Ask about this productRelated genes to: CREBBP antibody
- Gene:
- CREBBP NIH gene
- Name:
- CREB binding protein
- Previous symbol:
- RSTS
- Synonyms:
- RTS, CBP, KAT3A
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-01-10
- Date modifiied:
- 2015-09-11
Related products to: CREBBP antibody
Related articles to: CREBBP antibody
- Metastasis is the leading cause of cancer-related deaths. However, the core determinants and mechanistic principles underlying the metastatic cascade remain elusive. Small cell lung cancer (SCLC) is a highly aggressive malignancy with exceptional metastatic potential and limited therapeutic options. Here, we present Metastasis Originated Barcode Sequencing (MOBA-seq), a high-throughput platform that systematically maps genetic regulators across the metastatic cascade at single-colony resolution. MOBA-seq integrates scalable barcode-based lineage tracing with a computational pipeline that quantitatively deconvolutes genotype-specific effects on metastatic seeding, dormancy, and clonal expansion across hundreds of thousands of metastatic events. Applying this approach to more than 400 candidate regulators of SCLC, we uncovered tissue-specific metastatic suppressors and universal metastatic essential genes. We identified metastatic seeding as the predominant determinant of metastasis. Comparative analysis across recipient mice of distinct genetic backgrounds further revealed that innate immune surveillance constrains metastatic progression by reducing metastatic seeding and enforcing dormancy, with additional modulation by sex and tissue context. We validated the frequently mutated gene as a key metastasis suppressor whose loss enhances SCLC metastasis through both tumor-intrinsic and immune-modulatory mechanisms. This work establishes a scalable and quantitative platform for mapping the metastatic fitness landscape at single-colony resolution across hundreds of thousands of data points. Our approach offers a broadly applicable framework for dissecting the interactions between cancer-intrinsic and microenvironmental factors governing tumor initiation, progression, and therapeutic response. - Source: PubMed
Publication date: 2026/02/23
Roberts ChrisXu AndyFang XiangweiVisani AdriennePeng Chien-WeiQin XuleiChan Irenaeus C CDunterman MadelineGiles David AYou YaoxuanGuppy IsabellaYang ZhangKim Albert HStegh Alexander HLu GuolanChen FengDing LiTang Rui - A subset of triple negative breast cancer (TNBC) patients shows resistance to standard neoadjuvant chemotherapy (NAC), resulting in high relapse and mortality risk. This highlights the need for predictive biomarkers and alternative treatment strategies. Targeted molecular profiling was performed on post-NAC resection specimens from 138 TNBC patients, diagnosed across multiple centers between 2013 and 2022, all exhibiting extensive poor response, defined as >50% residual tumor and the development of distant metastasis. Integrated immunohistochemistry and genomic analyses were conducted to identify potentially targetable alterations. Most post-NAC TNBCs (60%) were HER2-ultralow or HER2-low. Among 85 patients with successful DNA sequencing, 2640 variants were detected, with TP53 mutations being most frequent (94%). Mutation count ranged from 3 to 1668 per patient (median n = 11). Several altered genes, including ERBB2, BRCA1/2, PIK3CA, and RB1, have been associated with favorable responses to targeted therapeutics in clinical trials. Moreover, 208 potential neo-peptide targets (median per patient n = 3) were detected across recurrently mutated genes such as ATM, CREBBP, IRS2, KEAP1, MSH6, NOTCH1, NOTCH2, POLD1, TP53, and TSC2. Molecular profiling of residual disease in extensively poor responding TNBC post-NAC revealed multiple potentially targetable variant, supporting the use of next-generation sequencing to guide personalized strategies for these high-risk TNBC patients. - Source: PubMed
Publication date: 2026/05/13
van den Ende Nadine SSmid MarcelMartens John W MDebets RenoJager Agnesvan Deurzen Carolien H M - Acute lymphoblastic leukemia (ALL) is a genetically heterogeneous malignancy characterized by a broad spectrum of chromosomal and gene abnormalities that define distinct genetic subtypes driving disease development. Although numerous driver fusion genes have been documented, a considerable proportion of ALL cases remain inadequately defined, classified, and consequently lack access to precisely targeted therapies. Herein, we report a case of high-risk B-ALL harboring four novel fusion gene transcripts-MAN1A1::GRIK2, ZCCHC7::CASC11, OSTM1-AS1::ZBTB24, and IGL::BCL6-along with concurrent mutations in CREBBP, BCL2, and ARID1B. These four novel fusion genes, particularly the BCL6 rearrangement, may represent a genetic feature that warrants further investigation in B-ALL. The patient received induction therapy with a modified COP regimen (cyclophosphamide, vindesine, dexamethasone) combined with the BCL2 inhibitor venetoclax, achieving a rapid and sustained complete remission. This case suggests that integrating deep genomic analysis can help identify potentially actionable therapeutic targets and provides preliminary clinical evidence supporting the efficacy of modified COP plus venetoclax in high-risk B-ALL with similar molecular features, highlighting a promising precision medicine strategy. - Source: PubMed
Tu JifangWang HuanpingWang YunguiZhou JunhaoGao XiangliLou YinjunTong Hongyan - - Source: PubMed
Publication date: 2026/05/11
Jackson Soyini R CDin Nasir UdQureshi Madiha BStoehr RobertAgaimy AbbasDickson Brendan C - Rubinstein Taybi syndrome (RSTS), a rare congenital disease, is caused by mutations in lysine acetyl transferase type 3 (KAT3) genes, EP300 and CREBBP. Many of the tissues affected in RSTS are derived from the neural crest (NC). Hence, we proposed that NC development would be perturbed in RSTS. - Source: PubMed
Publication date: 2026/05/11
Verma ShwetaDalabehera SujitGowda SubhashChandrasekaran KoushikaSingh DayanidhiPrasher BhavanaBapat SharmilaRamalingam SivaprakashSachidanandan Chetana