intensification via the addition of preoperative induction or consolidation chemotherapy (total neoadjuvant therapy [TNT]), have demonstrated improved tumor response rates while maintaining acceptable toxicity. In addition, TNT has led to an increased number of patients achieving a clinical complete response and thus eligible to pursue a nonoperative, organ-preserving, watch and wait approach, thereby avoiding toxicities associated with surgery, such as bowel dysfunction and stoma-related complications. Ongoing trials using immune checkpoint inhibitors in patients with mismatch repair-deficient tumors suggest that this subgroup of patients with LARC could potentially be treated with immunotherapy alone, sparing them the toxicity associated with preoperative treatment and surgery. However, the majority of rectal cancers are mismatch repair-proficient and less responsive to immune checkpoint inhibitors and require multimodal management. The synergy noted in preclinical studies between immunotherapy and radiotherapy on immunogenic tumor cell death has led to the design of ongoing clinical trials that explore the benefit of combining radiotherapy, chemotherapy, and immunotherapy (mainly of immune checkpoint inhibitors) and aim to increase the number of patients eligible for organ preservation.
Mesh-Begriff(e)	Humans ; Immune Checkpoint Inhibitors ; Rectal Neoplasms ; Immunotherapy ; Brain Neoplasms ; Chemotherapy, Adjuvant ; Neoplasms, Second Primary
Chemische Substanzen	Immune Checkpoint Inhibitors
Sprache	Englisch
Erscheinungsdatum	2023-06-10
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	2431126-1
ISSN	1548-8756 ; 1548-8748
ISSN (online)	1548-8756
ISSN	1548-8748
DOI	10.1200/EDBK_389558
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Evolving Landscape of Systemic Therapy for Hepatocellular Carcinoma: Breakthroughs, Toxicities, and Future Frontiers.

Grieb, Brian C / Goff, Laura W / Goyal, Lipika / Denlinger, Crystal S

American Society of Clinical Oncology educational book. American Society of Clinical Oncology. Annual Meeting

2019 Band 39, Seite(n) 248–260

Abstract: The incidence and death rates of hepatocellular carcinoma (HCC) are rising. For more than a decade, the multikinase inhibitor sorafenib was the only U.S. Food and Drug Administration (FDA)-approved systemic therapy for HCC. However, since 2017, five ... ...

Abstract	The incidence and death rates of hepatocellular carcinoma (HCC) are rising. For more than a decade, the multikinase inhibitor sorafenib was the only U.S. Food and Drug Administration (FDA)-approved systemic therapy for HCC. However, since 2017, five additional agents have been approved in the first- or second-line setting. Although this represents an incredible victory for the field, there are no clear guidelines for agent selection on the basis of either patient or tumor characteristics. Here, we review the available systemic therapy options for advanced HCC and reported clinical data for each. We outline each agent's unique toxicity profile, potential impact on patient quality of life, monitoring recommendations, and supportive strategies. Last, we review molecular and immunologic classifications of HCC as well as preclinical data that may serve as a basis for future biomarker enriched clinical trials to enable precision oncology care in HCC.
Mesh-Begriff(e)	Animals ; Biomarkers, Tumor ; Carcinoma, Hepatocellular/diagnosis ; Carcinoma, Hepatocellular/etiology ; Carcinoma, Hepatocellular/mortality ; Carcinoma, Hepatocellular/therapy ; Clinical Trials as Topic ; Combined Modality Therapy/adverse effects ; Combined Modality Therapy/methods ; Disease Management ; Humans ; Liver Neoplasms/diagnosis ; Liver Neoplasms/etiology ; Liver Neoplasms/mortality ; Liver Neoplasms/therapy ; Molecular Targeted Therapy/adverse effects ; Molecular Targeted Therapy/methods ; Neoplasm Metastasis ; Neoplasm Staging ; Precision Medicine ; Prognosis ; Treatment Outcome
Chemische Substanzen	Biomarkers, Tumor
Sprache	Englisch
Erscheinungsdatum	2019-05-17
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Review
ZDB-ID	2431126-1
ISSN	1548-8756 ; 1548-8748
ISSN (online)	1548-8756
ISSN	1548-8748
DOI	10.1200/EDBK_237555
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Ribosome subunit attrition and activation of the p53-MDM4 axis dominate the response of MLL-rearranged cancer cells to WDR5 WIN site inhibition.

bioRxiv : the preprint server for biology

2024

Abstract: The chromatin-associated protein WD Repeat Domain 5 (WDR5) is a promising target for cancer drug discovery, with most efforts blocking an arginine-binding cavity on the protein called the "WIN" site that tethers WDR5 to chromatin. WIN site inhibitors ( ... ...

Abstract	The chromatin-associated protein WD Repeat Domain 5 (WDR5) is a promising target for cancer drug discovery, with most efforts blocking an arginine-binding cavity on the protein called the "WIN" site that tethers WDR5 to chromatin. WIN site inhibitors (WINi) are active against multiple cancer cell types in vitro, the most notable of which are those derived from MLL-rearranged (MLLr) leukemias. Peptidomimetic WINi were originally proposed to inhibit MLLr cells via dysregulation of genes connected to hematopoietic stem cell expansion. Our discovery and interrogation of small molecule WIN site inhibitors, however, revealed that they act in MLLr cell lines to suppress ribosome protein gene (RPG) transcription, induce nucleolar stress, and activate p53. Because there is no precedent for an anti-cancer strategy that specifically targets RPG expression, we took an integrated multi-omics approach to further interrogate the mechanism of action of WINi in MLLr cancer cells. We show that WINi induce depletion of the stock of ribosomes, accompanied by a broad yet modest translational choke and changes in alternative mRNA splicing that inactivate the p53 antagonist MDM4. We also show that WINi are synergistic with agents including venetoclax and BET-bromodomain inhibitors. Together, these studies reinforce the concept that WINi are a novel type of ribosome-directed anti-cancer therapy and provide a resource to support their clinical implementation in MLLr leukemias and other malignancies.
Sprache	Englisch
Erscheinungsdatum	2024-01-10
Erscheinungsland	United States
Dokumenttyp	Preprint
DOI	10.1101/2023.07.26.550648
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Ribosome subunit attrition and activation of the p53-MDM4 axis dominate the response of MLL-rearranged cancer cells to WDR5 WIN site inhibition.

eLife

2024 Band 12

Abstract: The chromatin-associated protein WD Repeat Domain 5 (WDR5) is a promising target for cancer drug discovery, with most efforts blocking an arginine-binding cavity on the protein called the 'WIN' site that tethers WDR5 to chromatin. WIN site inhibitors ( ... ...

Abstract	The chromatin-associated protein WD Repeat Domain 5 (WDR5) is a promising target for cancer drug discovery, with most efforts blocking an arginine-binding cavity on the protein called the 'WIN' site that tethers WDR5 to chromatin. WIN site inhibitors (WINi) are active against multiple cancer cell types in vitro, the most notable of which are those derived from MLL-rearranged (MLLr) leukemias. Peptidomimetic WINi were originally proposed to inhibit MLLr cells via dysregulation of genes connected to hematopoietic stem cell expansion. Our discovery and interrogation of small-molecule WINi, however, revealed that they act in MLLr cell lines to suppress ribosome protein gene (RPG) transcription, induce nucleolar stress, and activate p53. Because there is no precedent for an anticancer strategy that specifically targets RPG expression, we took an integrated multi-omics approach to further interrogate the mechanism of action of WINi in human MLLr cancer cells. We show that WINi induce depletion of the stock of ribosomes, accompanied by a broad yet modest translational choke and changes in alternative mRNA splicing that inactivate the p53 antagonist MDM4. We also show that WINi are synergistic with agents including venetoclax and BET-bromodomain inhibitors. Together, these studies reinforce the concept that WINi are a novel type of ribosome-directed anticancer therapy and provide a resource to support their clinical implementation in MLLr leukemias and other malignancies.
Mesh-Begriff(e)	Humans ; Antineoplastic Agents/pharmacology ; Cell Cycle Proteins/metabolism ; Cell Cycle Proteins/genetics ; Cell Line, Tumor ; Histone-Lysine N-Methyltransferase/metabolism ; Histone-Lysine N-Methyltransferase/genetics ; Intracellular Signaling Peptides and Proteins/antagonists & inhibitors ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Myeloid-Lymphoid Leukemia Protein/metabolism ; Myeloid-Lymphoid Leukemia Protein/genetics ; Nuclear Proteins/metabolism ; Nuclear Proteins/genetics ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Ribosomes/drug effects ; Ribosomes/metabolism ; Tumor Suppressor Protein p53/metabolism ; Tumor Suppressor Protein p53/genetics ; Peptidomimetics/pharmacology
Chemische Substanzen	Antineoplastic Agents ; Cell Cycle Proteins ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; Intracellular Signaling Peptides and Proteins ; KMT2A protein, human ; MDM4 protein, human ; Myeloid-Lymphoid Leukemia Protein (149025-06-9) ; Nuclear Proteins ; Proto-Oncogene Proteins ; TP53 protein, human ; Tumor Suppressor Protein p53 ; WDR5 protein, human ; Peptidomimetics
Sprache	Englisch
Erscheinungsdatum	2024-04-29
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.90683
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Haploinsufficiency of the Myc regulator Mtbp extends survival and delays tumor development in aging mice.

Grieb, Brian C / Boyd, Kelli / Mitra, Ramkrishna / Eischen, Christine M

Aging

2016 Band 8, Heft 10, Seite(n) 2590–2602

Abstract: Alterations of specific genes can modulate aging. Myc, a transcription factor that regulates the expression of many genes involved in critical cellular functions was shown to have a role in controlling longevity. Decreased expression of Myc inhibited ... ...

Abstract	Alterations of specific genes can modulate aging. Myc, a transcription factor that regulates the expression of many genes involved in critical cellular functions was shown to have a role in controlling longevity. Decreased expression of Myc inhibited many of the deleterious effects of aging and increased lifespan in mice. Without altering Myc expression, reduced levels of Mtbp, a recently identified regulator of Myc, limit Myc transcriptional activity and proliferation, while increased levels promote Myc-mediated effects. To determine the contribution of Mtbp to the effects of Myc on aging, we studied a large cohort of
Mesh-Begriff(e)	Aging/genetics ; Aging/pathology ; Animals ; Body Weight/genetics ; Carcinogenesis/genetics ; Carcinogenesis/pathology ; Carrier Proteins/genetics ; Haploinsufficiency ; Litter Size/genetics ; Longevity/genetics ; Mice ; Motor Activity/genetics ; Proto-Oncogene Proteins c-myc/genetics
Chemische Substanzen	Carrier Proteins ; Mtbp protein, mouse ; Proto-Oncogene Proteins c-myc
Sprache	Englisch
Erscheinungsdatum	2016-10-31
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.101092
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: MTBP is overexpressed in triple-negative breast cancer and contributes to its growth and survival.

Grieb, Brian C / Chen, Xi / Eischen, Christine M

Molecular cancer research : MCR

2014 Band 12, Heft 9, Seite(n) 1216–1224

Abstract: Unlabelled: Triple-negative breast cancer (TNBC) is a clinically aggressive subtype of breast cancer commonly resistant to therapeutics that have been successful in increasing survival in patients with estrogen receptor-positive (ER(+)) and HER2(+) ... ...

Abstract	Unlabelled: Triple-negative breast cancer (TNBC) is a clinically aggressive subtype of breast cancer commonly resistant to therapeutics that have been successful in increasing survival in patients with estrogen receptor-positive (ER(+)) and HER2(+) breast cancer. As such, identifying factors that contribute to poor patient outcomes and mediate the growth and survival of TNBC cells remain important areas of investigation. MTBP (MDM2-binding protein), a gene linked to cellular proliferation and a transcriptional target of the MYC oncogene, is overexpressed in human malignancies, yet its contribution to cancer remains unresolved. Evaluation of mRNA expression and copy number variation data from The Cancer Genome Atlas (TCGA) revealed that MTBP is commonly overexpressed in breast cancer and 19% show amplification of MTBP. Increased transcript or gene amplification of MTBP significantly correlated with reduced breast cancer patient survival. Further analysis revealed that while MTBP mRNA is overexpressed in both ER(+) and HER2(+) breast cancers, its expression is highest in TNBC. MTBP mRNA and protein levels were also significantly elevated in a panel of human TNBC cell lines. Knockdown of MTBP in TNBC cells induced apoptosis and significantly reduced TNBC cell growth and soft agar colony formation, which was rescued by expression of shRNA-resistant Mtbp. Notably, inducible knockdown of MTBP expression significantly impaired TNBC tumor growth, in vivo, including in established tumors. Thus, these data emphasize that MTBP is important for the growth and survival of TNBC and warrants further investigation as a potential novel therapeutic target. Implications: MTBP significantly contributes to breast cancer survival and is a potential novel therapeutic target in TNBC.
Mesh-Begriff(e)	Apoptosis/genetics ; Carrier Proteins/biosynthesis ; Carrier Proteins/genetics ; Cell Line, Tumor ; Cell Proliferation/genetics ; Cell Survival/genetics ; DNA Copy Number Variations/genetics ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Molecular Targeted Therapy ; RNA, Small Interfering ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/pathology
Chemische Substanzen	Carrier Proteins ; MTBP protein, human ; RNA, Small Interfering
Sprache	Englisch
Erscheinungsdatum	2014-05-27
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-14-0069
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Synergistic action of WDR5 and HDM2 inhibitors in SMARCB1-deficient cancer cells.

Florian, Andrea C / Woodley, Chase M / Wang, Jing / Grieb, Brian C / Slota, Macey J / Guerrazzi, Kiana / Hsu, Chih-Yuan / Matlock, Brittany K / Flaherty, David K / Lorey, Shelly L / Fesik, Stephen W / Howard, Gregory C / Liu, Qi / Weissmiller, April M / Tansey, William P

NAR cancer

2022 Band 4, Heft 1, Seite(n) zcac007

Abstract: Rhabdoid tumors (RT) are rare and deadly pediatric cancers driven by loss ... ...

Abstract	Rhabdoid tumors (RT) are rare and deadly pediatric cancers driven by loss of
Sprache	Englisch
Erscheinungsdatum	2022-03-03
Erscheinungsland	England
Dokumenttyp	Journal Article
ISSN	2632-8674
ISSN (online)	2632-8674
DOI	10.1093/narcan/zcac007
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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