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  • 1
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    Comparative mutational evaluation of multiple lung cancers by multiplex oncogene mutation analysis
    Wiley ; 2018
    In:  Cancer Science Vol. 109, No. 11 ( 2018-11), p. 3634-3642
    Details
    In: Cancer Science, Wiley, Vol. 109, No. 11 ( 2018-11), p. 3634-3642
    Abstract: In patients presenting with synchronous or metachronous multiple lung cancer ( MLC ), it is important to distinguish between multiple primary lung cancer ( MP ) and intrapulmonary metastasis ( IM ). The present study was aimed at investigating the mutational profiles of synchronous/metachronous MLC and to compare the classification of paired tumors by multiplex gene mutation analysis with the histopathological evaluation. We carried out targeted sequencing of 20 lung cancer‐related oncogenes using next‐generation sequencing ( NGS ) in 82 tumors from 37 MLC patients who underwent surgical resection at our department. The patients were diagnosed as MP or IM cases based on the Martini and Melamed criteria, histopathological and gene mutational evaluations. Matching mutations between paired tumors was observed in 20 (54%) patients, who were diagnosed as IM cases by mutational evaluation. Patients who could not be clearly diagnosed by histopathological evaluation were classified as equivocal cases. Among the histopathological IM cases (n = 7), six (86%) were confirmed as IM cases also by mutational evaluation, and most of the paired tumors of these cases (n = 5) harbored multiple matching mutations. Among the histopathological MP cases (n = 17), mutational evaluation yielded a discordant diagnosis in eight (47%) cases. Of these, the paired tumors of four cases harbored multiple matching mutations, suggesting that the mutational diagnosis might be more suitable in these patients. Our findings suggest that multiplex mutational analysis could be a useful complementary tool for distinguishing between MP and IM in addition to histopathological evaluation.
    Type of Medium: Online Resource
    ISSN: 1347-9032 , 1349-7006
    URL: Issue
    URL: Article
    DOI: 10.1111/cas.2018.109.issue-11
    DOI: 10.1111/cas.13797
    Language: English
    Publisher: Wiley
    Publication Date: 2018
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  • 2
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    Abstract 4777: Antitumor effect of neratinib in lung cancers harboring HER2 oncogene alterations
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Research Vol. 78, No. 13_Supplement ( 2018-07-01), p. 4777-4777
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 4777-4777
    Abstract: Background The HER2-targeted therapy for non-small cell lung cancer (NSCLC) harboring HER2 oncogene alterations is one of promising strategy to improve the clinical outcome of treatment for NSCLC. In this study, we investigated the antitumor effect of neratinib, an irreversible pan-HER tyrosine kinase inhibitor (TKI) in NSCLC cells harboring HER2 alterations including mutation and amplification. Materials and Methods We examined the sensitivity of neratinib against normal bronchial epithelial cells BEAS-2B which ectopically overexpressing wild-type or mutant HER2. Furthermore, we examined the antitumor activity of neratinib in addition to afatinib in several NSCLC cell lines harboring HER2 or EGFR alterations in in vitro and in vivo experiments, and investigated the association between their genetic alterations and sensitivity to neratinib treatment. Results BEAS-2B cells ectopically overexpressing wild-type HER2 or mutants (A775insYVMA, G776VC, G776LC, P780insGSP, V659E, G660D, and S310F) showed constitutive autophosphorylation of HER2 and activation of downstream signaling by Western blotting. These BEAS-2B cells were sensitive to neratinib, but insensitive to erlotinib, a first generation EGFR-TKI. Neratinib also showed antiproliferative effects on both HER2-altered (H2170, Calu-3, and H1781) and EGFR-mutant (HCC827, PC9, and HCC4006) NSCLC cell lines. Neratinib administration showed strong antitumor effect on tumor growth in mouse xenograft model using HER2-altered lung cancer cell lines. Conclusions Our study strongly suggests that neratinib is a promising therapeutic option for the treatment of HER2-altered NSCLC. Citation Format: Yusuke Ogoshi, shinichi Toyooka, Jyunichi Soh, hiromasa Yamamoto, Kazuhiko Shien, Hidejiro torigoe, Hiroki sato, Takahiro Yoshioka, Kei Namba, Yuta Takahashi, Eisuke Kurihara. Antitumor effect of neratinib in lung cancers harboring HER2 oncogene alterations [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 4777.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2018-4777
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 3
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    Abstract 3680: Comparative mutational evaluation for multiple lung cancer by multiplex oncogene mutation analysis
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Research Vol. 78, No. 13_Supplement ( 2018-07-01), p. 3680-3680
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 3680-3680
    Abstract: [Background] In the treatment of synchronous or metachronous multiple lung cancer (MLC), determination whether multiple primary lung cancer (MP) or intrapulmonary metastases (IM) is very important to make an appropriate management. Clinical or pathological diagnoses have been adopted to distinguish whether MLC were MP or IM, however, the accuracy of these approaches seemed to be insufficient. On the other hand, recent evolution of high-throughput sequencing made it possible to perform comprehensive gene mutation analysis in cancer cells. The aims of this study were to investigate mutational profiles of synchronous or metachronous MLC, and to compare multiplex gene mutation analysis of MP or IM among paired tumors with clinical or pathological evaluations. [Methods] We performed targeted sequencing for 20 lung cancer related oncogenes using next-generation sequencing technology in 82 tumors from 37 patients (18 patients with synchronous MLC and 19 patients with metachronous MLC) who underwent surgical resection in our department from July 2002 to April 2013. Then, classification of MP or IM was made by clinical, pathological, and gene mutational evaluation. [Results] Among paired tumors, matching of mutation was observed in 20 (54%) cases (nine cases with completely matched and 11 cases with partially matched), which were diagnosed as IM by mutational evaluation. In pathologically suggested IM cases (n=7), six (86%) patients were interpreted as IM by mutational evaluation, and most of them (n=5) had multiple matched mutations, which suggested the clonality between paired tumors strongly. In pathologically suggested MP cases (n=17), the mutational diagnosis was discordant in eight (47%) patients. Among these cases, four paired tumors had multiple matched mutation, suggesting the pathological diagnosis in these cases might be incorrect. In addition, careful interpretation was required when the paired tumors harboring frequent mutation including TP53 or EGFR because such mutation may match accidentally. [Conclusion] Our findings suggest that multiplex mutational analysis of synchronous or metachronous MLC could complement the pathological diagnosis in differentiation whether MP or IM. In the cases with pathologically equivocal or those with discordant between pathological diagnosis and mutational evaluation, the frequency and the number of matched mutation may be helpful for the differentiation. Citation Format: Yuta Takahashi, Kazuhiko Shien, Shuta Tomida, Eisuke Kurihara, Yusuke Ogoshi, Kei Namba, Takahiro Yoshioka, Hidejiro Trigoe, Hiroki Sato, Hiromasa Yamamoto, Junichi Soh, Shinichi Toyooka. Comparative mutational evaluation for multiple lung cancer by multiplex oncogene mutation analysis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 3680.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2018-3680
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 4
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    Abstract 4776: Antitumor activity of pan-HER inhibitors in HER2-positive gastric cancer
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Research Vol. 78, No. 13_Supplement ( 2018-07-01), p. 4776-4776
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 4776-4776
    Abstract: Purpose: Molecularly targeted therapy has enabled outstanding advances in cancer treatment. Whereas various anti-HER2 drugs have been developed, trastuzumab is still the only anti-HER2 drug presently available for gastric cancer. Among HER2 targeting drug, afatinib and neratinib inhibit the activation of all HER family protein, and are called pan-HER inhibitors. In this study, we examined the effect of these pan-HER inhibitors to gastric cancer cells. Materials and Methods: We determined the molecular profiles of 12 gastric cancer cell lines. Protein level of HER2 and down-signal pathway molecules were analyzed by Western blotting, and copy number assay or gene expression assay were performed using qPCR. To detect HER2 mutation, we also performed direct-sequence of these cell lines. And next, we examined the antitumor effect of the pan-HER inhibitors afatinib and neratinib in those cell lines, in vitro and in vivo. In addition, we analyzed HER2 alteration in 123 primary gastric cancers resected from Japanese patients to clarify possible candidates with the potential to respond to these drugs. Results: HER2 was amplified in 5 out of 12 gastric cancer cell lines. Gene expression or protein level of HER2 were generally correlated with the copy number of HER2. HER2 mutation was found in one cell line, ECC10, at kinase domain (L755S). In the drug sensitivity analysis, both afatinib and neratinib showed an anti-tumor effect in all the HER2 amplified cell lines both in vitro and in vivo except MKN7 cell line. When the molecular profiles of the cells were compared based on the drug sensitivities, we found that cancer cells with lower mRNA expression levels of IGFBP7, a tumor suppressor gene by inhibiting the activation of IGF-1R, were less sensitive to pan-HER inhibitors. A combination therapy consisting of pan-HER inhibitors and an IGF-1R inhibitor, picropodophyllin, demonstrated a notable synergistic effect. Regarding HER2 alteration in 123 clinical samples, we found 19 cases of HER2 amplification and 3 cases of oncogenic mutations. Conclusion: Afatinib and neratinib are promising therapeutic options for the treatment of HER2-amplified gastric cancer. In addition to HER2 amplification, IGFBP7 might be a biomarker of sensitivity to these drugs, and IGF-1R-targeting therapy can overcome drug insensitiveness in HER2-amplified gastric cancer. Citation Format: Takahiro Yoshioka, Kazuhiko Shien, Yuta Takahashi, Eisuke Kurihara, Kei Namba, Yusuke Ogoshi, Hidejiro Torigoe, Hiroki Sato, Hiromasa Yamamoto, Junichi Soh, Toshiyoshi Fujiwara, Shinichi Toyooka. Antitumor activity of pan-HER inhibitors in HER2-positive gastric cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 4776.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2018-4776
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 5
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    Anti‑tumor effect of neratinib against lung cancer cells harboring HER2 oncogene alterations
    Spandidos Publications ; 2019
    In:  Oncology Letters ( 2019-01-08)
    Details
    In: Oncology Letters, Spandidos Publications, ( 2019-01-08)
    Type of Medium: Online Resource
    ISSN: 1792-1074 , 1792-1082
    URL: Journal
    URL: Article
    DOI: 10.3892/ol
    DOI: 10.3892/ol.2019.9908
    Language: Unknown
    Publisher: Spandidos Publications
    Publication Date: 2019
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  • 6
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    Activation of AXL as a Preclinical Acquired Resistance Mechanism Against Osimertinib Treatment in EGFR -Mutant Non–Small Cell Lung Cancer Cells
    American Association for Cancer Research (AACR) ; 2019
    In:  Molecular Cancer Research Vol. 17, No. 2 ( 2019-02-01), p. 499-507
    Details
    In: Molecular Cancer Research, American Association for Cancer Research (AACR), Vol. 17, No. 2 ( 2019-02-01), p. 499-507
    Abstract: Osimertinib (AZD9291) has an efficacy superior to that of standard EGFR-tyrosine kinase inhibitors for the first-line treatment of patients with EGFR-mutant advanced non–small cell lung cancer (NSCLC). However, patients treated with osimertinib eventually acquire drug resistance, and novel therapeutic strategies to overcome acquired resistance are needed. In clinical or preclinical models, several mechanisms of acquired resistance to osimertinib have been elucidated. However, the acquired resistance mechanisms when osimertinib is initially used for EGFR-mutant NSCLC remain unclear. In this study, we experimentally established acquired osimertinib-resistant cell lines from EGFR-mutant NSCLC cell lines and investigated the molecular profiles of resistant cells to uncover the mechanisms of acquired resistance. Various resistance mechanisms were identified, including the acquisition of MET amplification, EMT induction, and the upregulation of AXL. Using targeted next-generation sequencing with a multigene panel, no secondary mutations were detected in our resistant cell lines. Among three MET-amplified cell lines, one cell line was sensitive to a combination of osimertinib and crizotinib. Acquired resistance cell lines derived from H1975 harboring the T790M mutation showed AXL upregulation, and the cell growth of these cell lines was suppressed by a combination of osimertinib and cabozantinib, an inhibitor of multiple tyrosine kinases including AXL, both in vitro and in vivo. Our results suggest that AXL might be a therapeutic target for overcoming acquired resistance to osimertinib. Implications: Upregulation of AXL is one of the mechanisms of acquired resistance to osimertinib, and combination of osimertinib and cabozantinib might be a key treatment for overcoming osimertinib resistance.
    Type of Medium: Online Resource
    ISSN: 1541-7786 , 1557-3125
    URL: Article
    DOI: 10.1158/1541-7786.MCR-18-0628
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
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    SSG: 12
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  • 7
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    Abstract 1410: Clinicopathological characteristics of lung cancer patients with concomitant idiopathic pulmonary fibrosis
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Research Vol. 79, No. 13_Supplement ( 2019-07-01), p. 1410-1410
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 13_Supplement ( 2019-07-01), p. 1410-1410
    Abstract: Background: Idiopathic interstitial pneumonias (IIPs) are diffuse parenchymal lung disease of unknown etiology. Among IIPs, idiopathic pulmonary fibrosis (IPF) is the most frequent subtype. IPF is characterized by the accumulation of activated fibroblasts and extracellular matrix within the parenchyma. IPF is associated with pathologic and radiologic pattern of usual interstitial pneumonia (UIP). There are several possible underlying mechanisms linking lung cancer and IPF, however, many of them are still unknown. The purpose of this study is to reveal the clinicopathological characteristics of lung cancers patients with concomitant IPF. Materials and Methods: The clinical and pathological data of lung cancer patients with IPF who underwent surgical resection of lung cancer between 2001 to 2016 at our institution were analyzed. We defined IPF as IIPs with UIP pattern, based on the chest CT scan and pathological findings. Mutations of EGFR (L858R point mutation and exon19 deletion), AKT1, BRAF, EGFR, KRAS, MEK1, NRAS, PIK3CA, and PTEN were analyzed. Result: A total of 37 patients’ data of lung cancer with concomitant IPF was collected. Two patients had metachronous lung cancers. Thus, we analyzed 39 lung cancers from 37 patients. Based on the radiographic findings, 33 (84.2%) of the available 38 tumors arose from the fibrotic legion, which were mainly observed in peripheral region. The frequency of EGFR mutation was detected in 1 (2.6%) of 39 lung cancers. As control, we had EGFR mutation profile of 583 lung cancer without IPF. For this population, EGFR mutation was found in 164 (28.1%) of 583 cases. There was a significant difference in EGFR mutation between lung cancers with or without IPF (p = 0.0001). Among other examined genes in 16 tumors, one PIK3CA mutation was found. Conclusion: The lung cancer with IPF mainly arouse from fibrotic lesion. The frequency of EGFR mutation was less common in lung cancers with IPF than those without IPF. Our result suggests that molecular profile of lung cancer with IPF is different from that without IPF. Citation Format: Kota Araki, Kazuhiko Shien, Shunsaku Miyauchi, Akihiro Miura, Yuta Takahashi, Eisuke Kurihara, Yusuke Ogoshi, Kei Namba, Ken Suzawa, Hiromasa Yamamoto, Shuta Tomida, Junichi Soh, Masakiyo Sakaguchi, Shinichi Toyooka. Clinicopathological characteristics of lung cancer patients with concomitant idiopathic pulmonary fibrosis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1410.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2019-1410
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
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    detail.hit.zdb_id: 410466-3
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  • 8
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    Abstract 1233: Reducing sequence artifact in clinical sequencing of treatment-naïve NSCLC patient using molecular barcoding system
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Research Vol. 78, No. 13_Supplement ( 2018-07-01), p. 1233-1233
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 1233-1233
    Abstract: Background: Recently the clinical significance of compound mutations in cancer relapse and/or acquired resistance has been reported. Amplicon-based deep sequence enables analysis of tiny amount of input DNA, however, a major problem of these high-throughput DNA sequencing is the high rate (~1%) of errors causing potential sequence artifact. Molecular barcoding system, which has been developed to reduce sequencing artifacts as well as to improve mutation detection accuracy, was applied to analyze the frequency of compound EGFR mutations in early stage non-small-cell lung cancer (NSCLC) patients who undergo surgical resection without any presurgical treatment is less described. Materials and Methods: From 590 consecutive patients, 64 adenocarcinoma cases who underwent surgical resection for primary lung cancer were analyzed by using amplicon-based targeted sequencing method incorporating molecular barcodes in order to detect genetic alterations of 47 genes including EGFR. Results: Out of 64 samples, EGFR common mutation profiles of 63 (98.4%) by molecular-barcode sequencing corresponded to those by clinical test. Uncommon EGFR mutations were detected in 7 cases (10.9%). Among the three types of EGFR major mutation, G719X (60%, 3/5) showed a significantly higher incidence of EGFR double mutations than L858R (9.5%, 4/42) or Ex19del (0%, 0/17) (p = 0.0052). Co-mutations of other genes were observed in 20 EGFR-mutated cases. TP53 mutations were frequently detected in younger age (p = 0.0066) and pStage II-III cases (p = 0.042). Conclusion: Amplicon sequencing incorporating molecular barcoding system is a feasible approach to characterize predictive or prognostic mutations in early stage treatment naïve NSCLC patients, revealing those case who harbor EGFR G719X mutation have a significantly higher incidence of EGFR double mutations, likely to have worse prognosis. Citation Format: Kei Namba, Shuta Tomida, Yuta Takahashi, Eisuke Kurihara, Yusuke Ogoshi, Takahiro Yosioka, Hidejiro Torigoe, Hiroki Sato, Kazuhiko Shien, Hiromasa Yamamoto, Junichi Soh, Shinichi Toyooka. Reducing sequence artifact in clinical sequencing of treatment-naïve NSCLC patient using molecular barcoding system [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1233.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2018-1233
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 9
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    Application of amplicon-based targeted sequencing with the molecular barcoding system to detect uncommon minor EGFR mutations in patients with treatment-naïve lung adenocarcinoma
    Springer Science and Business Media LLC ; 2019
    In:  BMC Cancer Vol. 19, No. 1 ( 2019-12)
    Details
    In: BMC Cancer, Springer Science and Business Media LLC, Vol. 19, No. 1 ( 2019-12)
    Type of Medium: Online Resource
    ISSN: 1471-2407
    URL: Article
    DOI: 10.1186/s12885-019-5374-1
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2019
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  • 10
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    exSSSRs (extracellular S100 soil sensor receptors)‐Fc fusion proteins work as prominent decoys to S100A8/A9‐induced lung tropic cancer metastasis
    Wiley ; 2019
    In:  International Journal of Cancer Vol. 144, No. 12 ( 2019-06-15), p. 3138-3145
    Details
    In: International Journal of Cancer, Wiley, Vol. 144, No. 12 ( 2019-06-15), p. 3138-3145
    Abstract: What's new? The heterodimer complex S100A8/A9 is a suspected mediator of organ tropic metastasis, whereby tumor cells, or “seeds,” spread to preferred organ, or “soil,” sites as cancer progresses. Here, the S100 soil sensor receptors (SSSRs) EMMPRIN, NPTNβ, MCAM, and ALCAM, which display different expression patterns depending on cancer type, were investigated for their ability to serve as decoys to prevent S100A8/A9 binding to endogenous SSSRs. In experiments in cancer cells and in a lung metastasis model in vivo , purified chimera decoy SSSR proteins successfully suppressed S100A8/A9‐mediated metastasis. The findings warrant further investigation of SSSR biologics for the prevention of cancer metastasis.
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    URL: Article
    DOI: 10.1002/ijc.v144.12
    DOI: 10.1002/ijc.31945
    RVK:
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    Language: English
    Publisher: Wiley
    Publication Date: 2019
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