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  • American Association for Cancer Research (AACR)  (8)
  • 1
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    Online Resource
    Loss of Fbxw7 Impairs Development of and Induces Heterogeneous Tumor Formation in the Mouse Mammary Gland
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 24 ( 2020-12-15), p. 5515-5530
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 24 ( 2020-12-15), p. 5515-5530
    Abstract: Fbxw7 is an F-box protein that contributes to regulation of cell proliferation and cell fate determination as well as to tumor suppression in various tissues. In this study, we generated mice with mammary gland–specific ablation of Fbxw7 (Blg-Cre/Fbxw7F/F mice) and found that most neonates born to mutant dams die soon after birth as a result of defective maternal lactation. The mammary gland of mutant dams was markedly atrophic and manifested both excessive cell proliferation and apoptosis in association with the accumulation of Notch1 and p63. Despite the hypoplastic nature of the mutant mammary gland, Blg-Cre/Fbxw7F/F mice spontaneously developed mammary tumors that resembled basal-like carcinoma with marked intratumoral heterogeneity. Additional inactivation of Trp53 in Blg-Cre/Fbxw7F/F mice further promoted onset and development of mammary tumors, suggesting that spontaneous mutation of Trp53 may facilitate transition of hypoplastic mammary lesions to aggressive cancer in mice lacking Fbxw7. RNA-sequencing analysis of epithelial- and mesenchymal-like cell lines from a Blg-Cre/Fbxw7F/F mouse tumor revealed an increased mutation rate and structural alterations in the tumor and differential expression of upstream transcription factors including known targets of Fbxw7. Together, our results implicate Fbxw7 in the regulation of cell differentiation and in tumor suppression in the mammary gland. Loss of Fbxw7 increases mutation rate and chromosome instability, activates signaling pathways governed by transcription factors regulated by Fbxw7, and triggers the development of mammary tumors with prominent heterogeneity. Significance: Mammary gland–specific ablation of Fbxw7 in mice results in defective gland development and spontaneous mammary tumor formation reminiscent of human basal-like carcinoma with intratumoral heterogeneity.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-20-0271
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 2
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    The Combination of Multiple Receptor Tyrosine Kinase Inhibitor and Mammalian Target of Rapamycin Inhibitor Overcomes Erlotinib Resistance in Lung Cancer Cell Lines through c-Met Inhibition
    American Association for Cancer Research (AACR) ; 2010
    In:  Molecular Cancer Research Vol. 8, No. 8 ( 2010-08-01), p. 1142-1151
    Details
    In: Molecular Cancer Research, American Association for Cancer Research (AACR), Vol. 8, No. 8 ( 2010-08-01), p. 1142-1151
    Abstract: Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI) show antitumor activity in a subset of non–small cell lung cancer (NSCLC) patients. However, the initial tumor response is followed by recurrence. Several studies have suggested the importance of other receptor tyrosine kinases (RTK) and downstream kinases as potential targets in the treatment of NSCLC. We used the multiple-RTK inhibitor AEE788, which inhibits EGFR, vascular endothelial growth factor receptor, and human epidermal growth factor receptor 2, with and without the downstream kinase inhibitor RAD001 (an inhibitor of mammalian target of rapamycin). AEE788 inhibited cell growth more effectively than did erlotinib in three NSCLC cell lines examined (A549, H1650, and H1975). However, in the EGFR-TKI–resistant cell line H1975 harboring T790M resistance mutation, cell growth inhibition by AEE788 was only mild, and the phosphorylation of its leading targets such as EGFR and vascular endothelial growth factor receptor 2 was not inhibited. In H1975, AEE788 induced significantly greater cell growth inhibition when combined with RAD001 than when used alone. This cooperative effect was not seen with the combination of erlotinib and RAD001. We found that c-Met was highly phosphorylated in this cell line, and the phosphorylated c-Met was inhibited effectively by AEE788. Using a phospho-RTK array, the phosphorylation of c-Met and insulin-like growth factor-I receptor was inhibited by AEE788. These results suggest that upstream RTK inhibitor overcomes the acquired resistance to EGFR-TKI when combined with downstream kinase inhibitor. Thus, the combined inhibition of upstream and downstream RTKs is a promising strategy for the treatment of NSCLC. Mol Cancer Res; 8(8); 1142–51. ©2010 AACR.
    Type of Medium: Online Resource
    ISSN: 1541-7786 , 1557-3125
    URL: Article
    DOI: 10.1158/1541-7786.MCR-09-0388
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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    SSG: 12
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  • 3
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    Online Resource
    The Coordinated Actions of TIM-3 on Cancer and Myeloid Cells in the Regulation of Tumorigenicity and Clinical Prognosis in Clear Cell Renal Cell Carcinomas
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Immunology Research Vol. 3, No. 9 ( 2015-09-01), p. 999-1007
    Details
    In: Cancer Immunology Research, American Association for Cancer Research (AACR), Vol. 3, No. 9 ( 2015-09-01), p. 999-1007
    Abstract: Clear cell renal cell carcinoma (ccRCC) is one of most common cancers in urogenital organs. Although recent experimental and clinical studies have shown the immunogenic properties of ccRCC as illustrated by the clinical sensitivities to various immunotherapies, the detailed immunoregulatory machineries governing the tumorigenicity of human ccRCC remain largely obscure. In this study, we demonstrated the clinical significance and functional relevance of T-cell immunoglobulin and mucin domain-containing molecule-3 (TIM-3) expressed on tumor cells and myeloid cells in patients with ccRCC. TIM-3 expression was detected on cancer cells and CD204+ tumor-associated macrophages (TAM), and higher expression level of TIM-3 was positively correlated with shorter progression-free survival (PFS) in patients with ccRCC. We found that TIM-3 expression was detected on a large number of tumors, and there was significant correlation between an increased number of TAMs and high expression level of TIM-3 in patients with ccRCC. Furthermore, TIM-3 rendered RCC cells with the ability to induce resistance to sunitinib and mTOR inhibitors, the standard regimen for patients with ccRCC, as well as stem cell activities. TIM-3 expression was induced on CD14+ monocytes upon long-term stimulation with RCC cells, and TIM-3–expressing myeloid cells play a critical role in augmenting tumorigenic activities of TIM-3-negative RCC cells. More importantly, treatment with anti–TIM-3 mAb suppressed its tumorigenic effects in in vitro and in vivo settings. These findings indicate the coordinated action of TIM-3 in cancer cells and in myeloid cells regulates the tumorigenicity of human RCC. Cancer Immunol Res; 3(9); 999–1007. ©2015 AACR.
    Type of Medium: Online Resource
    ISSN: 2326-6066 , 2326-6074
    URL: Article
    DOI: 10.1158/2326-6066.CIR-14-0156
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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  • 4
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    p53 -Altered FBXW7 Expression Determines Poor Prognosis in Gastric Cancer Cases
    American Association for Cancer Research (AACR) ; 2009
    In:  Cancer Research Vol. 69, No. 9 ( 2009-05-01), p. 3788-3794
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 69, No. 9 ( 2009-05-01), p. 3788-3794
    Abstract: A molecular target associated with the progression of gastric cancer has not yet been uncovered. FBXW7 is a tumor suppressor gene transcriptionally controlled by p53 that plays a role in the regulation of cell cycle exit and reentry via c-Myc degradation. Few studies have addressed the clinical significance of FBXW7 expression in gastric cancer. Therefore, we examined FBXW7 mRNA expression to determine its clinicopathologic significance in 100 cases of gastric cancer. Low expression levels of FBXW7 in primary gastric cancer contributed to malignant potential, such as lymph node metastasis (P = 0.0012), tumor size (P = 0.0003), and poor prognosis (P = 0.018). In comparison with 52 cases of gastric cancer without the p53 mutation, 29 cases with the mutation exhibited lower expression levels of FBXW7 (P = 0.0034), revealing a significant relationship between p53 mutation and FBXW7 expression. Furthermore, we found that gastric cancer patients who had low FBXW7 expression levels and p53 mutation had a distinctively poor prognosis in comparison with other subgroups (P = 0.0033). In conclusion, we showed a role for p53 in the transcriptional regulation of FBXW7 expression in clinical gastric cancer cases and showed that disruption of both p53 and FBXW7 contributes to poor prognosis. [Cancer Res 2009;69(9):3788–94]
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-08-2846
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
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    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 5
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    Abstract 3081: SHOC2 is a critical modulator of the sensitivity to EGFR-TKI in non-small cell lung cancer cells
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 16_Supplement ( 2020-08-15), p. 3081-3081
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 16_Supplement ( 2020-08-15), p. 3081-3081
    Abstract: Epidermal Growth Factor Receptor tyrosine kinase inhibitors (EGFR-TKI) have become the first line treatment for patients with EGFR mutated non-small cell lung cancer (NSCLC) as a result of multiple clinical trials demonstrating superior response and less toxicity as compared to conventional cytotoxic agents. However, despite the clinical experience among nearly two decades, it is well known that EGFR-TKI monotherapy cannot cure EGFR mutation-positive lung cancer patients due to the occurrence of drug resistance. While dramatic initial tumor shrinkage is shown in most patients with EGFR-TKI treatment, therapeutic resistance is often observed in 1-2 years. This is likely caused by the outgrowth of rare pre-existing resistant clones and/or small fraction of drug tolerant persister cells (DTPs) which survive and acquire resistance to EGFR-TKIs. Several previous studies have clarified the acquired resistance mechanisms to EGFR-TKIs, but little is known how the DTPs survive during the initial phase of drug exposure and rapidly adapt to EGFR-TKIs. Utilizing the genome wide CRISPR/Cas9 screening, we have previously reported that DTPs were capable to exploit endoplasmic reticulum stress to survive EGFR-TKI exposure (Terai, et al, Cancer Research 2018). Further analysis of this data identified multiple genes which could affect the initial drug response to EGFR-TKIs, including the scaffold protein coding gene, SHOC2. In our present study we focused on this unique protein and revealed its critical function as a modulator of drug response to EGFR-TKIs in lung cancer cells. We confirmed that depletion/overexpression of SHOC2 in PC9 cells, an EGFR-dependent NSCLC cell line, renders the cells sensitive/resistant to all 1st to 3rd generation EGFR-TKIs. We have also confirmed similar findings with another EGFR dependent NSCLC cell line named H1975. Reduction of phosphorylation levels of ERK1/2 induced by EGFR-TKIs were stronger in PC9 or H1975 cells with SHOC2 knockout, indicating that SHOC2 can facilitate ERK1/2 reactivation during EGFR-TKI treatment. The above data indicate that SHOC2 is essential for DTPs and its function is correlated with MAPK-ERK pathway activity. Celastrol, a candidate SHOC2 inhibitor, inhibited the emergence of DTPs and synergized with EGFR-TKIs. Additionally, we showed that SHOC2 depletion enhanced the growth inhibitory effect of osimertinib in vivo. Lastly, we confirmed the increased expression of SHOC2 in clinical human samples which experienced EGFR-TKI failure. Our findings could offer a new treatment strategy for NSCLC patients with EGFR mutation leading to the increase of the degree and duration of EGFR TKIs response. Citation Format: Hideki Terai, Junko Hamamoto, Tadashi Manabe, Katsura Emoto, Takeshi Masuda, Satoshi Kuronuma, Keigo Kobayashi, Keita Masuzawa, Shinnosuke Ikemura, Sohei Nakayama, Ichiro Kawada, Yusuke Suzuki, Osamu Takeuchi, Yukio Suzuki, Sumio Ohtsuki, Hiroyuki Yasuda, Kenzo Soejima, Koichi Fukunaga. SHOC2 is a critical modulator of the sensitivity to EGFR-TKI in non-small cell lung cancer cells [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 3081.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2020-3081
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 6
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    SHOC2 Is a Critical Modulator of Sensitivity to EGFR–TKIs in Non–Small Cell Lung Cancer Cells
    American Association for Cancer Research (AACR) ; 2021
    In:  Molecular Cancer Research Vol. 19, No. 2 ( 2021-02-01), p. 317-328
    Details
    In: Molecular Cancer Research, American Association for Cancer Research (AACR), Vol. 19, No. 2 ( 2021-02-01), p. 317-328
    Abstract: EGFR mutation-positive patients with non–small cell lung cancer (NSCLC) respond well to treatment with EGFR–tyrosine kinase inhibitors (EGFR–TKI); however, treatment with EGFR–TKIs is not curative, owing to the presence of residual cancer cells with intrinsic or acquired resistance to this class of drugs. Additional treatment targets that may enhance the efficacy of EGFR–TKIs remain elusive. Using a CRISPR/Cas9-based screen, we identified the leucine-rich repeat scaffold protein SHOC2 as a key modulator of sensitivity to EGFR–TKI treatment. On the basis of in vitro assays, we demonstrated that SHOC2 expression levels strongly correlate with the sensitivity to EGFR–TKIs and that SHOC2 affects the sensitivity to EGFR–TKIs in NSCLC cells via SHOC2/MRAS/PP1c and SHOC2/SCRIB signaling. The potential SHOC2 inhibitor celastrol phenocopied SHOC2 depletion. In addition, we confirmed that SHOC2 expression levels were important for the sensitivity to EGFR–TKIs in vivo. Furthermore, IHC showed the accumulation of cancer cells that express high levels of SHOC2 in lung cancer tissues obtained from patients with NSCLC who experienced acquired resistance to EGFR–TKIs. These data indicate that SHOC2 may be a therapeutic target for patients with NSCLC or a biomarker to predict sensitivity to EGFR–TKI therapy in EGFR mutation-positive patients with NSCLC. Our findings may help improve treatment strategies for patients with NSCLC harboring EGFR mutations. Implications: This study showed that SHOC2 works as a modulator of sensitivity to EGFR–TKIs and the expression levels of SHOC2 can be used as a biomarker for sensitivity to EGFR–TKIs.
    Type of Medium: Online Resource
    ISSN: 1541-7786 , 1557-3125
    URL: Article
    DOI: 10.1158/1541-7786.MCR-20-0664
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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    SSG: 12
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  • 7
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    Abstract PS13-31: Prospective observational study to explore the effectiveness of eribulin as first- or second- line chemotherapy in patients with HER2-negative hormone-resistant advanced or metastatic breast cancer (KBCRN A001: E-SPEC study)
    American Association for Cancer Research (AACR) ; 2021
    In:  Cancer Research Vol. 81, No. 4_Supplement ( 2021-02-15), p. PS13-31-PS13-31
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 81, No. 4_Supplement ( 2021-02-15), p. PS13-31-PS13-31
    Abstract: BackgroundEribulin (E) is a chemotherapeutic drug that prolongs overall survival (OS) of patients with HER2-negative advanced or metastatic breast cancer (AMBC), mainly in multi-line chemotherapy (ChT) or later. However, the effectiveness and optimal scheduling of E remain unclear. We prospectively investigated the impact of E use in 1st- and 2nd-line ChT (early E) for patients with endocrine-resistant AMBC. Methods In this multi-institutional prospective cohort study, we registered patients with hormone receptor-positive AMBC who relapsed during or within 6 months after ending adjuvant endocrine therapy, were refractory to at least one previous endocrine therapy, or patients with triple negative AMBC. The endpoints were 1st-line OS (OS1), 2nd-line OS (OS2), and 3rd-line OS (OS3), defined as the time from the start of treatment to death. In addition, the time from the start of 1st-line ChT to death was also analyzed for 2nd-line and 3rd-line ChT groups. In addition to E therapy, oral FU-based therapies (FU) and anthracycline or taxane-based therapies (A/T) were also analyzed (ClinicalTrial.gov number, NCT02551263). Results Between June 2015 and July 2017, a total of 201 patients were enrolled, and full analysis was conducted for 180 patients. The median OS1, OS2, and OS3 of all patients was 2.69, 1.74, and 1.13 years, respectively. Major patient characteristics are described in the Table. Concurrent or maintenance endocrine therapy was used by 14.9%, 31.6%, and 12.9% of patients receiving E, FU and A/T in 1st-line ChT, respectively. The median OS of patients using E was OS1: 2.25 years (N=47), OS2: 1.75 years (N=70) and OS3: 0.94 years (N=16). The median OS of patients using A/T was OS1: 2.60 years (N=70), OS2: 1.69 years (N=44) and OS3: 0.96 years (N=49). The median OS of patients using FU was OS1: 3.49 years (N=57), OS2: 2.33 years (N=27), and OS3: 1.45 years (N=24). The time from the start of 1st-line ChT to death was 2.58 and 3.18 years among patients who received E in 2nd- and 3rd-line ChT, respectively. Multivariate analysis of patients who used 1st-line and 2nd-line E demonstrated that higher LDH (≥300) (HR 3.50, 95% CI 1.78-6.73; p & lt;0.001), brain metastasis (HR 2.64, 95% CI 1.02-6.83; p=0.045) and smoker (HR 2.33, 95% CI 1.20-4.53; p=0.013) were associated with shorter OS. Overall, OS data for E were comparable to those for A/T. While OS tended to be better for FU, patient characteristics for 1st-line ChT showed that FU was often used for patients with less aggressive AMBC. We also present data on second progression-free survival and new metastasis-free survival, prognostic factor analysis and prognostic factor-adjusted comparison, and predictive factor analysis for early E. Conclusions This prospective observational study of AMBC patients showed that E and A/T had similar survival outcomes in each treatment line. While FU led to relatively longer survival, it was often used for patients with less aggressive AMBC. Analysis data on survival outcomes will also be presented. Patient characteristics according to 1st-line therapyE (n=47)Oral FU based (n=57)A/T based (n=70)Median age (IQR)61(54-71)64(51-68)59(48-66)Triple negative, n (%)15(31.9)11(19.3)23(32.9)Disease-free interval, n (%) & lt;2 years15(31.9)9(15.8)12(17.1)2-5 years12(25.5)18(31.6)15(21.4)5-8 years4(8.5)9(15.8)9(12.9) & gt;8years3(6.4)10(17.5)8(11.4)Stage49(19.1)9(15.8)23(32.9)(neo) Adjuvant chemotherapy, n (%)30(63.8)36(63.2)32(45.7)Metastatic sites at 1st-line ChT, n (%)Liver16(34.0)12(21.1)22(31.4)Lung15(31.9)17(29.8)25(35.7)Bone24(51.1)27(47.3)36(51.4)Brain6(12.8)1(1.8)2(2.9) Citation Format: Yuri Fujimoto, Yuichiro Kikawa, Takeshi Kotake, Shigeru Tsuyuki, Sachiko Takahara, Hiroyasu Yamashiro, Hiroshi Yoshibayashi, Masahiro Takada, Rie Yasuoka, Kazuhiko Yamagami, Hirofumi Suwa, Toshitaka Okuno, Ichiro Nakayama, Tatsuji Kato, Nobuko Ogura, Yoshio Moriguchi, Hiroshi Ishiguro, Tatsuo Kagimura, Tetsuya Taguchi, Tomoharu Sugie, Masakazu Toi. Prospective observational study to explore the effectiveness of eribulin as first- or second- line chemotherapy in patients with HER2-negative hormone-resistant advanced or metastatic breast cancer (KBCRN A001: E-SPEC study) [abstract]. In: Proceedings of the 2020 San Antonio Breast Cancer Virtual Symposium; 2020 Dec 8-11; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2021;81(4 Suppl):Abstract nr PS13-31.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.SABCS20-PS13-31
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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  • 8
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    A Phase I Study of In vitro Expanded Natural Killer T Cells in Patients with Advanced and Recurrent Non–Small Cell Lung Cancer
    American Association for Cancer Research (AACR) ; 2006
    In:  Clinical Cancer Research Vol. 12, No. 20 ( 2006-10-15), p. 6079-6086
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 12, No. 20 ( 2006-10-15), p. 6079-6086
    Abstract: Purpose: Human Vα24 natural killer T (Vα24 NKT) cells bearing an invariant Vα24JαQ antigen receptor are activated by a glicolipid ligand α-galactosylceramide (αGalCer; KRN7000) in a CD1d-dependent manner. The human Vα24 NKT cells activated with αGalCer and interleukin-2 have been shown to produce large amounts of cytokines, such as IFN-γ, and also exerting a potent killing activity against various tumor cell lines. We did a phase I study with autologous activated Vα24 NKT cell therapy. Experimental Design: Patients with advanced or recurrent non–small cell lung cancer received i.v. injections of activated Vα24 NKT cells (level 1: 1 × 107/m2 and level 2: 5 × 107/m2) to test the safety, feasibility, and clinical response of this therapeutic strategy. Immunomonitoring was also done in all cases. Results: Six patients were enrolled in this study. No severe adverse events were observed during this study in any patients. After the first and second injection of activated Vα24 NKT cells, an increased number of peripheral blood Vα24 NKT cells was observed in two of three cases receiving a level 2 dose of activated Vα24 NKT cells. The number of IFN-γ-producing cells in peripheral blood mononuclear cells increased after the administration of activated Vα24 NKT cells in all three cases receiving the level 2 dose. No patient was found to meet the criteria for either a partial or a complete response. Conclusions: The clinical trial with activated Vα24 NKT cell administration was well tolerated and carried out safely with minor adverse events even in patients with advanced diseases.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-06-0114
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2006
    detail.hit.zdb_id: 1225457-5
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