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  • American Association for Cancer Research (AACR)  (112)
  • 1
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    Bacterial Prostatitis Enhances 2-Amino-1-Methyl-6-Phenylimidazo[4,5- b ]Pyridine (PhIP)–Induced Cancer at Multiple Sites
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Prevention Research Vol. 8, No. 8 ( 2015-08-01), p. 683-692
    Details
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 8, No. 8 ( 2015-08-01), p. 683-692
    Abstract: Dietary carcinogens, such as 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), and chronic inflammation have each been implicated as etiologic agents in prostate cancer. We hypothesized that bacterial prostatitis would accelerate PhIP-induced preinvasive lesions in the rat prostate. Male Fischer 344 rats were assigned into 4 groups: Control (untreated), PhIP (200 ppm in the diet for 20 weeks), Escherichia coli (E. coli, prostatic inoculation in week 10), or PhIP + E. coli. Study animals were monitored for a total of 52 weeks and were euthanized as necessary based on strict criteria for health status and tumor burden. Animals treated with E. coli initially developed acute and chronic inflammation in all lobes of the prostate, whereas inflammation was observed predominantly in the ventral lobe at time of death. PhIP + E. coli–treated animals exhibited a marked decrease in survival compared with PhIP-alone–treated animals as a result of an increase in the number of invasive cancers that developed at multiple sites, including the skin, small intestine, and Zymbal's gland. Despite their earlier mortality, PhIP + E. coli–treated animals developed an increased average number of precancerous lesions within the prostate compared with PhIP-treated animals, with a significantly increased Ki-67 index. Multiplexed serum cytokine analysis indicated an increase in the level of circulating IL6 and IL12 in PhIP + E. coli–treated animals. Elevated serum IL6 levels correlated with the development of precancerous lesions within the prostate. These results suggest that bacterial infections and dietary carcinogens, two conceivably preventable cancer risk factors, may synergistically promote tumorigenesis. Cancer Prev Res; 8(8); 683–92. ©2015 AACR.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.CAPR-15-0090
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
    detail.hit.zdb_id: 2422346-3
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  • 2
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    Abstract SS02-02: A long walk from FGFR2 alternative splicing to cancer progression
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 23, No. 11_Supplement ( 2014-11-01), p. SS02-02-SS02-02
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 23, No. 11_Supplement ( 2014-11-01), p. SS02-02-SS02-02
    Abstract: Previously, our group developed fluorescence-based alternative splicing reporters of epithelial plasticity to visualize phenotypic transitions in real time in vivo (Oltean et al., 2008; Oltean et al., 2006; Somarelli et al., 2013). We reasoned that our mesenchymal-epithelial transition (MET) reporters could be extremely useful to test the hypothesis that MET is a modulator of metastatic colonization in undifferentiated, sarcomatoid-like cancers. Along these lines, we generated a lineage-tracing reporter based on combined transcription and alternative splicing regulatory elements to measure the frequency of MET-like events during tumor growth and metastasis in the post-EMT Dunning rat AT3 model of prostate cancer. In a parallel set of experiments, we also used the combinatorial control strategy to drive a suicide reporter that kills cells undergoing MET to test the hypothesis that MET is required for metastatic colonization in undifferentiated, mesenchymal-like cancers. The combinatorial use of both transcription and alternative splicing regulation provided exquisite cell-type discrimination in the expression of enzymes, such as the Cre recombinase and Diphtheria A (DipA) toxin. Using the lineage tracing reporter system, we were able to quantify, for the first time, overall frequencies of MET during primary tumor and metastatic growth. Remarkably, we observed that the frequency of MET within primary tumors and metastatic nodules was not significantly different, with very low rates of MET taking place during the growth of tumors and metastases. Moreover, targeted killing of cells undergoing MET did not reduce the number of macrometastatic colonies in the lungs. This work demonstrates the ability of tumors to metastasize efficiently without the need for MET, and we suggest that this may be similar to the behavior of highly aggressive prostate carcinosarcomas or undifferentiated carcinomas. Using this system we will describe new experiments that will address differential behavior in different types of prostate cancer. Citation Format: Jason A. Somarelli, Jason A. Somarelli, Daneen Schaeffer, Daneen Schaeffer, Mathew S. Marengo, Mathew S. Marengo, Tristan Bepler, Tristan Bepler, Douglas Rouse, Anne F. Buckley, Jonathan I. Epstein, Andrew J. Armstrong, Mariano A. Garcia-Blanco, Mariano A. Garcia-Blanco. A long walk from FGFR2 alternative splicing to cancer progression. [abstract] . In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr SS02-02. doi:10.1158/1538-7755.DISP13-SS02-02
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1538-7755.DISP13-SS02-02
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 3
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    Abstract A018: Optimizing cancer immunotherapy response prediction by tumor aneuploidy score and fraction of copy number alterations
    American Association for Cancer Research (AACR) ; 2023
    In:  Molecular Cancer Therapeutics Vol. 22, No. 12_Supplement ( 2023-12-01), p. A018-A018
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 22, No. 12_Supplement ( 2023-12-01), p. A018-A018
    Abstract: Identifying patients that are likely to respond to cancer immunotherapy is an important, yet highly challenging clinical need. Using 3139 patients across 17 different cancer types, we comprehensively studied the ability of two common copy-number alteration (CNA) scores—the tumor aneuploidy score (AS) and the fraction of genome single nucleotide polymorphism encompassed by copy-number alterations (FGA)—to predict survival following immunotherapy in both pan-cancer and individual cancer types. First, we show that choice of cutoff during CNA calling significantly influences the predictive power of AS and FGA for patient survival following immunotherapy. Remarkably, by using proper cutoff during CNA calling, AS and FGA can predict pan-cancer survival following immunotherapy for both high-TMB and low-TMB patients. However, at the individual cancer level, our data suggest that the use of AS and FGA for predicting immunotherapy response is currently limited to only a few cancer types. Therefore, larger sample sizes are needed to evaluate the clinical utility of these measures for patient stratification in other cancer types. Finally, we propose a simple, non-parameterized, elbow-point-based method to help determine the cutoff used for calling CNAs. Citation Format: Tian-Gen Chang, Yingying Cao, Eldad D Shulman, Uri Ben-David, Alejandro A. Schäffer, Eytan Ruppin. Optimizing cancer immunotherapy response prediction by tumor aneuploidy score and fraction of copy number alterations [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 A018.
    Type of Medium: Online Resource
    ISSN: 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.TARG-23-A018
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
    detail.hit.zdb_id: 2062135-8
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  • 4
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    AXL Inhibition in Macrophages Stimulates Host-versus-Leukemia Immunity and Eradicates Naïve and Treatment-Resistant Leukemia
    American Association for Cancer Research (AACR) ; 2021
    In:  Cancer Discovery Vol. 11, No. 11 ( 2021-11-01), p. 2924-2943
    Details
    In: Cancer Discovery, American Association for Cancer Research (AACR), Vol. 11, No. 11 ( 2021-11-01), p. 2924-2943
    Abstract: Acute leukemias are systemic malignancies associated with a dire outcome. Because of low immunogenicity, leukemias display a remarkable ability to evade immune control and are often resistant to checkpoint blockade. Here, we discover that leukemia cells actively establish a suppressive environment to prevent immune attacks by co-opting a signaling axis that skews macrophages toward a tumor-promoting tissue repair phenotype, namely the GAS6/AXL axis. Using aggressive leukemia models, we demonstrate that ablation of the AXL receptor specifically in macrophages, or its ligand GAS6 in the environment, stimulates antileukemic immunity and elicits effective and lasting natural killer cell– and T cell–dependent immune response against naïve and treatment-resistant leukemia. Remarkably, AXL deficiency in macrophages also enables PD-1 checkpoint blockade in PD-1–refractory leukemias. Finally, we provide proof-of-concept that a clinical-grade AXL inhibitor can be used in combination with standard-of-care therapy to cure established leukemia, regardless of AXL expression in malignant cells. Significance: Alternatively primed myeloid cells predict negative outcome in leukemia. By demonstrating that leukemia cells actively evade immune control by engaging AXL receptor tyrosine kinase in macrophages and promoting their alternative priming, we identified a target which blockade, using a clinical-grade inhibitor, is vital to unleashing the therapeutic potential of myeloid-centered immunotherapy. This article is highlighted in the In This Issue feature, p. 2659
    Type of Medium: Online Resource
    ISSN: 2159-8274 , 2159-8290
    URL: Article
    DOI: 10.1158/2159-8290.CD-20-1378
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
    detail.hit.zdb_id: 2607892-2
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  • 5
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    Deconvolving Clinically Relevant Cellular Immune Cross-talk from Bulk Gene Expression Using CODEFACS and LIRICS Stratifies Patients with Melanoma to Anti–PD-1 Therapy
    American Association for Cancer Research (AACR) ; 2022
    In:  Cancer Discovery Vol. 12, No. 4 ( 2022-04-01), p. 1088-1105
    Details
    In: Cancer Discovery, American Association for Cancer Research (AACR), Vol. 12, No. 4 ( 2022-04-01), p. 1088-1105
    Abstract: The tumor microenvironment (TME) is a complex mixture of cell types whose interactions affect tumor growth and clinical outcome. To discover such interactions, we developed CODEFACS (COnfident DEconvolution For All Cell Subsets), a tool deconvolving cell type–specific gene expression in each sample from bulk expression, and LIRICS (Ligand–Receptor Interactions between Cell Subsets), a statistical framework prioritizing clinically relevant ligand–receptor interactions between cell types from the deconvolved data. We first demonstrate the superiority of CODEFACS versus the state-of-the-art deconvolution method CIBERSORTx. Second, analyzing The Cancer Genome Atlas, we uncover cell type–specific ligand–receptor interactions uniquely associated with mismatch-repair deficiency across different cancer types, providing additional insights into their enhanced sensitivity to anti–programmed cell death protein 1 (PD-1) therapy compared with other tumors with high neoantigen burden. Finally, we identify a subset of cell type–specific ligand–receptor interactions in the melanoma TME that stratify survival of patients receiving anti–PD-1 therapy better than some recently published bulk transcriptomics-based methods. Significance: This work presents two new computational methods that can deconvolve a large collection of bulk tumor gene expression profiles into their respective cell type–specific gene expression profiles and identify cell type–specific ligand–receptor interactions predictive of response to immune-checkpoint blockade therapy. This article is highlighted in the In This Issue feature, p. 873
    Type of Medium: Online Resource
    ISSN: 2159-8274 , 2159-8290
    URL: Article
    DOI: 10.1158/2159-8290.CD-21-0887
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
    detail.hit.zdb_id: 2607892-2
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  • 6
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    Abstract PO093: Identifying the landscape of intratumoral microbes via a single cell transcriptomic analysis
    American Association for Cancer Research (AACR) ; 2021
    In:  Cancer Immunology Research Vol. 9, No. 2_Supplement ( 2021-02-01), p. PO093-PO093
    Details
    In: Cancer Immunology Research, American Association for Cancer Research (AACR), Vol. 9, No. 2_Supplement ( 2021-02-01), p. PO093-PO093
    Abstract: The goal of this study is to develop a new method to characterize taxonomically which microbes are present intracellularly in which cell types in the tumor microenvironment. The tumor microbiome impacts many aspects of tumor development including tumorigenesis, mutagenesis, response to chemotherapy and the immune response. A recent computational approach showed that bacterial reads found in sequencing tumor samples and taxon abundances are predictive of cancer type. Recent experimental evidence suggests that some bacteria in the tumor microbiome may reside intracellularly. We sought to answer two questions: 1) which microbes, especially bacteria, reside intracellularly in a tumor sample and 2) in which cell types do these microbes preferentially reside? We developed a computational pipeline, CSI-Microbes (computational identification of Cell-type-Specific Intracellular Microbes), to identify cell-type-specific intracellular microbes from single cell RNA-seq (scRNA-seq) data. CSI-Microbes builds on the observation that in contrast to extracellular microbes and contaminants, some cell-type-specific intracellular microbes would exhibit differential abundance between cell types. For validation, we show that CSI-Microbes identifies Salmonella as the only differentially abundant microbe in a scRNA-seq dataset in the subset of immune cells that were deliberately infected with Salmonella. Next, we recapitulate known findings that Merkel cell polyomavirus and Fusobacterium exist intracellularly in tumor cells in Merkel cell carcinoma and in colorectal carcinoma, respectively. We then apply CSI-Microbes to analyze scRNA-seq data from numerous cancer types. We find that Streptomyces is differentially abundant in the tumor cells of both breast and head-and-neck cancer. We identify three bacterial genera and four fungal genera that are differentially abundant specifically in the tumor cells of melanoma samples. We additionally find evidence for the reactivation of herpesvirus in the plasma cells of a patient with basal cell carcinoma after immune checkpoint blockade therapy. These sequence-based findings raise the possibility that these tumor-specific intracellular microbes may play functional roles in tumor metabolism and drug response in these cancer types. As such, they also may be a source of neo-antigens, which can potentially be targeted using T cell therapies. In sum, CSI-Microbes offers a new way for fast, single cell RNA-seq based identification of likely intracellular bacteria living within specific cell populations in tumors, markedly extending upon previous studies aimed at inferring microbial abundance from bulk tumor samples. Citation Format: Welles Robinson, Fiorella Schischlik, E. Michael Gertz, Alejandro A. Schäffer, Eytan Ruppin. Identifying the landscape of intratumoral microbes via a single cell transcriptomic analysis [abstract]. In: Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; 2020 Oct 19-20. Philadelphia (PA): AACR; Cancer Immunol Res 2021;9(2 Suppl):Abstract nr PO093.
    Type of Medium: Online Resource
    ISSN: 2326-6066 , 2326-6074
    URL: Article
    DOI: 10.1158/2326-6074.TUMIMM20-PO093
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
    detail.hit.zdb_id: 2732517-9
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  • 7
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    Altered Gene Expression along the Glycolysis–Cholesterol Synthesis Axis Is Associated with Outcome in Pancreatic Cancer
    American Association for Cancer Research (AACR) ; 2020
    In:  Clinical Cancer Research Vol. 26, No. 1 ( 2020-01-01), p. 135-146
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 26, No. 1 ( 2020-01-01), p. 135-146
    Abstract: Identification of clinically actionable molecular subtypes of pancreatic ductal adenocarcinoma (PDAC) is key to improving patient outcome. Intertumoral metabolic heterogeneity contributes to cancer survival and the balance between distinct metabolic pathways may influence PDAC outcome. We hypothesized that PDAC can be stratified into prognostic metabolic subgroups based on alterations in the expression of genes involved in glycolysis and cholesterol synthesis. Experimental Design: We performed bioinformatics analysis of genomic, transcriptomic, and clinical data in an integrated cohort of 325 resectable and nonresectable PDAC. The resectable datasets included retrospective The Cancer Genome Atlas (TCGA) and the International Cancer Genome Consortium (ICGC) cohorts. The nonresectable PDAC cohort studies included prospective COMPASS, PanGen, and BC Cancer Personalized OncoGenomics program (POG). Results: On the basis of the median normalized expression of glycolytic and cholesterogenic genes, four subgroups were identified: quiescent, glycolytic, cholesterogenic, and mixed. Glycolytic tumors were associated with the shortest median survival in resectable (log-rank test P = 0.018) and metastatic settings (log-rank test P = 0.027). Patients with cholesterogenic tumors had the longest median survival. KRAS and MYC-amplified tumors had higher expression of glycolytic genes than tumors with normal or lost copies of the oncogenes (Wilcoxon rank sum test P = 0.015). Glycolytic tumors had the lowest expression of mitochondrial pyruvate carriers MPC1 and MPC2. Glycolytic and cholesterogenic gene expression correlated with the expression of prognostic PDAC subtype classifier genes. Conclusions: Metabolic classification specific to glycolytic and cholesterogenic pathways provides novel biological insight into previously established PDAC subtypes and may help develop personalized therapies targeting unique tumor metabolic profiles. See related commentary by Mehla and Singh, p. 6
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-19-1543
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 8
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    T-Cell Infiltration and Adaptive Treg Resistance in Response to Androgen Deprivation With or Without Vaccination in Localized Prostate Cancer
    American Association for Cancer Research (AACR) ; 2020
    In:  Clinical Cancer Research Vol. 26, No. 13 ( 2020-07-01), p. 3182-3192
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 26, No. 13 ( 2020-07-01), p. 3182-3192
    Abstract: Previous studies suggest that androgen deprivation therapy (ADT) promotes antitumor immunity in prostate cancer. Whether a vaccine-based approach can augment this effect remains unknown. Patients and Methods: We conducted a neoadjuvant, randomized study to quantify the immunologic effects of a GM-CSF–secreting allogeneic cellular vaccine in combination with low-dose cyclophosphamide (Cy/GVAX) followed by degarelix versus degarelix alone in patients with high-risk localized prostate adenocarcinoma who were planned for radical prostatectomy. Results: Both Cy/GVAX plus degarelix and degarelix alone led to significant increases in intratumoral CD8+ T-cell infiltration and PD-L1 expression as compared with a cohort of untreated, matched controls. However, the CD8+ T-cell infiltrate was accompanied by a proportional increase in regulatory T cells (Treg), suggesting that adaptive Treg resistance may dampen the immunogenicity of ADT. Although Cy/GVAX followed by degarelix was associated with a modest improvement in time-to-PSA progression and time-to-next treatment, as well as an increase in PD-L1, there was no difference in the CD8+ T-cell infiltrate as compared with degarelix alone. Gene expression profiling demonstrated that CHIT1, a macrophage marker, was differentially upregulated with Cy/GVAX plus degarelix compared with degarelix alone. Conclusions: Our results highlight that ADT with or without Cy/GVAX induces a complex immune response within the prostate tumor microenvironment. These data have important implications for combining ADT with immunotherapy. In particular, our finding that ADT increases both CD8+ T cells and Tregs supports the development of regimens combining ADT with Treg-depleting agents in the treatment of prostate cancer.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-19-3372
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 9
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    Subtype-Discordant Pancreatic Ductal Adenocarcinoma Tumors Show Intermediate Clinical and Molecular Characteristics
    American Association for Cancer Research (AACR) ; 2021
    In:  Clinical Cancer Research Vol. 27, No. 1 ( 2021-01-01), p. 150-157
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 27, No. 1 ( 2021-01-01), p. 150-157
    Abstract: RNA-sequencing–based subtyping of pancreatic ductal adenocarcinoma (PDAC) has been reported by multiple research groups, each using different methodologies and patient cohorts. “Classical” and “basal-like” PDAC subtypes are associated with survival differences, with basal-like tumors associated with worse prognosis. We amalgamated various PDAC subtyping tools to evaluate the potential of such tools to be reliable in clinical practice. Experimental Design: Sequencing data for 574 PDAC tumors was obtained from prospective trials and retrospective public databases. Six published PDAC subtyping strategies (Moffitt regression tools, clustering-based Moffitt, Collisson, Bailey, and Karasinska subtypes) were used on each sample, and results were tested for subtype call consistency and association with survival. Results: Basal-like and classical subtype calls were concordant in 88% of patient samples, and survival outcomes were significantly different (P & lt; 0.05) between prognostic subtypes. Twelve percent of tumors had subtype-discordant calls across the different methods, showing intermediate survival in univariate and multivariate survival analyses. Transcriptional profiles compatible with that of a hybrid subtype signature were observed for subtype-discordant tumors, in which classical and basal-like genes were concomitantly expressed. Subtype-discordant tumors showed intermediate molecular characteristics, including subtyping gene expression (P & lt; 0.0001) and mutant KRAS allelic imbalance (P & lt; 0.001). Conclusions: Nearly 1 in 6 patients with PDAC have tumors that fail to reliably fall into the classical or basal-like PDAC subtype categories, based on two regression tools aimed toward clinical practice. Rather, these patient tumors show intermediate prognostic and molecular traits. We propose close consideration of the non-binary nature of PDAC subtypes for future incorporation of subtyping into clinical practice.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-20-2831
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 10
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    Abstract CC01-01: The landscape of precision cancer combination therapy: A single-cell perspective
    American Association for Cancer Research (AACR) ; 2021
    In:  Molecular Cancer Therapeutics Vol. 20, No. 12_Supplement ( 2021-12-01), p. CC01-01-CC01-01
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 20, No. 12_Supplement ( 2021-12-01), p. CC01-01-CC01-01
    Abstract: The availability of single-cell transcriptomics data opens new opportunities for rational design of combination cancer treatments in a systematic manner. Mining such data, we employed combinatorial optimization techniques to explore the landscape of optimal combination therapies in solid tumors, including brain, head and neck, melanoma, lung, breast and colon cancers. We assume that each individual therapy can target any one of 1269 genes encoding cell surface receptors, which may be targets of CAR-T, conjugated antibodies or coated nanoparticle therapies. In most cancer types, personalized combinations composed of at most four targets are sufficient to kill at least 80% of the tumor cells while killing at most 10% of the non-tumor cells in each patient. The number of distinct targets needed to do that for all patients in 8 of the 9 cohorts we studied is at most 11, while one larger melanoma cohort requires over 30 distinct targets. Further requiring that the target genes be lowly expressed across many different healthy tissues uncovers qualitatively similar trends. However, as one requires either more stringent killing thresholds or more stringent sparing of non-cancerous tissues beyond these baseline values, the number of targets needed rises rapidly. Emerging promising targets include the gene PTPRZ1, which is frequently found in the optimal combinations for brain and head and neck cancers, and EGFR, a recurring target in multiple tumor types. In sum, this is the first systematic single-cell based characterization of the landscape of combinatorial receptor-mediated cancer treatments, identifying promising targets for future development. Citation Format: Saba Ahmadi, Pattara Sukprasert, Rahulsimham Vegesna, Sanju Sinha, Fiorella Schischlik, Natalie Artzi, Samir Khuller, Alejandro A. Schäffer, Eytan Ruppin. The landscape of precision cancer combination therapy: A single-cell perspective [abstract]. In: Proceedings of the AACR-NCI-EORTC Virtual International Conference on Molecular Targets and Cancer Therapeutics; 2021 Oct 7-10. Philadelphia (PA): AACR; Mol Cancer Ther 2021;20(12 Suppl):Abstract nr CC01-01.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.TARG-21-CC01-01
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
    detail.hit.zdb_id: 2062135-8
    SSG: 12
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