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Study of Growth Defects and Structure in Nonlinear-Optical Crystals of Lithium Boric Oxide (1995)

Zhao, Q. L. ; Huang, Y. S. ; Tang, D. Y. ; [et al.]

Copenhagen : International Union of Crystallography (IUCr)

Applied crystallography online 28 (1995), S. 294-301

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ISSN: 1600-5767

Source: Crystallography Journals Online : IUCR Backfile Archive 1948-2001

Topics: Geosciences , Physics

Notes: Imperfections in the (100), (010) and (001) plates of an inorganic nonlinear crystal of lithium boric oxide [lithium triboron (III) tetraoxide] (LiB3O5), prepared from different blocks, have been studied by means of X-ray projection topography. The experimental results show that there are mainly grown-in dislocations with b = [100], [101], [10{\bar 1}], [001] and [011], glide dislocations in the system of (010)[101], inclusion-induced dislocations almost all with b = [101], [10{\bar 1}] and [001], distributed in a network parallel to the (010) plane, inclusions with the orthorhombic configuration and a long stripe to which there is only one gas bubble attached, and assigned to be the negative crystals. All dislocations run nearly straight and are of the pure screw type. The origins of defect formation and some other crystal properties are discussed in terms of the structure.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1107/S002188989401112X

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NSCLC with Concomitant EGFR Mutations and ALK Rearrangements (2014)

Yang, J.-J., Zhang, X.-C., Su, J., Xu, C.-R., Zhou, Q., Tian, H.-X., Xie, Z., Chen, H.-J., Huang, Y.-S., Jiang, B.-Y., Wang, Z., Wang, B.-C., Yang, X.-N., Zhong, W.-Z., Nie, Q., Liao, R.-Q., Mok, T. S., Wu, Y.-L.

The American Association for Cancer Research (AACR)

In: Clinical Cancer Research

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Publication Date: 2014-03-04

Description: Purpose: We investigated the incidence of concomitant epidermal growth factor receptor ( EGFR ) mutations and anaplastic lymphoma kinase ( ALK ) rearrangements in Chinese patients with non–small cell lung cancer (NSCLC), and assessed responses to EGFR tyrosine kinase inhibitors (EGFR-TKIs) and crizotinib in such tumors. Experimental Design: We screened 977 consecutive patients with NSCLC for the presence of concomitant EGFR mutations and ALK rearrangements by rapid amplification of cDNA ends-coupled PCR sequencing and FISH. Immunohistochemistry (IHC) and Western blotting were used to correlate the activation of EGFR, ALK, and downstream proteins with responses to EGFR-TKIs and crizotinib. Results: The overall frequency of concomitant EGFR mutations and ALK rearrangements was 1.3% (13/977). EGFR/ALK co-alterations were found in 3.9% (13/336) EGFR- mutant and 18.6% (13/70) ALK- rearranged patients. Ten tumors were treated with first-line EGFR-TKIs, with a response rate of 80% (8/10). Two tumors with high phospho-ALK levels and low phospho-EGFR levels achieved stable and progressive disease, respectively. Median progression-free survival was 11.2 months. Coexpression of mutant EGFR and ALK fusion proteins in the same tumor cell populations was detected by IHC. Two cases with high phospho-ALK levels treated with crizotinib achieved partial responses; two cases with low phospho-ALK levels had progressive or stable disease. Conclusion: ALK rearrangements and EGFR mutations could coexist in a small subgroup of NSCLC. Advanced pulmonary adenocarcinomas with such co-alterations could have diverse responses to EGFR-TKIs and crizotinib. Relative phospho-ALK and phospho-EGFR levels could predict the efficacy of EGFR-TKI and crizotinib. Clin Cancer Res; 20(5); 1383–92. ©2014 AACR .

Print ISSN: 1078-0432

Electronic ISSN: 1557-3265

Topics: Medicine

Published by The American Association for Cancer Research (AACR)

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Acquired MET Y1248H and D1246N Mutations Mediate Resistance to MET Inhibitors in Non-Small Cell Lung Cancer (2017)

Li, A., Yang, J.-j., Zhang, X.-c., Zhang, Z., Su, J., Gou, L.-y., Bai, Y., Zhou, Q., Yang, Z., Han-Zhang, H., Zhong, W.-Z., Chuai, S., Zhang, Q., Xie, Z., Gao, H., Chen, H., Wang, Z., Wang, Z., Yang, X.-n., Wang, B.-c., Gan, B., Chen, Z.-h., Jiang, B.-y., Wu, S.-p., Liu, S.-y., Xu, C.-r., Wu, Y.-l.

The American Association for Cancer Research (AACR)

In: Clinical Cancer Research

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Publication Date: 2017-08-16

Description: Purpose: MET amplification, responsible for 20% of acquired resistance to EGFR tyrosine kinase inhibitor (TKI) in patients with advanced non–small cell lung cancer (NSCLC), presents an attractive target. Numerous studies have conferred susceptibility of MET mutations and focal amplification to targeted MET-TKIs. However, the mechanism underlying MET-TKIs–induced resistance remains elusive. Experimental Design: We conducted a cohort of 12 patients with advanced NSCLC who developed resistance to a combinatorial therapy consisting of gefitinib and a type I MET-TKI. We performed capture-based targeted ultra-deep sequencing on serial tumor biopsies and plasmas ctDNA samples to detect and quantify genetic alterations. Results: We identified 2 newly acquired MET mutations, Y1248H and D1246N, in 2 patients and further confirmed their resistance against type I MET-TKIs in silco, in vitro , and in vivo . Interestingly, NIH3T3 cells harboring either mutation exhibited responses to type II MET-TKIs, suggesting sequential use of MET-TKIs may offer a more durable response. In addition, we also discovered that EGFR amplification may act as an alternative MET-TKI resistance mechanism. Conclusions: Our study provides insight into the diversity of mechanisms underlying MET-TKI–induced resistance and highlights the potential of sequential use of MET-TKIs. Clin Cancer Res; 23(16); 4929–37. ©2017 AACR .

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Topics: Medicine

Published by The American Association for Cancer Research (AACR)

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Potential Predictive Value of TP53 and KRAS Mutation Status for Response to PD-1 Blockade Immunotherapy in Lung Adenocarcinoma (2017)

Dong, Z.-Y., Zhong, W.-Z., Zhang, X.-C., Su, J., Xie, Z., Liu, S.-Y., Tu, H.-Y., Chen, H.-J., Sun, Y.-L., Zhou, Q., Yang, J.-J., Yang, X.-N., Lin, J.-X., Yan, H.-H., Zhai, H.-R., Yan, L.-X., Liao, R.-Q., Wu, S.-P., Wu, Y.-L.

The American Association for Cancer Research (AACR)

In: Clinical Cancer Research

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Publication Date: 2017-06-16

Description: Purpose: Although clinical studies have shown promise for targeting programmed cell death protein-1 (PD-1) and ligand (PD-L1) signaling in non–small cell lung cancer (NSCLC), the factors that predict which subtype patients will be responsive to checkpoint blockade are not fully understood. Experimental Design: We performed an integrated analysis on the multiple-dimensional data types including genomic, transcriptomic, proteomic, and clinical data from cohorts of lung adenocarcinoma public (discovery set) and internal (validation set) database and immunotherapeutic patients. Gene set enrichment analysis (GSEA) was used to determine potentially relevant gene expression signatures between specific subgroups. Results: We observed that TP53 mutation significantly increased expression of immune checkpoints and activated T-effector and interferon- signature. More importantly, the TP53/KRAS comutated subgroup manifested exclusive increased expression of PD-L1 and a highest proportion of PD-L1 + /CD8A + . Meanwhile, TP53- or KRAS -mutated tumors showed prominently increased mutation burden and specifically enriched in the transversion-high (TH) cohort. Further analysis focused on the potential molecular mechanism revealed that TP53 or KRAS mutation altered a group of genes involved in cell-cycle regulating, DNA replication and damage repair. Finally, immunotherapeutic analysis from public clinical trial and prospective observation in our center were further confirmed that TP53 or KRAS mutation patients, especially those with co-occurring TP53/KRAS mutations, showed remarkable clinical benefit to PD-1 inhibitors. Conclusions: This work provides evidence that TP53 and KRAS mutation in lung adenocarcinoma may be served as a pair of potential predictive factors in guiding anti–PD-1/PD-L1 immunotherapy. Clin Cancer Res; 23(12); 3012–24. ©2016 AACR .

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Electronic ISSN: 1557-3265

Topics: Medicine

Published by The American Association for Cancer Research (AACR)

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Detection of Driver and Resistance Mutations in Leptomeningeal Metastases of NSCLC by Next-Generation Sequencing of Cerebrospinal Fluid Circulating Tumor Cells (2017)

Jiang, B.-Y., Li, Y.-S., Guo, W.-B., Zhang, X.-C., Chen, Z.-H., Su, J., Zhong, W.-Z., Yang, X.-N., Yang, J.-J., Shao, Y., Huang, B., Liu, Y.-H., Zhou, Q., Tu, H.-Y., Chen, H.-J., Wang, Z., Xu, C.-R., Wang, B.-C., Wu, S.-Y., Gao, C.-Y., Zhang, X., Wu, Y.-L.

The American Association for Cancer Research (AACR)

In: Clinical Cancer Research

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Publication Date: 2017-09-16

Description: Purpose: Leptomeningeal metastases are more common in non–small cell lung cancer (NSCLC) with EGFR mutations. The diagnosis is difficult by traditional imaging only, and leads to poor understanding of resistance mechanisms of leptomeningeal metastases. Experimental Design: We compared the CellSearch Assay, the Thinprep cytologic test (TCT), and brain magnetic resonance imaging (MRI) in 21 NSCLC patients with suspected leptomeningeal metastases. Next-generation sequencing that included 416 cancer-associated genes was also performed on cerebrospinal fluid circulating tumor cells (CSFCTC) of 19 patients. Results: Twenty-one patients were diagnosed with leptomeningeal metastases, and CSFCTCs were captured by CellSearch in 20 patients (median, 969 CSFCTCs/7.5 mL; range, 27–14,888). CellSearch had a sensitivity of 95.2% for leptomeningeal metastases diagnosis, which was higher than that of TCT (12/21, 57.1%), MRI (10/21, 47.6%), and MRI plus TCT (19/21, 90.5%), respectively. CTCs were found only in 5 of 14 patients (median, 2 CTCs/7.5 mL; range, 2–4), which was a much lower ratio than CSFCTCs. Genetic profiles of CSFCTCs were highly concordant with molecular mutations identified in the primary tumor (17/19, 89.5%). The resistance gene EGFR T790M was detected in 7 of 9 patients with extracranial lesions, but was detected in only 1 of 14 CSFCTC samples. Other potential resistant mutations, such as MET amplification and ERBB2 mutation, were also identified in CSFCTCs. Conclusions: CSFCTCs captured by CellSearch may be a more sensitive and effective way to diagnose leptomeningeal metastases, and may serve as a liquid biopsy medium for gene profiles in NSCLC patients with leptomeningeal metastases. Clin Cancer Res; 23(18); 5480–8. ©2017 AACR .

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Topics: Medicine

Published by The American Association for Cancer Research (AACR)

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Pemetrexed versus gefitinib as a second-line treatment in advanced nonsquamous nonsmall-cell lung cancer patients harboring wild-type EGFR (CTONG0806): a multicenter randomized trial (2014)

Zhou, Q., Cheng, Y., Yang, J.- J., Zhao, M.- F., Zhang, L., Zhang, X.- C., Chen, Z.- H., Yan, H.- H., Song, Y., Chen, J.- H., Feng, W.- N., Xu, C.- R., Wang, Z., Chen, H.- J., Zhong, W.- Z., Liu, Y.- P., Wu, Y.- L.

Oxford University Press

In: Annals of Oncology

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Publication Date: 2014-11-21

Description: Background CTONG0806 assessed the efficacy of pemetrexed versus gefitinib as second-line treatment in advanced nonsquamous nonsmall-cell lung cancer (NSCLC) harboring wild-type epidermal growth factor receptor ( EGFR ). Patients and methods Patients with locally advanced or metastatic nonsquamous NSCLC harboring wild-type EGFR , detected by direct sequencing, and previously treated with platinum-based chemotherapy were randomized to receive gefitinib (250 mg/day) orally or pemetrexed (500 mg/m 2 ) i.v. on day 1 of a 21-day cycle until disease progression or unacceptable toxicity. The primary end point was progression-free survival (PFS). The Independent Review Committee (IRC) evaluated all pictorial data. Results From February 2009 to August 2012, 161 patients were enrolled, and 157 were assessable (81 in the gefitinib arm, 76 in the pemetrexed arm). Baseline characteristics were balanced between the two arms. The median PFSs were 4.8 versus 1.6 months in the pemetrexed and gefitinib arms, respectively [hazard ratio (HR) 0.54, 95% confidence interval (CI) 0.40–0.75, P 〈 0.001] as confirmed by IRC evaluation (5.6versus 1.7 months, HR 0.53, 95% CI 0.38–0.75, P 〈 0.001). The median overall survival (OS) showed a trend of superiority in the pemetrexed arm (12.4 versus 9.6 months, HR 0.72, 95% CI 0.49–1.04, P = 0.077). Quality-of-life assessment showed no marked difference between the arms. No unexpected adverse events were found. Of 108 patients with sufficient DNA samples, EGFR mutation status was re-tested by Scorpion amplification refractory mutation system (ARMS); 32 (29.6%) tested positive (19 in the pemetrexed arm, 13 in the gefitinib arm; median PFS: 8.1 versus 7.0 months, HR 0.94, 95% CI 0.43–2.08, P = 0.877). Conclusions CTONG0806 is the first trial to show significant improvement in PFS and an improved OS trend with pemetrexed compared with gefitinib as second-line setting treatment of EGFR wild-type advanced nonsquamous NSCLC. ARMS is superior to direct sequencing in excluding false-negative patients. ClinicalTrials.gov Identifier NCT00891579.

Print ISSN: 0923-7534

Electronic ISSN: 1569-8041

Topics: Medicine

Published by Oxford University Press

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