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  • American Association for Cancer Research (AACR)  (61)
  • 1
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    Abstract 1115: p32 is a downstream effector of c-Myc induced glutamine addiction
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1115-1115
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1115-1115
    Abstract: Genetic alterations of oncogenes and tumor suppressor genes are the main drivers not only of deregulated cell proliferation but also altered cancer cell metabolism. Compared with normal cells, malignant cells exhibit enhanced utilization of glucose and glutamine. As such, efforts to understand the molecular basis of the addiction to these two nutrients is likely to lead to the identification of new drug targets for the specific killing of cancer cells. A major player in tumor cell addiction to glutamine is the c-Myc oncogene. By stimulating the expression of glutamine transporters and glutaminase, this transcription factor promotes glutamine oxidation through the mitochondria. This rewiring of glutamine metabolism must be sustained by efficient mitochondrial function. The mitochondrial p32 protein was previously demonstrated to be critical in mitochondria metabolism by maintaining oxidative phosphorylation, yet the factors regulating its expression are not clear. Deregulated c-Myc is a frequent feature of gliomas and recent discoveries suggest the importance of metabolic alterations, in particular glutamine addiction, in the pathogenesis of these cancers. Interestingly, medulloblastoma can be clustered into six subgroups based on gene signature and the c-Myc amplified subgroup exhibits high p32 expression. In the present study, we hypothesized that p32 may be a downstream effector of c-Myc induced glutamine addiction. Using a c-Myc and estrogen receptor fusion protein construct in immortalized fibroblast, we demonstrated that p32 expression was up regulated upon c-Myc nuclear translocation. shRNA mediated stable knock-down of p32 in glioma cell lines and patient-derived tumor initiating cells impaired cell proliferation and tumorigenic potential in mouse models. Furthermore, attenuation of p32 expression reduced glioma cells sensitivity to glutamine deprivation and abrogated c-Myc induced glutamine consumption. Additional work is underway to determine whether c-Myc and p32 work in the same or parallel pathways to confer glutamine addiction on glioma cells and to establish the implications of this co-operation on tumor metabolism in vivo. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1115. doi:1538-7445.AM2012-1115
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-1115
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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  • 2
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    Comutations and KRASG12C Inhibitor Efficacy in Advanced NSCLC
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Discovery Vol. 13, No. 7 ( 2023-07-07), p. 1556-1571
    Details
    In: Cancer Discovery, American Association for Cancer Research (AACR), Vol. 13, No. 7 ( 2023-07-07), p. 1556-1571
    Abstract: Molecular modifiers of KRASG12C inhibitor (KRASG12Ci) efficacy in advanced KRASG12C-mutant NSCLC are poorly defined. In a large unbiased clinicogenomic analysis of 424 patients with non–small cell lung cancer (NSCLC), we identified and validated coalterations in KEAP1, SMARCA4, and CDKN2A as major independent determinants of inferior clinical outcomes with KRASG12Ci monotherapy. Collectively, comutations in these three tumor suppressor genes segregated patients into distinct prognostic subgroups and captured ∼50% of those with early disease progression (progression-free survival ≤3 months) with KRASG12Ci. Pathway-level integration of less prevalent coalterations in functionally related genes nominated PI3K/AKT/MTOR pathway and additional baseline RAS gene alterations, including amplifications, as candidate drivers of inferior outcomes with KRASG12Ci, and revealed a possible association between defective DNA damage response/repair and improved KRASG12Ci efficacy. Our findings propose a framework for patient stratification and clinical outcome prediction in KRASG12C-mutant NSCLC that can inform rational selection and appropriate tailoring of emerging combination therapies. Significance: In this work, we identify co-occurring genomic alterations in KEAP1, SMARCA4, and CDKN2A as independent determinants of poor clinical outcomes with KRASG12Ci monotherapy in advanced NSCLC, and we propose a framework for patient stratification and treatment personalization based on the comutational status of individual tumors. See related commentary by Heng et al., p. 1513. This article is highlighted in the In This Issue feature, p. 1501
    Type of Medium: Online Resource
    ISSN: 2159-8274 , 2159-8290
    URL: Article
    DOI: 10.1158/2159-8290.CD-22-1420
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
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  • 3
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    Fibrinogen Alpha Chain Knockout Promotes Tumor Growth and Metastasis through Integrin–AKT Signaling Pathway in Lung Cancer
    American Association for Cancer Research (AACR) ; 2020
    In:  Molecular Cancer Research Vol. 18, No. 7 ( 2020-07-01), p. 943-954
    Details
    In: Molecular Cancer Research, American Association for Cancer Research (AACR), Vol. 18, No. 7 ( 2020-07-01), p. 943-954
    Abstract: Fibrinogen is an extracellular matrix protein composed of three polypeptide chains with fibrinogen alpha (FGA), beta (FGB) and gamma (FGG). Although fibrinogen and its related fragments are involved in tumor angiogenesis and metastasis, their functional roles are incompatible. A recent genome-scale screening reveals that loss of FGA affects the acceleration of tumor growth and metastasis of lung cancer, but the mechanism remains elusive. We used CRISPR/Cas9 genome editing to knockout (KO) FGA in human lung adenocarcinoma (LUAD) cell lines A549 and H1299. By colony formation, transwell migration and matrix invasion assays, FGA KO increased cell proliferation, migration, and invasion but decreased the expressions of epithelial–mesenchymal transition marker E-cadherin and cytokeratin 5/8 in A549 and H1299 cells. However, administration of FGA inhibited cell proliferation and migration but induced apoptosis in A549 cells. Of note, FGA KO cells indirectly cocultured by transwells with FGA wild-type cells increased FGA in the culture medium, leading to decreased migration of FGA KO cells. Furthermore, our functional analysis identified a direct interaction of FGA with integrin α5 as well as FGA–integrin signaling that regulated the AKT–mTOR signaling pathway in A549 cells. In addition, we validated that FGA KO increased tumor growth and metastasis through activation of AKT signaling in an A549 xenograft model. Implications: These findings demonstrate that that loss of FGA facilities tumor growth and metastasis through the integrin–AKT signaling pathway in lung cancer.
    Type of Medium: Online Resource
    ISSN: 1541-7786 , 1557-3125
    URL: Article
    DOI: 10.1158/1541-7786.MCR-19-1033
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 4
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    Abstract A82: Immune checkpoint protein VISTA controls antitumor immunity via regulating Toll-like receptor signaling and myeloid cells-mediated inflammation
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Immunology Research Vol. 8, No. 4_Supplement ( 2020-04-01), p. A82-A82
    Details
    In: Cancer Immunology Research, American Association for Cancer Research (AACR), Vol. 8, No. 4_Supplement ( 2020-04-01), p. A82-A82
    Abstract: Introduction: V-domain Ig suppressor of T-cell activation (VISTA, gene Vsir) is an inhibitory immune-checkpoint molecule that suppresses CD4+ and CD8+ T-cell activation. Vsir-/- mice developed chronic inflammatory phenotypes, and Vsir-/- CD4+ and CD8+ T cells were hyper-responsive towards self- and foreign antigens. Our recent study (Li et al., Sci Rep 2017) has identified a novel role of VISTA as a critical regulator of IL-23/IL-17 inflammatory axis induced by Toll-like receptor (TLR) stimulation. The molecular mechanisms by which VISTA inhibits TLR signaling remain to be elucidated. Methods: Peritoneal macrophages from WT or Vsir-/- mice were isolated and stimulated with TLR agonists. Alternatively, human monocyte THP-1 cells overexpressing VISTA were stimulated by TLR2 agonist Pam3CSK4. The activation of TLR signaling pathways and the production of inflammatory cytokines were examined by Western blotting, gel shift assay, or ELISA. Tumor-bearing mice were treated with VISTA-specific monoclonal antibody (mAb) and a peptide vaccine containing TLR agonists. The production of inflammatory cytokines and chemokines was examined via RT-PCR and ELISA. Results: VISTA downregulates Toll-like receptor (TLR)/TRAF6/TAK1-mediated signaling pathway via promoting K48-linked polyubiquitination and proteasomal degradation of TRAF6 and inhibiting K63-linked polyubiquitination and activation of TRAF6. VISTA blockade by an antibody or genetic deletion augments the activation of MAPKs/AP-1 and IKK/NF-kB signaling cascades in myeloid cells and induces the accumulation of inflammatory cytokines and chemokines within tumor tissues. Inflamed tumor tissues promote the infiltration and effector function of tumor-reactive CD8+ T cells. TLR/TRAF6-mediated inflammatory responses promote the antitumor efficacy of VISTA-blocking antibodies and contribute to a synergistic outcome when VISTA blockade is combined with a TLR agonistic vaccine. Conclusions: Our study establishes that VISTA critically regulates the inflammatory responses of myeloid cells mediated by TLR signaling. Unlike targeting other immune checkpoint proteins, the therapeutic efficacy of VISTA inhibition benefits from the activation of myeloid cells and early induction of inflammatory cytokines may predict positive clinical responses. Citation Format: Wenwen Xu, Yongwei Zheng, Juan Zhou, Ying Yuan, Hieu Minh Ta, Jun Dong, Halli E. Miller, Michael Olson, Kamalakannan Rajasekaran, Marc S. Ernstoff, Demin Wang, Subramaniam Malarkannan, Li Wang. Immune checkpoint protein VISTA controls antitumor immunity via regulating Toll-like receptor signaling and myeloid cells-mediated inflammation [abstract]. In: Proceedings of the AACR Special Conference on Tumor Immunology and Immunotherapy; 2018 Nov 27-30; Miami Beach, FL. Philadelphia (PA): AACR; Cancer Immunol Res 2020;8(4 Suppl):Abstract nr A82.
    Type of Medium: Online Resource
    ISSN: 2326-6066 , 2326-6074
    URL: Article
    DOI: 10.1158/2326-6074.TUMIMM18-A82
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 5
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    RGS-GAIP–Interacting Protein Controls Breast Cancer Progression
    American Association for Cancer Research (AACR) ; 2010
    In:  Molecular Cancer Research Vol. 8, No. 12 ( 2010-12-01), p. 1591-1600
    Details
    In: Molecular Cancer Research, American Association for Cancer Research (AACR), Vol. 8, No. 12 ( 2010-12-01), p. 1591-1600
    Abstract: Although the importance of RGS-GAIP–interacting protein (GIPC) in the biology of malignant cells is well known, the molecular mechanism of GIPC in the inhibition of tumor progression has not been identified. This study focused on elucidating the molecular role of GIPC in breast cancer progression. By using a human breast tumor specimen, an in vivo mouse model, and breast cancer cell lines, we showed for the first time that GIPC is involved in breast cancer progression through regulation of breast cancer cell proliferation, survival, and invasion. Furthermore, we found that the Akt/Mdm2/p53 axis, insulin-like growth factor-1 receptor, matrix metalloproteinase-9, and Cdc42 were downstream of GIPC signaling in breast cancer cells. Moreover, we showed that wild-type p53 reduced GIPC-induced breast cancer cell survival, whereas mutant p53 inhibited GIPC-induced cell invasion. Finally, we demonstrated that an N-myristoylated GIPC peptide (CR1023, N-myristoyl-PSQSSSEA) capable of blocking the PDZ domain of GIPC successfully inhibited MDA-MB-231 cell proliferation, survival, and further in vivo tumor growth. Taken together, these findings demonstrate the importance of GIPC in breast tumor progression, which has a potentially significant impact on the development of therapies against many common cancers expressing GIPC, including breast and renal cancer. Mol Cancer Res; 8(12); 1591–600. ©2010 AACR.
    Type of Medium: Online Resource
    ISSN: 1541-7786 , 1557-3125
    URL: Article
    DOI: 10.1158/1541-7786.MCR-10-0209
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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    SSG: 12
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  • 6
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    Characterization of Phosphoglycerate Kinase-1 Expression of Stromal Cells Derived from Tumor Microenvironment in Prostate Cancer Progression
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 2 ( 2010-01-15), p. 471-480
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 2 ( 2010-01-15), p. 471-480
    Abstract: Tumor and stromal interactions in the tumor microenvironment are critical for oncogenesis and cancer progression. Our understanding of the molecular events by which reactive stromal fibroblasts—myofibroblast or cancer-associated fibroblasts (CAF)—affect the growth and invasion of prostate cancer remains unclear. Laser capture microdissection and cDNA microarray analysis of CAFs in prostate tumors revealed strong upregulation of phosphoglycerate kinase-1 (PGK1), an ATP-generating glycolytic enzyme that forms part of the glycolytic pathway and is directly involved in CXCL12-CXCR4 signaling. Normal fibroblasts overexpressing PGK1 resembled myofibroblasts in their expression of smooth muscle α-actin, vimentin, and high levels of CXCL12. These cells also displayed a higher proliferative index and the capability to contribute to prostate tumor cell invasion in vitro, possibly through expression of MMP-2 and MMP-3 and activation of the AKT and ERK pathways. Coimplantation of PGK1-overexpressing fibroblasts with prostate tumor cells promoted tumor cell growth in vivo. Collectively, these observations suggest that PGK1 helps support the interactions between cancer and its microenvironment. Cancer Res; 70(2); 471–80
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-09-2863
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 7
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    Neratinib-Plus-Cetuximab in Quadruple-WT ( KRAS, NRAS, BRAF, PIK3CA ) Metastatic Colorectal Cancer Resistant to Cetuximab or Panitumumab: NSABP FC-7, A Phase Ib Study
    American Association for Cancer Research (AACR) ; 2021
    In:  Clinical Cancer Research Vol. 27, No. 6 ( 2021-03-15), p. 1612-1622
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 27, No. 6 ( 2021-03-15), p. 1612-1622
    Abstract: In metastatic colorectal cancer (mCRC), HER2 (ERBB2) gene amplification is implicated in anti-EGFR therapy resistance. We sought to determine the recommended phase II dose (RP2D) and efficacy of neratinib, a pan-ERBB kinase inhibitor, combined with cetuximab, in patients with progressive disease (PD) on anti-EGFR treatment. Patients and Methods: Twenty-one patients with quadruple-wild-type, refractory mCRC enrolled in this 3+3 phase Ib study. Standard dosage cetuximab was administered with neratinib at 120 mg, 160 mg, 200 mg, and 240 mg/day orally in 28-day cycles. Samples were collected for molecular and pharmacokinetic studies. Results: Sixteen patients were evaluable for dose-limiting toxicity (DLT). 240 mg was determined to be the RP2D wherein a single DLT occurred (1/7 patients). Treatment-related DLTs were not seen at lower doses. Best response was stable disease (SD) in 7 of 16 (44%) patients. HER2 amplification (chromogenic in situ IHC) was detected in 2 of 21 (9.5%) treatment-naïve tumors and 4 of 16 (25%) biopsies upon trial enrollment (post-anti-EGFR treatment and progression). Compared with matched enrollment biopsies, 6 of 8 (75%) blood samples showed concordance for HER2 CNV in circulating cell-free DNA. Five SD patients had HER2 amplification in either treatment-naïve or enrollment biopsies. Examination of gene-expression, total protein, and protein phosphorylation levels showed relative upregulation of ≥2 members of the HER-family receptors or ligands upon enrollment versus matched treatment-naïve samples. Conclusions: The RP2D of neratinib in this combination was 240 mg/day, which was well tolerated with low incidence of G3 AEs. There were no objective responses; SD was seen at all neratinib doses. HER2 amplification, detectable in both tissue and blood, was more frequent post-anti-EGFR therapy.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-20-1831
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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    detail.hit.zdb_id: 2036787-9
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  • 8
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    Accounting for EGFR Mutations in Epidemiologic Analyses of Non–Small Cell Lung Cancers: Examples Based on the International Lung Cancer Consortium Data
    American Association for Cancer Research (AACR) ; 2022
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 31, No. 3 ( 2022-03-01), p. 679-687
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 31, No. 3 ( 2022-03-01), p. 679-687
    Abstract: Somatic EGFR mutations define a subset of non–small cell lung cancers (NSCLC) that have clinical impact on NSCLC risk and outcome. However, EGFR-mutation-status is often missing in epidemiologic datasets. We developed and tested pragmatic approaches to account for EGFR-mutation-status based on variables commonly included in epidemiologic datasets and evaluated the clinical utility of these approaches. Methods: Through analysis of the International Lung Cancer Consortium (ILCCO) epidemiologic datasets, we developed a regression model for EGFR-status; we then applied a clinical-restriction approach using the optimal cut-point, and a second epidemiologic, multiple imputation approach to ILCCO survival analyses that did and did not account for EGFR-status. Results: Of 35,356 ILCCO patients with NSCLC, EGFR-mutation-status was available in 4,231 patients. A model regressing known EGFR-mutation-status on clinical and demographic variables achieved a concordance index of 0.75 (95% CI, 0.74–0.77) in the training and 0.77 (95% CI, 0.74–0.79) in the testing dataset. At an optimal cut-point of probability-score = 0.335, sensitivity = 69% and specificity = 72.5% for determining EGFR-wildtype status. In both restriction-based and imputation-based regression analyses of the individual roles of BMI on overall survival of patients with NSCLC, similar results were observed between overall and EGFR-mutation-negative cohort analyses of patients of all ancestries. However, our approach identified some differences: EGFR-mutated Asian patients did not incur a survival benefit from being obese, as observed in EGFR-wildtype Asian patients. Conclusions: We introduce a pragmatic method to evaluate the potential impact of EGFR-status on epidemiological analyses of NSCLC. Impact: The proposed method is generalizable in the common occurrence in which EGFR-status data are missing.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-21-0747
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
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  • 9
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    CREBBP Inactivation Promotes the Development of HDAC3-Dependent Lymphomas
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Discovery Vol. 7, No. 1 ( 2017-01-01), p. 38-53
    Details
    In: Cancer Discovery, American Association for Cancer Research (AACR), Vol. 7, No. 1 ( 2017-01-01), p. 38-53
    Abstract: Somatic mutations in CREBBP occur frequently in B-cell lymphoma. Here, we show that loss of CREBBP facilitates the development of germinal center (GC)–derived lymphomas in mice. In both human and murine lymphomas, CREBBP loss-of-function resulted in focal depletion of enhancer H3K27 acetylation and aberrant transcriptional silencing of genes that regulate B-cell signaling and immune responses, including class II MHC. Mechanistically, CREBBP-regulated enhancers are counter-regulated by the BCL6 transcriptional repressor in a complex with SMRT and HDAC3, which we found to bind extensively to MHC class II loci. HDAC3 loss-of-function rescued repression of these enhancers and corresponding genes, including MHC class II, and more profoundly suppressed CREBBP-mutant lymphomas in vitro and in vivo. Hence, CREBBP loss-of-function contributes to lymphomagenesis by enabling unopposed suppression of enhancers by BCL6/SMRT/HDAC3 complexes, suggesting HDAC3-targeted therapy as a precision approach for CREBBP-mutant lymphomas. Significance: Our findings establish the tumor suppressor function of CREBBP in GC lymphomas in which CREBBP mutations disable acetylation and result in unopposed deacetylation by BCL6/SMRT/HDAC3 complexes at enhancers of B-cell signaling and immune response genes. Hence, inhibition of HDAC3 can restore the enhancer histone acetylation and may serve as a targeted therapy for CREBBP-mutant lymphomas. Cancer Discov; 7(1); 38–53. ©2016 AACR. See related commentary by Höpken, p. 14. This article is highlighted in the In This Issue feature, p. 1
    Type of Medium: Online Resource
    ISSN: 2159-8274 , 2159-8290
    URL: Article
    DOI: 10.1158/2159-8290.CD-16-0975
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
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  • 10
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    Retraction: Characterization of Phosphoglycerate Kinase-1 Expression of Stromal Cells Derived from Tumor Microenvironment in Prostate Cancer Progression
    American Association for Cancer Research (AACR) ; 2022
    In:  Cancer Research Vol. 82, No. 18 ( 2022-09-16), p. 3405-3405
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 82, No. 18 ( 2022-09-16), p. 3405-3405
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-22-2398
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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