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Gotowa bibliografia na temat „=aacr2 700=aacr2”

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Data publikacji: 29 lipca 2024
Data aktualizacji: 31 lipca 2024

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Artykuły w czasopismach na temat "=aacr2 700=aacr2"

1

Yang, Yuanchu J., Sam Rubinstein i Jeremy Lyle Warner. "Markers of immune checkpoint inhibitor efficacy in the AACR Project GENIE database." Journal of Clinical Oncology 38, nr 15_suppl (20.05.2020): e15091-e15091. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e15091.

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e15091 Background: Although immune checkpoint inhibitors (ICIs) have been shown to be effective in many tumor types, some highly lethal cancers are not responsive to ICI. Potential biomarkers of ICI response include tumor mutational burden (TMB), which is thought to correlate with increased neoantigen production, and 9p24.1 copy number gain (CNG), which can result in over-expression of programmed death ligand 1 (PD-L1). 9p24.1 CNGs have been described in ICI-sensitive (ICI-S) hematologic malignancies (e.g., Hodgkin lymphoma), but are not well described in solid malignancy. We sought to investigate TMB and 9p24.1 CNG for ICI-S and ICI-resistant (ICI-R) tumor types in the publicly available AACR Project GENIE database, version 7.0. Methods: TMB was calculated by counting somatic mutations with tumor reference allele frequency ≥5% and sequencing depth ≥200X. Samples with < 0.5 MB sequenced were excluded. 9p24.1 CNG was extrapolated from gene-level data. Samples with two or more consecutive gene amplifications in the 9p24.1 region were determined to have 9p24.1 CNG. Samples whose sequencing assay did not include at least two genes in 9p24.1 were excluded. Using an overall response rate (ORR) of ≥10% to define ICI-S, we assessed three ICI-S cancers: hepatobiliary cancer (HBC), melanoma (MEL), non-small cell lung cancer (NSCLC); and two ICI-R types: metastatic breast cancer (MBC) & pancreatic ductal adenocarcinoma (PDAC). Groupwise TMB was compared using Wilcoxon rank-sum and 9p24.1 CNG was compared using Chi-squared. Results: MEL had the highest median TMB but a low 9p24.1 CNG rate; NSCLC had the highest rate of 9p24.1 CNG (Table). PDAC had both the lowest median TMB and 9p24.1 CNG rate. As a group, the ICI-S cancers had higher median TMB (p < .001) and 9p24.1 CNG rate (p < .001). Conclusions: Although rates of 9p24.1 CNG were low across the database as a whole, the NSCLC finding replicates findings described in early stage resected NSCLC (Inoue et al. 2016). Relatively high median TMB in MEL may explain ICI-sensitivity in this cancer type. The combination of low median TMB and low rates of 9p24.1 CNG in PDAC may explain the general lack of efficacy of ICIs in this disease. These findings demonstrate the utility of GENIE as a clinico-genomic database, and also highlight the need to identify better markers of responsiveness to these potentially effective but toxic therapies. [Table: see text]
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Emond, Wei B., Rajiv Sawant, Matthis Geitmann, Johan Winquist, Peter Brandt, Ulf Bremberg, Per Källblad i in. "Abstract 705: Potentiation of immunotherapy by LSD1 modulation". Cancer Research 83, nr 7_Supplement (4.04.2023): 705. http://dx.doi.org/10.1158/1538-7445.am2023-705.

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Abstract LSD1 has emerged as a potential therapeutic target to increase the effectiveness of cancer immunotherapy. We have developed a series of novel small molecules, exemplified by the lead substance BEA-17, that modulates LSD1 via binding to an allosteric site, without directly inhibiting its enzymatic activity. In cells, BEA-17 induces a reduction of LSD1 levels. In addition, BEA-17 upregulates the expression of endogenous retroviral genes and T cell-attractant chemokines and does so in an LSD1-dependent manner. In a co-culture of HeLa and PBMCs, BEA-17 increases cell kill of cancer cells by immune effector T cells, also in an LSD1-dependent manner. In a CT26 syngeneic animal model of colon cancer, BEA-17 potentiates the activity of anti-PD1 inhibitors. Finally, in a syngeneic GL261 animal model of glioblastoma, BEA-17 increases the effectiveness of standard-of-care temozolomide + radiation. Citation Format: Wei B. Emond, Rajiv Sawant, Matthis Geitmann, Johan Winquist, Peter Brandt, Ulf Bremberg, Per Källblad, Vendela Parrow, Claes Andersson, Kristin Blom, Nasrin Najafi, Tobias Bergström, Fredrik J. Swartling, Mats Hellström, Konrad F. Koehler. Potentiation of immunotherapy by LSD1 modulation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 705.
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Lee, John J., Bernice C. Nounamo, Fariba Jousheghany, Issam Makhoul, Eric R. Siegel, Thomas Kieber-Emmons i Behjatolah Monzavi-Karbassi. "Abstract 700: Induction of cancer-specific T-cell responses in patients immunized with P10s-PADRE vaccine". Cancer Research 83, nr 7_Supplement (4.04.2023): 700. http://dx.doi.org/10.1158/1538-7445.am2023-700.

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Abstract Introduction: HR+/HER2− breast cancer is the most common form of breast cancer in the United States. HR+/HER2− tumors are known for a low number of tumor-infiltrating lymphocytes (TILs) and considered less immunogenic than other breast cancer subtypes. We have demonstrated that vaccination with P10s-PADRE, a carbohydrate-mimetic-based peptide, cancer vaccine in combination with standard-of-care chemotherapy in HR+/HER2− breast cancer patients led to an increase in TILs and stromal CD3+ T cells. The current study was performed to determine the vaccine specificity and anti-tumor functionality of T cells in treated patients. Methods: Peripheral blood mononuclear cells (PBMCs) collected at the baseline and after vaccination were used in T-cell assays by multi-color ELISpot, examining Th1, Th2, and cytotoxic responses. PBMCs were also interrogated for the vaccine-induced changes in immune gene expression by next-generation RNA-seq analysis. Results: We observed a significant increase in IFN-g, but not in IL-5 or IL-10, responses in post-immune PBMCs after stimulation with P10s, P10s-PADRE and polyclonal stimulation of T cells by anti-CD3/CD28 antibodies. Stimulation with cancer cell lysate resulted in a strikingly high IFN-g response in post-immune samples. Determining the trio of IFN-g, GzB, and IL-2 together with CD4/CD8 cell proliferation assays of consequent post vaccination specimens established the dynamics of effector T-cell populations. RNA-seq data clearly distinguished post-treatment samples by the increase in immune cell activation, cytokine response, and antigen presentation. Conclusions: The data indicate that immunization of HR+/HER2− breast cancer patients with P10s-PADRE in combination with chemotherapy leads to specific activation of T-cells that recognize breast cancer cells. Improving immunogenicity of such immunologically cold tumors could increase the effectiveness of standard therapeutic approaches. Citation Format: John J. Lee, Bernice C. Nounamo, Fariba Jousheghany, Issam Makhoul, Eric R. Siegel, Thomas Kieber-Emmons, Behjatolah Monzavi-Karbassi. Induction of cancer-specific T-cell responses in patients immunized with P10s-PADRE vaccine [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 700.
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Miller, Madison E., Myah Bell, Priscella Holland, Vanessa Ibrahim, Gordon Jacobsen i Monique Swain. "Abstract A069: The impact of race and glycemic control on triple negative breast cancer in type 2 diabetics". Cancer Epidemiology, Biomarkers & Prevention 32, nr 1_Supplement (1.01.2023): A069. http://dx.doi.org/10.1158/1538-7755.disp22-a069.

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Abstract Although the association between type 2 diabetes (T2D) and breast cancer is well established, the relationship between glycemic control and breast cancer by hormone receptor subtype is poorly understood. We sought to investigate the relationship between glycemic control and the incidence of triple negative breast cancer (TNBC) among patients with T2D. Furthermore, we hoped to elucidate whether this hypothesized risk was further moderated by demographic factors, such as patient race. METHODS: A retrospective cohort study evaluating 1,679 patients with T2D diagnosed with breast cancer between 2010-2020 was conducted. Data including tumor hormone receptor status, Hgb A1c measured within 3 months of cancer diagnosis date, and patient race were ascertained via chart review. Tumor subtype was categorized as either hormone receptor-positive (ER+, PR+ or both) or triple-negative (ER/PR- and HER2/neu-). Based on Hgb A1c measurements, subjects were assigned to one of three categories of glycemic control: well-controlled (Hgb A1c less than 7.0), moderately controlled (Hgb A1c 7.0-9.4), or poorly controlled (Hgb A1c greater than or equal to 9.5) T2D. RESULTS: Accounting for all study subjects, the incidence of TNBC increased with worsening glycemic control (12.7% vs 15.2% vs 21.8%, P=0.040). Among non-Hispanic White patients, a significant increase in the incidence of TNBC with worsening glycemic control was also observed (9.2% vs 13.2% vs 21.9%, P=.010). Among Black patients, the incidence of TNBC did not significantly change across the three levels of glycemic control (17.6% vs 17.6% vs 22.7%, P=.700). Comparing the incidence rates of breast cancer by subtype between non-Hispanic White and Black patients across the three categories of glycemic control, a significant difference was only observed among patients with well-controlled T2D (17.6% of Black patients with TNBC versus 9.2% of non-Hispanic White patients, P&lt;.001; 87.4% of non-Hispanic White patients with hormone receptor positive breast cancer versus 75.6% of Black patients, P&lt;.001). CONCLUSION: Poor glycemic control is associated with a higher incidence of TNBC in patients with T2D overall. A significant increase in the incidence of TNBC with lesser degrees of glycemic control was only observed in the population of non-Hispanic white patients. Although previous studies have shown that Black patients are 2-3 times more likely to develop TNBC than their non-Hispanic White counterparts, a statistically significant racial difference in the rates of breast cancer by subtype was only noted among those with well-controlled T2D. Together our data not only suggests that T2D may serve as a modifiable risk factor for the development of TNBC, but also that the risk conferred by poor glycemic control may bear more significance for non-Hispanic White patients than Black patients. Citation Format: Madison E. Miller, Myah Bell, Priscella Holland, Vanessa Ibrahim, Gordon Jacobsen, Monique Swain. The impact of race and glycemic control on triple negative breast cancer in type 2 diabetics [abstract]. In: Proceedings of the 15th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2022 Sep 16-19; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2022;31(1 Suppl):Abstract nr A069.
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Chen, Jiani, Jinhua Wu, Jeff Schubert, Fumin Lin, Elizabeth H. Denenberg, Alison Muir, Edward J. Romasko i in. "The spectrum of RAF1 fusion positive solid tumors in children and young adults." Journal of Clinical Oncology 41, nr 16_suppl (1.06.2023): e22013-e22013. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.e22013.

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e22013 Background: The RAF1 gene encodes a kinase protein in the MAPK signaling pathway. Fusions involving RAF1 have been reported in solid tumors with a higher prevalence in melanoma, breast cancer, non-small cell lung cancer, and brain tumors. The fusions typically replace the N-terminal autoinhibitory domain with the 5’ partner genes leading to autonomous activation of RAF1 kinase. The efficacy of MEK inhibitors as a potential treatment for RAF1 fusion positive tumors is under investigation. Here we present a cohort of 8 RAF1 fusions involved in a spectrum of tumors in children and young adults. Methods: A retrospective search for tumors harboring RAF1 fusion was performed using our clinical database from 2016 to date. The RNA fusion analysis targets >700 exons of 117 genes for known and novel fusions. Additional genomic alterations, tumor type, and patient demographics were also collected. Results: A total of 8 cases positive for RAF1 fusion were identified from 2526 solid tumors including 6 brain tumors, 1 sarcoma, and 1 hepatoblastoma. Histologic diagnoses of the brain tumors were mostly low grade gliomas with no other driver mutations. Two pilocytic astrocytomas harbored RAF1 fusions without the pathognomonic KIAA1549: BRAF fusions. Although RAF1 fusions have been reported in rhabdomyosarcomas, it is the first time that a RAF1 fusion is associated with hepatoblastoma. 4 of the 8 RAF1 fusions identified are novel (noted with * in the table). The break points in RAF1 were at exon 7, 8, or 10, demonstrating the retention of the kinase domain. Conclusions: We report 8 RAF1 fusion positive solid tumors in children and young adults, mainly in low-grade gliomas. Although rare, the presence of a RAF1 fusion not only facilitates the tumor diagnosis but also provides genomic evidence for potential targeted therapies. References: 1. The AACR Project GENIE Consortium. AACR Project GENIE: powering precision medicine through an international consortium. Cancer Discovery. 2017;7(8):818-831. 2. McEvoy CR et al. Profound MEK inhibitor response in a cutaneous melanoma harboring a GOLGA4-RAF1 fusion. J Clin Invest. 2019; 129:1940-1945. [Table: see text]
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Wang, Zhishen. "Abstract 1419: Single molecule detection of human heparanase". Cancer Research 82, nr 12_Supplement (15.06.2022): 1419. http://dx.doi.org/10.1158/1538-7445.am2022-1419.

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Abstract Heparanase, a mammalian endo-β-D-glucuronidase, is the only known enzyme responsible for the cleavage of heparan sulfate (HS) side chains of heparan sulfate proteoglycans (HSPGs). Its activity is implicated in various disease conditions such as tumor growth, angiogenesis, metastasis, chronic inflammation and diabetic nephropathy. Detecting the activity of heparanase thus is a promising approach for the discovery of diagnostics and therapeutics for these diseases. We have developed an activity-based disaccharide probe for heparanase, which offers over 700-fold of fluorescence increase in the presence of human heparanase. In this project, we aim to build up an ultrasensitive single heparanase detection system by coupling a sensitive fluorogenic probe with a microwell-based device. The microwell-based device is designed to achieve single enzyme separation and significantly increase the sensitivity of detection. This system is being validated using recombinant human heparanase and will be used to analyze clinical samples from breast cancer patients. Citation Format: Zhishen Wang. Single molecule detection of human heparanase [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1419.
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Pecoraro, Adam F., Tooba Rashid, Breanne A. Burgess, Corinne M. Linardic i Michael D. Deel. "Abstract 700: Targeting transcriptional co-activators YAP1/TAZ in fusion-positive rhabdomyosarcoma demonstrates a novel strategy in ablating fusion-driven sarcoma transcriptional programing". Cancer Research 82, nr 12_Supplement (15.06.2022): 700. http://dx.doi.org/10.1158/1538-7445.am2022-700.

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Abstract Background: Approximately one third of all sarcomas are characterized by recurrent chromosomal translocations, and these fusion-positive sarcomas remain among the most difficult to treat of all malignancies. Rhabdomyosarcoma is the most common soft tissue sarcoma of childhood and a prototype fusion-oncogene-driven tumor. Fusion-positive rhabdomyosarcoma (FP-RMS) is driven by a chromosomal translocation encoding for the pathognomonic chimeric fusion product PAX3-FOXO1 (P3F). Because it is a large inherently disordered transcription factor lacking drug-binding sites, conventional efforts to directly target P3F have thus far proven futile, and 5-yr overall survival rates remain below 50%. Objective: We thus sought to identify therapeutically tractable co-activators or co-regulators that represent vulnerabilities to P3F transcriptional programing. Methods/Results: Interrogation of transcriptomic data and immunohistochemical (IHC) staining of human tissue microarrays demonstrated the transcriptional co-activators YAP1 and TAZ are highly abundant in FP-RMS tumors. We performed genetic gain- and loss-of-function experiments using RNAi and CRISPR/Cas9 to determine that YAP1/TAZ regulate many FP-RMS cancer phenotypes, including proliferation and xenograft tumor growth. Mechanistic studies using co-immunoprecipitation (co-IP) and co-IP-coupled mass spectrometry revealed a YAP1/TAZ-P3F physical interaction and that YAP1/TAZ and P3F share an enrichment for co-immunoprecipitated proteins involved in chromatin remodeling and DNA binding as well as transcriptional regulation. Functional studies using qRT-PCR, immunoblots, and reporter assays demonstrated YAP1/TAZ are positive regulators of P3F-mediated transcriptional activity. Unbiased approaches using RNA-Seq and quantitative tandem mass tag proteomics also demonstrated that YAP1/TAZ positively regulate the differential expression of P3F’s targets and gene signature. Pharmacologically targeting the YAP1/TAZ-P3F axis using novel NUAK1/2 kinase inhibitors that lead to YAP1/TAZ nuclear exclusion cause cell cycle arrest at the G2/M checkpoint as well as a decrease in FP-RMS cell viability through induction of apoptosis. Main Conclusions: Transcriptional co-activators YAP1/TAZ are highly abundant in FP-RMS tumors and are required for numerous FP-RMS cancer phenotypes. YAP1/TAZ physically associate with P3F to regulate P3F-mediated transcriptional activity. Therefore, while directly targeting P3F is not currently viable, we have identified YAP1/TAZ as therapeutically tractable dependencies to P3F transcriptional programing. Citation Format: Adam F. Pecoraro, Tooba Rashid, Breanne A. Burgess, Corinne M. Linardic, Michael D. Deel. Targeting transcriptional co-activators YAP1/TAZ in fusion-positive rhabdomyosarcoma demonstrates a novel strategy in ablating fusion-driven sarcoma transcriptional programing [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 700.
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Zhu, Xiangzhu, Xiang Huang, Yinan Zheng, Wei Zhang, Lihua Shu, Reid Ness, Harvey J. Murff i in. "Abstract CT534: Magnesium treatment on the demethylation of chemokine (C-X-C motif) ligand 9 (CXCL9) gene, results from the personalized prevention of colorectal cancer trial". Cancer Research 82, nr 12_Supplement (15.06.2022): CT534. http://dx.doi.org/10.1158/1538-7445.am2022-ct534.

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Abstract Background: Chemokine ligand 9 (CXCL9), a T-cell chemoattractant, plays a critical role in regulating antitumor immunity in cancer immunotherapy, i.e., clinical responses to anti-PD(L)-1 treatment. Very recently, CXCL9 was identified as the strongest contributor to the “inflammatory clock of aging”, linked to age-related chronic inflammation. Due to the critical role of magnesium (Mg) in regulating inflammatory responses, this study aims to investigate the effect of Mg treatment on DNA methylation changes in CXCL9. Methods: The Personalized Prevention of Colorectal Cancer Trial conducted at Vanderbilt University Medical Center was a double-blind 2 × 2 factorial randomized controlled trial of 240 participants who completed the study. Participants aged from 40 to 85 years, had a daily calcium intake 700-2000 mg and calcium:magnesium intake ratio ≥2.6 based on the average of the two baseline 24-hour dietary recalls. Results: Among three CpG sites, a 12-week personalized dose of Mg supplementation marginally increased the 5-hydroxymethylcytosine methylation, a measure of active demethylation, at CpG site 04038163 (3'UTR of CXCL9 gene) by 7.0% compared to the placebo group (p=0.07). Although the overall effect was not significant or of borderline significance, Mg treatment significantly reduced the levels of 5-hydroxymethylcytosine by 3.7% at the CpG site 12793812 (body of CXCL9 gene) among those with aged 60 years or above (p=0.03). Conclusions: These findings indicate that Mg treatment modified the demethylation process in the CXCL9 gene, a critical regulator of immune responses and inflammation. Future studies are needed to examine if Mg treatment also changes the circulating levels of CXCL9. Citation Format: Xiangzhu Zhu, Xiang Huang, Yinan Zheng, Wei Zhang, Lihua Shu, Reid Ness, Harvey J Murff, Chang Yu, Martha J Shrubsole, Lifang Hou, Qi Dai. Magnesium treatment on the demethylation of chemokine (C-X-C motif) ligand 9 (CXCL9) gene, results from the personalized prevention of colorectal cancer trial [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr CT534.
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Brake, Rachael, Zhaopeng Sun, Mo Dan, Lu Lv, Congcong Niu, Yang Zhang, Mingyue Shen, XiXin Hu, Xiwu Hui i Andrew Kolodziej. "Abstract C121: Development of CRB-701 (SYS6002): A novel site-specific, Nectin-4 targeting ADC". Molecular Cancer Therapeutics 22, nr 12_Supplement (1.12.2023): C121. http://dx.doi.org/10.1158/1535-7163.targ-23-c121.

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Abstract CRB-701 (SYS6002) is a clinical stage, next generation ADC targeting Nectin-4 wherein two monomethyl auristatin E (MMAE) moieties are site-specifically conjugated to a novel Nectin-4 targeting IgG1 antibody via a cleavable linker. Nectin proteins are cell adhesion molecules belonging to the immunoglobulin (Ig) superfamily that participate in cell-to-cell interactions and form adhesion junctions between cells. Nectin-4 is widely expressed in epithelial cancers including bladder, breast, lung, colorectal, pancreatic, and ovarian. By contrast the expression level of Nectin-4 is very low in healthy adult human tissues. Due to this differential expression, Nectin-4 has emerged as a robust tumor associated antigen (TAA) that has been clinically validated in urothelial carcinoma by Enfortumab Vedotin (EV). While approved, EV carries associated toxicity concerns including skin rash, peripheral neuropathy and ocular toxicities that can lead to EV discontinuations and lasting adverse effects. CRB-701 (SYS6002) has demonstrated high affinity Nectin-4 binding (~2ng/ml) across species and has selectivity for Nectin-4 among the Nectin family of proteins (&gt;5000 ng/ml). The antibody retains potent in vitro activity against FcgRI and C1q (&lt;10nM) conferring antibody dependent cellular cytotoxicity (ADCC) and complement dependent cytotoxicity (CDC) activity in vitro. Compared to EV, CRB-701 (SYS6002) reduces free MMAE exposure by 4.8-9.7-fold when adjusted to ADC exposure (AUC) and there is a 2.2-7.4-fold reduction in MMAE in circulation based on Cmax in rats and non-human primates. Collectively these data reflect lower free MMAE in plasma, reducing the risk of MMAE-induced toxicities observed with EV in the clinic. This improved PK and safety profile coincides with a longer half-life of the ADC in plasma potentially reducing the frequency of administration to achieve efficacy. The internalization rate of CRB-701 (SYS6002) was 2-fold faster than EV when assessed in nectin-4 expressing cells. These data may explain the statistically significant reduction in tumor growth observed in a BL0597 patient derived xenograft model (PDX) of bladder cancer with low Nectin-4 protein expression by IHC (H score =50) when compared to EV at the same dose and frequency. Collectively these data suggest that CRB-701 (SYS6002) could demonstrate an improved therapeutic index and PK profile relative to EV and as such could achieve higher tolerated concentrations at lower dose frequency. The stability of the site-specific linker and the reduction in the drug-antibody ratio (DAR) could lead to a differentiated profile clinically that enables higher doses, longer treatment duration and a greater potential in drug combinations in nectin-4 positive tumors. CRB-701 (SYS6002) is currently being explored clinically in a phase 1 dose escalation with an anticipated completion date mid-2024. Citation Format: Rachael Brake, Zhaopeng Sun, Mo Dan, Lu Lv, Congcong Niu, Yang Zhang, Mingyue Shen, XiXin Hu, Xiwu Hui, Andrew Kolodziej. Development of CRB-701 (SYS6002): A novel site-specific, Nectin-4 targeting ADC [abstract]. In: Proceedings of the AACR-NCI-EORTC Virtual International Conference on Molecular Targets and Cancer Therapeutics; 2023 Oct 11-15; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2023;22(12 Suppl):Abstract nr C121.
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Wang, Stephanie. "Abstract A008: An in vivo screening platform based on Ba/F3 kinase-engineered cell lines for discovering next-generation kinase inhibitors". Molecular Cancer Therapeutics 22, nr 12_Supplement (1.12.2023): A008. http://dx.doi.org/10.1158/1535-7163.targ-23-a008.

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Abstract Tongtong Liu, Feng He, Xuyang Duan, Shuliang Li, Chang Liu, Jingying Ning, Feng Hao* KYinno Biotechnology (Beijing) Co., Ltd. No.3 Building, Yizhuang Biomedical Park, Beijing, China. Correspondence: Feng.hao@kyinno.com Protein kinases have become very popular targets in the treatment of cancer and other diseases, and since 2001, the FDA has approved more than 70 kinase inhibitor drugs. However, due to innate or acquired resistance in tumors, most of these small molecule inhibitors only delay tumor progression. The development of next-generation kinase inhibitors with better specificity and lower resistance is still ongoing. Ba/F3 is a mouse pro-B cell line whose survival and proliferation depend on IL-3. After transduction with driver genes such as kinase genes or their mutants, Ba/F3 cells switch from IL-3 dependence to driver gene dependence, making Ba/F3 cells a powerful tool for discovering new kinase inhibitors. Our group has constructed over 700 Ba/F3 engineered cell lines stably transfected with kinase gene mutants. These Ba/F3 kinase cell lines have been fully validated by sequencing, western blotting, and inhibitor testing, covering many popular kinases including EGFR (&gt;150 cell lines), RAS (80 cell lines), FGFR (55 cell lines), ERBB2 (49 cell lines), MET (41 cell lines), RET (39 cell lines), BCR-ABL (37 cell lines), EML4-ALK (33 cell lines), and FLT3 (26 cell lines), etc. Most of these transformed Ba/F3 cell lines can be used for xenograft models in immunodeficient mice. Based on these Ba/F3 kinase cell line-derived xenograft models, we have established an in vivo screening platform to evaluate the efficacy and toxicity of candidate drugs against specific kinase mutation types, as well as their comparison with previous generation drugs. Overall, our data suggest that xenograft models derived from Ba/F3 kinase cell lines are powerful models for discovering next-generation kinase inhibitors. Citation Format: Stephanie Wang. An in vivo screening platform based on Ba/F3 kinase-engineered cell lines for discovering next-generation kinase inhibitors [abstract]. In: Proceedings of the AACR-NCI-EORTC Virtual International Conference on Molecular Targets and Cancer Therapeutics; 2023 Oct 11-15; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2023;22(12 Suppl):Abstract nr A008.
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Książki na temat "=aacr2 700=aacr2"

1

J, Jeník, red. Tropical forest and its environment. Wyd. 2. Harlow: Longman Scientific & Technical, 1987.

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C, Lindberg David, i Westman Robert S, red. Reappraisals of the scientific revolution. Cambridge, [England] ; New York: Cambridge University Press, 1990.

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E, Bottoms A., Light Roy, University of Cambridge. Institute of Criminology. i Cropwood Round-Table Conference (18th : 1986 : Cambridge, England), red. Problems of long-term imprisonment. Aldershot: Gower, 1987.

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Ben, Brewster, red. Life to those shadows. London: BFI Publishing, 1990.

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Ben, Brewster, red. Life to those shadows. Berkeley: University of California Press, 1990.

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Giuseppe, Verdi. La Traviata: Melodramma in tre atti = Oper in drei Akten : Textbuxh Italienisch/Deutsch. Stuttgart: Philipp Reclam jun., 1995.

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E, Dreyfus Stuart, i Athanasiou Tom, red. Mind over machine: The power of human intuition and expertise in the era of the computer. Oxford, UK: B. Blackwell, 1986.

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E, Dreyfus Stuart, i Athanasiou Tom, red. Mind over machine: The power of human intuition and expertise in the era of the computer. New York: Free Press, 1986.

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L, Solow Barbara, i Engerman Stanley L, red. British capitalism and Caribbean slavery: The legacy of Eric Williams. Cambridge [Cambridgeshire]: Cambridge University Press, 1987.

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Homer. Homer's Odyssey. New York: Garland, 1987.

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Streszczenia konferencji na temat "=aacr2 700=aacr2"

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Yamaoka, Masuo, Takahito Hara, Hiroshi Miki, Takenori Hitaka, Tomohiro Kaku, Naohiro Kawaguchi, Hitomi Yamasaki, Toshiyuki Takeuchi, Akihiro Tasaka i Masami Kusaka. "Abstract DD01-03: TAK-700, an inhibitor of 17,20-lyase". W Proceedings: AACR 101st Annual Meeting 2010; Apr 17-21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-dd01-03.

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Kaur, Pali, Victoria Sachs, Amanda L. Christie, David M. Weinstock i James G. Keck. "Abstract 700: Characterization of new AML PDX models: Engraftment kinetics and mutational profile". W Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-700.

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Scrace, Simon F., Elpida Tsonou, Paul Russell, Julie A. Wickenden, Steffen Lawo, Tim M. Scales, Ceri M. Wiggins i Jonathan D. Moore. "Abstract 700: Investigating KRAS synthetic lethal/co-dependency interactions using siRNA and CRISPR". W Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-700.

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Ottaviani, Silvia, Sean Delaney, Hetal Patel, Manikandan Periyasamy, Alexander Bondke, Brian Slafer, Richard Starkey i in. "Abstract 700: Gene expression profiling of cyclin-dependent kinase (CDK) inhibition in cancer cells." W Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-700.

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Brack, Eva, Marco Wachtel i Beat W. Schaefer. "Abstract 700: Characterization of the mode of action of Fenretinide treatment in alveolar rhabdomyosarcoma cells". W Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-700.

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Ghassemifar, Sara, Yasmin Hashambhoy-Ramsay, Haluk Yuzugullu, Tamara Utermark, Violette Paragas, Tim Maiwald, Lia Luus i in. "Abstract 700: Development of a second-generation TRAIL agonist and predictive biomarker profile for colorectal cancer". W Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-700.

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Ghassemifar, Sara, Yasmin Hashambhoy-Ramsay, Haluk Yuzugullu, Tamara Utermark, Violette Paragas, Tim Maiwald, Lia Luus i in. "Abstract 700: Development of a second-generation TRAIL agonist and predictive biomarker profile for colorectal cancer". W Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-700.

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Roos, Alison, Zachary Mayo, Heather Sonnemann, Michael Pineda, Gil Lambert, Harshil D. Dhruv, Jeffrey A. Winkles, Michael E. Berens i Nhan L. Tran. "Abstract 700: Regulation of Fn14 expression by EGFRvIII-STAT signaling enhances glioblastoma cell invasion and survival". W Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-700.

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Sawicki, Janet A., Weidan Peng, Kelly Rhodes i Robert Getts. "Abstract 700: Systemic administration of DNA nanoparticles containing the diphtheria toxin gene reduces pancreatic tumor load in mice". W Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-700.

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Li, Aofei, Marco Marzulli, Lucia Mazzacurati, Hiroaki Uchida, Justus Cohen, Joseph Glorioso i Paola Grandi. "Abstract 703: Highly selective HSV virotherapy for glioblastoma". W Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-703.

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