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  • American Association for Cancer Research (AACR)  (28)
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  • American Association for Cancer Research (AACR)  (28)
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  • 1
    Online Resource
    Online Resource
    Antitumor Activity of a Mitochondrial-Targeted HSP90 Inhibitor in Gliomas
    American Association for Cancer Research (AACR) ; 2022
    In:  Clinical Cancer Research Vol. 28, No. 10 ( 2022-05-13), p. 2180-2195
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 28, No. 10 ( 2022-05-13), p. 2180-2195
    Abstract: To investigate the antitumor activity of a mitochondrial-localized HSP90 inhibitor, Gamitrinib, in multiple glioma models, and to elucidate the antitumor mechanisms of Gamitrinib in gliomas. Experimental Design: A broad panel of primary and temozolomide (TMZ)-resistant human glioma cell lines were screened by cell viability assays, flow cytometry, and crystal violet assays to investigate the therapeutic efficacy of Gamitrinib. Seahorse assays were used to measure the mitochondrial respiration of glioma cells. Integrated analyses of RNA sequencing (RNAseq) and reverse phase protein array (RPPA) data were performed to reveal the potential antitumor mechanisms of Gamitrinib. Neurospheres, patient-derived organoids (PDO), cell line–derived xenografts (CDX), and patient-derived xenografts (PDX) models were generated to further evaluate the therapeutic efficacy of Gamitrinib. Results: Gamitrinib inhibited cell proliferation and induced cell apoptosis and death in 17 primary glioma cell lines, 6 TMZ-resistant glioma cell lines, 4 neurospheres, and 3 PDOs. Importantly, Gamitrinib significantly delayed the tumor growth and improved survival of mice in both CDX and PDX models in which tumors were either subcutaneously or intracranially implanted. Integrated computational analyses of RNAseq and RPPA data revealed that Gamitrinib exhibited its antitumor activity via (i) suppressing mitochondrial biogenesis, OXPHOS, and cell-cycle progression and (ii) activating the energy-sensing AMP-activated kinase, DNA damage, and stress response. Conclusions: These preclinical findings established the therapeutic role of Gamitrinib in gliomas and revealed the inhibition of mitochondrial biogenesis and tumor bioenergetics as the primary antitumor mechanisms in gliomas.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-21-0833
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 2
    Online Resource
    Online Resource
    Prediction of Chemotherapeutic Efficacy in Non–Small Cell Lung Cancer by Serum Metabolomic Profiling
    American Association for Cancer Research (AACR) ; 2018
    In:  Clinical Cancer Research Vol. 24, No. 9 ( 2018-05-01), p. 2100-2109
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 24, No. 9 ( 2018-05-01), p. 2100-2109
    Abstract: Purpose: No validated biomarkers that could identify the subset of patients with lung adenocarcinoma who might benefit from chemotherapy have yet been well established. This study aimed to explore potential biomarker model predictive of efficacy and survival outcomes after first-line pemetrexed plus platinum doublet based on metabolomics profiling. Experimental Design: In total, 354 consecutive eligible patients were assigned to receive first-line chemotherapy of pemetrexed in combination with either cisplatin or carboplatin. Prospectively collected serum samples before initial treatment were utilized to perform metabolomics profiling analyses under the application of LC/MS-MS. Binary logistic regression analysis was carried out to establish discrimination models. Results: There were 251 cases randomly sorted into discovery set, the rest of 103 cases into validation set. Seven metabolites including hypotaurine, uridine, dodecanoylcarnitine, choline, dimethylglycine, niacinamide, and l-palmitoylcarnitine were identified associated with chemo response. On the basis of the seven-metabolite panel, a discriminant model according to logistic regression values g(z) was established with the receiver operating characteristic curve (AUC) of 0.912 (Discovery set) and 0.909 (Validation set) in differentiating progressive disease (PD) groups from disease control (DC) groups. The median progression-free survival (PFS) after chemotherapy in patients with g(z) ≤0.155 was significantly longer than that in those with g(z) & gt; 0.155 (10.3 vs.4.5 months, P & lt; 0.001). Conclusions: This study developed an effective and convenient discriminant model that can accurately predict the efficacy and survival outcomes of pemetrexed plus platinum doublet chemotherapy prior to treatment delivery. Clin Cancer Res; 24(9); 2100–9. ©2018 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-17-2855
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 3
    Online Resource
    Online Resource
    Time distributions and prognosis factors of breast cancer recurrence in different sites after operation.
    American Association for Cancer Research (AACR) ; 2009
    In:  Cancer Research Vol. 69, No. 2_Supplement ( 2009-01-15), p. 2080-
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 69, No. 2_Supplement ( 2009-01-15), p. 2080-
    Abstract: Abstract #2080 Objective Our study aims to analyze the breast caner patients with different sites of recurrence, and to have knowledge of the regular patterns and influence factors of metastastic breast cancer. & #x2028; Methods We performed a retrospective study of 210 female breast cancer patients who were continuously followed up in our hospital from January 2005 to May 2007 and had complete data of metastasis. The clinical and biological characteristics were compared between the patients with organ metastases (lung, liver, brain) and non-viscera metastases (lymph node, bone). & #x2028; Results Cox regression analysis-hazard function showed that patients with elder age (RR=0.927 95%CI 0.877∼0.981, P=0.008) and HER-2 negative(RR=0.253 95%CI 0.076∼0.836, P=0.024)tended to develop non-viscera metastases, while patients with larger tumors (RR=3.832 95%CI 1.073∼13.687, P=0.039) tended to develop organ metastasesp. & #x2028; & #x2028; When stratified by the prognostic factors, the annual risk hazard curve of the patients with high risk of recurrence had double peaks at the second year and the ninth years after mastectomy respectively, and it was significantly higher than those of the patients with middle and low risk.[figure1]Annual risk hazard curves of both local relapse and metastasis also showed a double-peaked pattern. The curves for lymph node, bone, lung and liver metastasis showed a similar pattern, but all the peaks of curve emerged later than that of the local relapse. & #x2028; & #x2028; Conclusion Patients with different clinical and biological characteristics may develop recurrence in different sites. There are certain regular patterns of time distribution for different metastasis sites after mastectomy. The local recurrence may be the foreboding for the metastasis and we should pay attention to the local relapse signs especially in the patients with high risk. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 2080.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.SABCS-2080
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 4
    Online Resource
    Online Resource
    Intermittent Hypoxia: Potential Factor of Resistance to Endocrine Therapy.
    American Association for Cancer Research (AACR) ; 2009
    In:  Cancer Research Vol. 69, No. 24_Supplement ( 2009-12-15), p. 5148-5148
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 69, No. 24_Supplement ( 2009-12-15), p. 5148-5148
    Abstract: Background: It has been reported that intermittent hypoxia, which is likely more prevalent than acute hypoxia in breast cancers, can cause persistent depression of estrogen receptor alpha (ER-α) expression in breast cell lines. However, it remains suspension whether intermittent hypoxia may be associated with resistance to endocrine therapy.Material and methods: The role of intermittent hypoxia in resistance to endocrine therapy was investigated in ER-α positive breast cell lines and animal models.Results: We observed that intermittent hypoxia promoted cancer cell proliferation in vitro and in vivo compared with normoxia. At both mRNA and protein levels, intermittent hypoxia induced down-regulation of ER-α and factor inhibiting HIF-1 (FIH) as well as up-regulation of hypoxia inducible factor-1 alpha (HIF-1α) and carbonic anhydrase IX (CA-IX). ER-α positive breast cancer cells under normoxic condition were capable of an intact response to ICI 182,780 (Tocris), whereas the inhibitory effect of ICI 182,780 (Tocris) was significantly reduced in those after intermittent hypoxia. Such effect was further validated with fulvestrant (Astrazeneca) in the animal models. To clarify whether intermittent hypoxia was associated with resistance to endocrine therapy, the expression of HIF-1α, a critical regulator of hypoxia-related pathway, was blocked by a reformed type of small interfering RNA (siRNA), stealth RNAi (Invitrogen), which can reduce the cytotoxic interferon response unlike conventional siRNA. Interestingly, knock-down of HIF-1α did result in the restoration of not only the ER-α expression but also the response to endocrine therapy, which was reproducible with administration of Bortezomib, a proteasome inhibitor of HIF-1α.Discussion: These data provide functional evidence that intermittent hypoxia may confer resistance to endocrine therapy in breast cancers through the crosstalk between HIF-1α and ER-α signaling, which holds a promise to overcome endocrine resistance. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 5148.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.SABCS-09-5148
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 5
    Online Resource
    Online Resource
    LOXL2 Upregulates Phosphorylation of Ezrin to Promote Cytoskeletal Reorganization and Tumor Cell Invasion
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Research Vol. 79, No. 19 ( 2019-10-01), p. 4951-4964
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 19 ( 2019-10-01), p. 4951-4964
    Abstract: Lysyl oxidase-like 2 (LOXL2), a copper-dependent enzyme of the lysyl oxidase family and its nonsecreted, catalytically dead spliced isoform L2Δ13, enhance cell migration and invasion, stimulate filopodia formation, modulate the expression of cytoskeletal genes, and promote tumor development and metastasis in vivo. We previously showed that LOXL2 reorganizes the actin cytoskeleton in esophageal squamous cell carcinoma (ESCC) cells, however, the underlying molecular mechanisms were not identified. Here, using interactome analysis, we identified ezrin (EZR), fascin (FSCN1), heat shock protein beta-1 (HSPB1), and tropomodulin-3 (TMOD3) as actin-binding proteins that associate with cytoplasmic LOXL2, as well as with its L2Δ13 variant. High levels of LOXL2 and L2Δ13 and their cytoskeletal partners correlated with poor clinical outcome in patients with ESCC. To better understand the significance of these interactions, we focused on the interaction of LOXL2 with ezrin. Phosphorylation of ezrin at T567 was greatly reduced following depletion of LOXL2 and was enhanced following LOXL2/L2Δ13 reexpression. Furthermore, LOXL2 depletion inhibited the ability of ezrin to promote tumor progression. These results suggest that LOXL2-induced ezrin phosphorylation, which also requires PKCα, is critical for LOXL2-induced cytoskeletal reorganization that subsequently promotes tumor cell invasion and metastasis in ESCC. In summary, we have characterized a novel molecular mechanism that mediates, in part, the protumorigenic activity of LOXL2. These findings may enable the future development of therapeutic agents targeting cytoplasmic LOXL2. Significance: LOXL2 and its spliced isoform L2Δ13 promote cytoskeletal reorganization and invasion of esophageal cancer cells by interacting with cytoplasmic actin-binding proteins such as ezrin.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-19-0860
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 6
    Online Resource
    Online Resource
    Consumption of the Fish Oil High-Fat Diet Uncouples Obesity and Mammary Tumor Growth through Induction of Reactive Oxygen Species in Protumor Macrophages
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 12 ( 2020-06-15), p. 2564-2574
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 12 ( 2020-06-15), p. 2564-2574
    Abstract: Obesity is associated with increased risk of many types of cancer and can be induced by various high-fat diets (HFD) from different fat sources. It remains unknown whether fatty acid composition in different HFD influences obesity-associated tumor development. Here we report that consumption of either a cocoa butter or fish oil HFD induced similar obesity in mouse models. While obesity induced by the cocoa butter HFD was associated with accelerated mammary tumor growth, consumption of the fish oil HFD uncoupled obesity from increased mammary tumor growth and exhibited a decrease in protumor macrophages. Compared with fatty acid (FA) components in both HFDs, n-3 FA rich in the fish oil HFD induced significant production of reactive oxygen species (ROS) and macrophage death. Moreover, A-FABP expression in the protumor macrophages facilitated intracellular transportation of n-3 FA and oxidation of mitochondrial FA. A-FABP deficiency diminished n-3 FA–mediated ROS production and macrophage death in vitro and in vivo. Together, our results demonstrate a novel mechanism by which n-3 FA induce ROS-mediated protumor macrophage death in an A-FABP–dependent manner. Significance: This study provides mechanistic insight into dietary supplementation with fish oil for breast cancer prevention and advances a new concept that not all HFDs leading to obesity are tumorigenic.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-19-3184
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 7
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    Online Resource
    Seroma formation after breast cancer surgery and its risk factors.
    American Association for Cancer Research (AACR) ; 2009
    In:  Cancer Research Vol. 69, No. 2_Supplement ( 2009-01-15), p. 4085-
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 69, No. 2_Supplement ( 2009-01-15), p. 4085-
    Abstract: Abstract #4085 Background:. Seroma formation is one of the most common complications after breast cancer surgery including modified radical mastectomy and breast conservative surgery. Our study aims to investigate the risk factors of postoperative seroma in Chinese breast cancer patients. & #x2028; Methods: Clinical data of 158 women who underwent surgerical therapy for breast cancer in our hospital were collected prospectively and all patients were followed up. The risk factors for seroma occurrence were compared between the seroma group and control group using X 2 test or t test, as well as the logistic regression was used as multivariate analysis. & #x2028; Results: Univariate analysis showed that the average age of the seroma group was significantly higher than those without seroma formation(58.71vs51.00, P=0.0019), but the total serum protein and albumin content were lower (68.47g/L vs 72.53g/L, P=0.009 and 40.75g/L vs 42.52g/L,P=0.020, respectively). In seroma group, the drainage volume of the first three days, the total and daily drainage volume were all higher (all p values less than 0.01), as well as drainage duration and hospital stay were longer(8.3d vs 14.4d, P=0.000 and 11.5d vs 23.7d, P=0.000, respectively). Logistic regression showed that older patients (OR=1.080, 95%CI 1.016∼1.148, P=0.013), lower total serum protein content(OR=0.814, 95%CI 0.705∼0.940, P=0.005)and higher drainage volume in d1(OR=1.009, 95%CI 1.001∼1.016, P=0.022) and d3 (OR=1.017, 95%CI 1.005∼1.029, P=0.005) were all independent risk factors for subcutaneous seroma. The daily average drainage curve showed a gradually decreasing trend with a highest collections in the first three days. The seroma group had significantly higher average daily drainage volume( P=0.034) and longer duration (P=0.000). & #x2028; Conclusion:The risk factors of seroma formation after breast cancer surgery are complicated. However in order to prevent its occurrence effectively, the factors including age, nutrition status and daily drainage volume should be taken into consideration. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 4085.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.SABCS-4085
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 8
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    Online Resource
    Abstract 3965: KIFC1 is a therapeutic target in lung cancers with extra centrosomes
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Research Vol. 83, No. 7_Supplement ( 2023-04-04), p. 3965-3965
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 83, No. 7_Supplement ( 2023-04-04), p. 3965-3965
    Abstract: Introduction: Lung cancer is a deadly malignancy and new treatments targeting mechanisms promoting its growth and progression are needed. Genomic instability (GIN) is a recurrent feature of lung tumours that promotes drug resistance and other cancer hallmarks. One mechanism that enables tumour-promoting GIN is centrosome amplification (CA). Centrosomes are organelles involved in chromosome segregation during cell division and two centrosomes in a bipolar arrangement normally ensure equal division of the genome during mitosis. CA, an abnormal increase in centrosome number, is frequently observed in lung and other cancers despite the fact that it can cause lethal multipolar mitotic spindles that potentiate aneuploidy. To mitigate detrimental consequences of CA, cancer cells can cluster extra centrosomes into pseudo-bipolar mitotic spindles. This process is facilitated by a protein called KIFC1 which is upregulated in a large proportion of lung cancers. However, KIFC1’s potential as a therapeutic target in lung cancers with CA has not been explored. Here we investigate the hypothesis that lung cancers with CA are dependent on KIFC1 and sensitive to its inhibition. Methods: Western blotting for KIFC1 and immunofluorescence (IF) for the centrosomal protein, CEP192, were used to measure basal expression and CA, respectively, across a panel of 21 lung adenocarcinoma (LUAD) and 3 non-malignant (NM) cell lines. KIFC1 loss-of-function (LOF) in H1299 and PC9 (LUAD), and BEAS-2B (NM) was achieved using CRISPR/Cas9 and siRNA. In vitro competition assays were done to assess the relative fitness of mCherry-tagged wild-type and GFP-tagged KIFC1-LOF cells in mixed populations over 3-4 cell passages using flow cytometry. CA was potentiated in cells using low doses of the compound, CFI-400945. Clonogenic survival and IF experiments were also done to determine the consequences of KIFC1 LOF. Results: Our findings suggests that basal KIFC1 expression and CA across 21 LUAD cell lines and 3 NM controls are variable. However, we observed a positive correlation (R2 = 0.52, p = 0.01) between KIFC1 expression and CA in LUAD lines. Competition assays revealed that KIFC1 LOF sensitizes LUAD cells with high KIFC1 expression, but not LUAD with low KIFC1 expression or NM cells, to pharmacologically-induced CA. Complementary siRNA experiments confirmed that KIFC1 LOF impairs the survival of cells with CA. Finally, we found that KIFC1 LOF was associated with an increase in multi-polar spindles. Conclusion: These findings support our hypothesis that LUAD with CA are dependent on KIFC1. We suspect its role in centrosome clustering explains this phenotype. Ongoing work is focused on validating these observations in additional models and clinical tumours to confirm its therapeutic potential in LUAD with CA, since combining KIFC1 inhibition with standard of care therapies that induce CA (eg. cisplatin, radiation) could represent an effective therapeutic strategy. Citation Format: Christopher Z. Zhang, Benson Z. Wu, Yin Fang Wu, Caterina di Ciano-Oliveira, Ju-Yoon Yoon, Tak W. Mak, David W. Cescon, Kelsie L. Thu. KIFC1 is a therapeutic target in lung cancers with extra centrosomes. [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 3965.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2023-3965
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 9
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    Online Resource
    P5-13-13: The Role of Topoisomerase IIa in Predicting Sensitivity to Anthracyclines in Breast Cancer Patients: A Meta-Analysis of Published Literatures.
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 24_Supplement ( 2011-12-15), p. P5-13-13-P5-13-13
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 24_Supplement ( 2011-12-15), p. P5-13-13-P5-13-13
    Abstract: Topoisomerase IIα is not only a proliferation marker of tumor cells but also a target for anthracycline-based chemotherapy. Both in vitro and in vivo studies have shown that there was a relationship between topo IIα and chemosensitivity to anthracyclines, but the predictive role of topo IIα is still controversial in breast cancer patients. A meta-analysis based on published studies was performed with the aim of obtaining an accurate evaluation of the association between topo IIα and sensitivity to anthracycline-based chemotherapy. A total of 13 eligible studies including 2,633 cases and 2,118 controls were identified. Topo IIα was associated with sensitivity to anthracyclines in locally advanced breast cancer patients who received neoadjuvant chemotherapy (RR = 1.93, 95%CI: 1.27−2.94, P=0.002; RR =1.98, 95%CI: 1.37−2.86, P & lt;0.001). In early breast cancer patients who received anthracycline-based adjuvant chemotherapy compared with non-taxane-based polychemotherapy, amplification(HR = 0.64, 95%CI: 0.49−0.83, P=0.001; HR = 0.59, 95% CI: 0.35−1.01, P=0.056) or deletion (HR = 0.82, 95%CI: 0.67−1.00, P=0.051; HR =0.58, 95%CI: 0.35−0.97, P=0.036) of topo IIα was significantly associated with better RFS and OS. The subgroup analysis in the early breast cancer patients indicated that taxane could be an interference for evaluation of the predictive role of topo IIα. In summary, the present meta-analysis suggests that topo IIα is a predictive factor for breast cancer patients who received anthracycline-based chemotherapy. Larger and well-designed prospective studies are required to further evaluate the predictive role of topo IIα in clinical practice. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P5-13-13.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.SABCS11-P5-13-13
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 10
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    Online Resource
    Abstract B040: Novel immunotherapy strategies targeting PTEN and TP53 defects in advanced prostate cancer
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Research Vol. 83, No. 11_Supplement ( 2023-06-02), p. B040-B040
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 83, No. 11_Supplement ( 2023-06-02), p. B040-B040
    Abstract: Prostate cancer is the most diagnosed cancer in men worldwide and the leading cause of cancer death in men worldwide. Genetic inactivation of PTEN and TP53 are common in advanced prostate cancers. Checkpoint immunotherapy has yielded meaningful responses across many cancers but shown modest activity in advanced prostate cancer. Prior studies showed that overexpression of immune checkpoint B7-H3 (CD276) correlates with the increased risks of clinical recurrence, disease spread, and poor outcomes in various cancer types, including prostate cancer. However, the roles of B7-H3 in prostate cancer development and its tumor microenvironment remain unclear, partially due to the lack of tissue-specific deletion mouse models. This gap in knowledge hinders the application of immunotherapy targeting B7-H3 in prostate cancers. To identify PTEN- and p53-associated immune checkpoints, we performed multi-omics analyses of expression patterns of 51 checkpoint molecules in human prostate cancer samples and found that B7-H3 is one of the most significantly overexpressed immune checkpoints in prostate tumors containing PTEN and TP53 genetic inactivation. Mechanistically, we found that the PTEN-AKT pathway co-operates with p53 pathway in modulating B7-H3 expression in cancer cells. In Pten/Trp53 genetically engineered mouse (GEM) models, prostate-specific deletion of Cd276 resulted in markedly delayed tumor progression and reversed immunosuppression in the tumor microenvironment. Furthermore, we developed and evaluated novel combinatorial immunotherapy strategies targeting B7-H3 in advanced prostate cancer with PTEN and TP53 deficiencies. Citation Format: Wei Shi, Yin Wang, Yuehui Zhao, Di Zhao. Novel immunotherapy strategies targeting PTEN and TP53 defects in advanced prostate cancer [abstract]. In: Proceedings of the AACR Special Conference: Advances in Prostate Cancer Research; 2023 Mar 15-18; Denver, Colorado. Philadelphia (PA): AACR; Cancer Res 2023;83(11 Suppl):Abstract nr B040.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.PRCA2023-B040
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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