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  • American Association for Cancer Research (AACR)  (4)
  • 2020-2024  (4)
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  • American Association for Cancer Research (AACR)  (4)
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  • 2020-2024  (4)
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  • 1
    Online Resource
    Online Resource
    Abstract 1670: Characterization of the chick chorioallantoic membrane tumor model in comparison with various xenograft mouse tumors
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 16_Supplement ( 2020-08-15), p. 1670-1670
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 16_Supplement ( 2020-08-15), p. 1670-1670
    Abstract: Background: The chick chorioallantoic membrane (CAM) tumor model is an in vivo three-dimensional culture model that is easy to use and inexpensive, has no ethical issues, and has been used in cancer research, although the success rate of generating CAM tumors varies among reports. We analyzed the success rate of CAM tumors from patient-derived xenograft (PDX) of esophageal squamous cell carcinoma (ESCC) and many cell line-derived xenograft (CDX) tumors of different cancer types, and we sought to determine which factors affected the success rate of generating CAM tumors. Method: We used patient cancer tissue (ESCC) and/or commercially available 12 tumorigenic cancer cell lines (esophageal cancer [TE-11 and HCE4], pancreatic cancer [CFPA-1, MIA PaCa2, and PANC-1] , lung cancer [A549 and H358], skin cancer [A431 and B16F10] , and biliary tract cancer [HuCCT-1, TFK-1, and MzchA2]) to generate xenograft tumors. Small (1- to 2-mm) pieces of xenograft tumors were grafted onto the CAMs of fertilized eggs. After incubating for an additional 7 to 9 days at 37.5°C and 65% humidity, nodules were observed on the assigned locations of each CAM. On the basis of hematoxylin and eosin (H & E) staining, we calculated the success rate of the CAM tumor engraftment. H & E staining was also performed with parental PDX or CDX tumors as well as parental ESCC tissues, to compare them with CAM tumors. Results: A total of 29 xenograft tumors were transplanted onto CAMs. The overall success rate in generating CAM tumors was 19/29 (66%). The CAM tumors were histologically quite similar to those of their parental CDX or PDX tumors, and the CAM tumors from PDX ESCC were also histologically similar to their parent ESCC tumors. Tumor pieces from poorly-differentiated xenograft tumors (including PDX ESCC) generated CAM tumors with a 90% success rate (19/21), in comparison with well-differentiated xenograft tumors, whose success rate was 0% (0/8). Conclusion: The overall success rate in generating CAM tumors, especially from poorly differentiated tumors, seems acceptable. The histological similarity between CAM tumors and both parent xenograft and parent tumors from humans indicates that the CAM tumor model is a promising in vivo model for the study of poorly differentiated tumors. As for well-differentiated tumors, this model has to be further optimized to increase the success rate of engraftment. Citation Format: Tomoki Saito, Shinya Ohashi, Ayaka Mizumoto, Osamu Kikuchi, Kotaro Matsumoto, Aoi Komatsu, Seiji Naganuma, Yoshihiro Yamamoto, Kenshiro Hirohashi, Masahiro Yoshioka, Masashi Tamaoki, Makiko Funakoshi, Fuyuhiko Tamanoi, Manabu Muto. Characterization of the chick chorioallantoic membrane tumor model in comparison with various xenograft mouse tumors [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 1670.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2020-1670
    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
    Location Call Number Limitation Availability
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  • 2
    Online Resource
    Online Resource
    Abstract 321: Novel bone microenvironment model of prostate cancer with chitosan fiber matrix and osteoblast in 3D culture
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 16_Supplement ( 2020-08-15), p. 321-321
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 16_Supplement ( 2020-08-15), p. 321-321
    Abstract: BACKGROUND: The interaction between prostate cancer cells and osteoblast is essential for the development of bone metastasis. Recently, novel androgen receptor signal inhibitors (ARSi) have been approved for metastatic castration naïve (mCNPC), or non-metastatic castration resistant prostate cancer (nmCRPC), both of which should be pivotal to investigate the association between bone microenvironment and tumor. We established a novel 3D in vitro culture method reflecting bone microenvironment and evaluated the drug susceptibility of ARSi including enzalutamide, apalutamide, darolutamide, and abiraterone (Abi) with/without dutasteride (Duta). METHODS: GFP-transferred C4-2 (CRPC cell line) and RFP-transferred human osteoblast differentiated from human-mesenchymal stem cell was co-cultured in chitosan nanofiber, a mimicry of 3D scaffold of bone microenvironment, coated culture plate (Cosmo bio Co., LTD). The growth of C4-2 cell was quantified using live-cell imaging and analysis system, Cell3 iMager duos (SCREEN). Abi metabolites including delta-4 abiraterone (D4A) and 3-keto-5-alfa abiraterone in C4-2 cells were measured by ESI-TOF-MS method. RESULTS: We could non-invasively quantify the sustained growth of C4-2 cells at maximum of 30 days. IC50 of each drugs and combination effect of Abi and Duta was evaluated using this model. Combination treatment synergistically inhibited the growth of C2-4 cells compared with each drug alone. D4A, the strongest anti-proliferative metabolite of Abi under the CRPC-specific backdoor pathway, was detected from the treated C4-2 cell. These results were coincided with the effective cases of pharmacokinetics of Abi metabolites in our ongoing phase II clinical trial of combination therapy of Abi with Duta for CRPC (UMIN000027795). Furthermore, combination of abiraterone and dutasteride was most potent cell growth inhibitor than other ARis tested in this model. This model is applying for international patent (C12N 5/09). CONCLUSIONS: Our bone microenvironment model is unique and useful to evaluate the new drug susceptibility testing in prostate cancer cells. This model may help in disclose unknown mechanisms from micro- to clinical bone metastasis in prostate cancer. Citation Format: Masahiro Samoto, Hiroaki Matsumoto, Hiroshi Hirata, Sho Ozawa, Junichi Mori, Ryo Inoue, Seiji Yano, Yoshiaki Yamamoto, Hideyasu Matsuyama. Novel bone microenvironment model of prostate cancer with chitosan fiber matrix and osteoblast in 3D culture [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 321.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2020-321
    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
    Location Call Number Limitation Availability
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    Online Resource
  • 3
    Online Resource
    Online Resource
    Abstract 4478: Effective prediction of treatment responders with anti-PD-1 antibody in malignant pleural mesothelioma by diversity of peripheral CD8+PD-1+ T cell subpopulation
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 16_Supplement ( 2020-08-15), p. 4478-4478
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 16_Supplement ( 2020-08-15), p. 4478-4478
    Abstract: Background: Programmed death 1 (PD-1) blockade with Nivolumab are effective in patients with malignant pleural mesothelioma (MPM), however; successful predictive biomarker has not been available. Unlike invasive test with tumor biopsy, peripheral blood is safe and easily obtainable source of biomarkers. We have previously reported that T cell receptor (TCR) diversity of CD8+PD-1+ T cells were effective to predict response to anti-PD-1 antibody treatment in non-small cell lung cancer (NSCLC) patients (AACR2019: Abstract nr 2230). In this study, Next generation sequence(NGS)-based TCR α and β repertoires were examined with peripheral CD8+PD-1+ T cells isolated from 11 patients with MPM and treatment responses were evaluated 2 months after anti-PD-1 antibody treatment. Methods: Peripheral blood mononuclear cells were collected from 11 MPM patients enrolled in this study before administration of anti-PD-1 antibody (Nivolumab). NGS-based TCR α and β repertoire analysis were performed with CD8+PD-1+ T cells isolated with FACS sorting by Repertoire Genesis Inc. TCR diversity was statistically evaluated by Shannon, Simpson and Diversity Evenness 50 (DE50) indices. CT scan was performed during week 8 of treatment and used to determine response to nivolumab. This study was approved by the Ethical Committee of Hyogo College of Medicine. Results: Three of 11 (27.3%) MPM patients responded to anti-PD-1 treatment. There were good correlation of all diversity indices between TCRα and TCRβ. TCRβ diversity was significantly higher among responders than non-responders based on DE50 (0.0019 ± 0.00032 vs 0.0011 ± 0.00042, P & lt; 0.05). Also, responders exhibited a clear trend to have higher TCR diversity of CD8+PD-1+ T cells in terms of Shannon, normalized Shannon and Simpson indices. Conclusion: Like NSCLC patients, PD-1 blockade was more effective in MPM patients who had higher levels of TCR diversity in peripheral CD8+PD-1+ T cells. This result suggested the TCR diversity of peripheral CD8+PD-1+ T cells has potential to predict response to immune checkpoint inhibitors in various tumor patient. Further clinical study would be needed to verify effectiveness of this biomarker. Citation Format: Seiji Matsumoto, Takaji Matsutani, Yoshiko Fujita, Ryo Takahashi, Takashi Yokoi, Hiroshi Kodama, Yoshie Inao, Kazutaka Kitaura, Tohoru Nakamichi, Akifumi Nakamura, Ayumi Kuroda, Aki Kobayashi, Masaki Hashimoto, Nobuyuki Kondo, Ryuji Suzuki, Koichiro Yamakado, Takashi Kijima, Seiki Hasegawa. Effective prediction of treatment responders with anti-PD-1 antibody in malignant pleural mesothelioma by diversity of peripheral CD8+PD-1+ T cell subpopulation [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 4478.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2020-4478
    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
    Location Call Number Limitation Availability
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  • 4
    Online Resource
    Online Resource
    Proteasome Inhibition Overcomes ALK-TKI Resistance in ALK -Rearranged/ TP53 -Mutant NSCLC via Noxa Expression
    American Association for Cancer Research (AACR) ; 2021
    In:  Clinical Cancer Research Vol. 27, No. 5 ( 2021-03-01), p. 1410-1420
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 27, No. 5 ( 2021-03-01), p. 1410-1420
    Abstract: In ALK-rearranged non–small cell lung cancer (NSCLC), impacts of concomitant genetic alterations on targeted therapies with ALK-tyrosine kinase inhibitors (ALK-TKI) are not yet well understood. Here, we investigated genetic alterations related to ALK-TKI resistance using clinico-genomic data and explored effective therapies to overcome the resistance in preclinical models through the identification of underlying molecular mechanisms. Experimental Design: We used integrated clinical and next-generation sequencing data generated in a nationwide lung cancer genome screening project (LC-SCRUM-Japan). ALK-rearranged NSCLC cell lines expressing wild-type or mutant TP53 were used to evaluate cellular apoptosis induced by ALK-TKIs. Results: In 90 patients with ALK-rearranged NSCLC who were treated with a selective ALK-TKI, alectinib, TP53 comutated patients showed significantly worse progression-free survival (PFS) than TP53 wild-type patients [median PFS, 11.7 months (95% confidence interval, CI, 6.3–not reached, NR) vs. NR (23.6–NR); P = 0.0008; HR, 0.33 (95% CI, 0.17–0.65)]. ALK-rearranged NSCLC cell lines that lost p53 function were resistant to alectinib-induced apoptosis, but a proteasome inhibitior, ixazomib, markedly induced apoptosis in the alectinib-treated cells by increasing the expression of a proapoptotic protein, Noxa, which bound to an antiapoptotic protein, Mcl-1. In subcutaneous tumor models, combination of ixazomib and alectinib prominently induced tumor regression and apoptosis even though the tumors were generated from ALK-rearranged NSCLC cells with nonfunctional p53. Conclusions: These clinical and preclinical results indicate concomitant TP53 mutations reduce the efficacy of alectinib for ALK-rearranged NSCLC and the combined use of a proteasome inhibitor with alectinib is a promising therapy for ALK-rearranged/TP53-mutated NSCLC.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-20-2853
    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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