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Zhangzhou Huang
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EP1.03 - Biology (ID 193)
- Event: WCLC 2019
- Type: E-Poster Viewing in the Exhibit Hall
- Track: Biology
- Presentations: 6
- Moderators:
- Coordinates: 9/08/2019, 08:00 - 18:00, Exhibit Hall
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EP1.03-03 - Association Between Molecular Spectrum of EZH2 Variants and Prognosis in Patients with Non-Small-Cell Lung Cancer in Chinese Patients (ID 93)
08:00 - 18:00 | Author(s): Zhangzhou Huang
- Abstract
Background
Enhancer of zeste homolog 2 (EZH2) shows upregulated expression in tumors and is an important driver of tumor development and progression. However, the mechanism underlying the mediation of tumor aggressiveness in non-small-cell lung cancer (NSCLC) by EZH2 remains unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring EZH2 mutations.
Method
A total of 1122 patients with non-small-cell lung cancer were recruited between July 2012 and December 2016. The status of EZH2 mutations and other genes were detected by next generation sequencing.
Result
EZH2 gene mutation rate was 0.62% (7/1122) in non-small cell lung cancer, including K515R (1 patient), I55M (1 patient), D142H (1 patient), K222N (1 patient), Q66R (1 patient), P486S (1 patient), and S652C (1 patient), and median overall survival (OS) for these patients was 20.0 months. Among them, all patients were EZH2 gene with co-occurring mutations. Briefly, patients with (n=2) or without (n=5) co-occurring EGFR mutations had a median OS of 16.0 months and 20.0 months respectively (P=0.88); patients with (n=6) or without (n=1) co-occurring TP53 mutations had a median OS of not up to now and 20.0 months respectively (P=0.79); patients with (n=2) or without (n=5) co-occurring BRAF mutations had a median OS of 14.0 months and 20.0 months respectively (P=0.45); patients with (n=2) or without (n=5) co-occurring SMARCA4 mutations had a median OS of 20.0 months and not up to now respectively (P=0.88).
Conclusion
EZH2 mutation may predict a worse prognosis of NSCLC. Methyltransferase inhibitor may be beneficial for NSCLC patients with specific EZH2 mutations. EGFR, TP53, BRAF, SMARCA4 gene accompanied may have less correlation with EZH2 mutation in NSCLC patients. The findings of this study could facilitate both clinical trial design and therapeutic strategies.
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EP1.03-09 - Epidemiological Study of TSC1 Mutations Among Non-Small Cell Lung Cancer Patients in China (ID 115)
08:00 - 18:00 | Author(s): Zhangzhou Huang
- Abstract
Background
The tuberous sclerosis complex 1 (TSC1) is an endogenous regulator of the mechanistic target of rapamycin (mTOR). While mTOR has been shown to play an important role in neoplasm. The aim of this study is to investigate mutations and prognosis of NSCLC harboring TSC1 mutations.
Method
A total of 1106 patients with non-small-cell lung cancer were recruited between July 2012 and December 2016. The status of TSC1 mutations and other genes were detected by next generation sequencing.
Result
TSC1 gene mutation rate was 1.90% (21/1106) in non-small cell lung cancer, including Q654E (2 patients), R429K (2 patients), A1072D (1 patient), R850S (1 patient), E625K (1 patient), R715Q (1 patient), A84T (1 patient), S1038G (1 patient), M1090I (1 patient), D903H (1 patient), I143N (1 patient), Q3H (1 patient), L134F (1 patient), T1065M (1 patient), V407M (1 patient), S673F (1 patient), D675Y (1 patient), Q149H (1 patient) and T1144P plus L916M (1 patient), and median overall survival (OS) for these patients was 14.0 months. Among them, all patients were TSC1 gene with co-occurring mutations. Briefly, patients with (n=12) or without (n=9) co-occurring TP53 mutations had a median OS of 14.0 months and 15.0 months respectively (P=0.58); patients with (n=9) or without (n=12) co-occurring KRAS mutations had a median OS of not up to now and 14.0 months respectively (P=0.56); patients with (n=2) or without (n=19) co-occurring BRAF mutations had a median OS of 18.5 months and 12.0 months respectively (P=0.71); patients with (n=4) or without (n=17) co-occurring CDKN2A mutations had a median OS of 8.0 months and 18.0 months respectively (P=0.47).
Conclusion
Accompanied gene has not well been connected with TSC1 gene mutations. Our finding expands the mutant spectrum of TSC1 gene and adds new understanding of the phenotype.
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EP1.03-13 - Molecular Characteristics of East Asian Patients with VHL-Mutated Non-Small-Cell Lung Cancer: A Retrospective Study (ID 113)
08:00 - 18:00 | Author(s): Zhangzhou Huang
- Abstract
Background
The von Hippel-Lindau (VHL) gene is inactivated frequently in sporadic clear-cell renal cell carcinomas (ccRCCs) by genetic alteration. However, the pathological or prognostic significance of VHL gene alteration has not been well defined in the other cancers, especially non-small cell lung cancer (NSCLC). The aim of this study is to investigate mutations and prognosis of NSCLC harboring VHL mutations.
Method
A total of 972 patients with non-small-cell lung cancer were recruited between July 2012 and December 2016. The status of VHL mutations and other genes were detected by next generation sequencing.
Result
VHL gene mutation rate was 0.72% (7/972) in non-small cell lung cancer, including W117fs*15 (1 patient), G44A (1 patient), G44V (1 patient), P81S (1 patient), R120T (1 patient), E51K (1 patient) and T100A (1 patient), and median overall survival (OS) for these patients was 22.0 months. Among them, all patients were VHL gene with co-occurring mutations. Briefly, patients with (n=2) or without (n=5) co-occurring EGFR mutations had a median OS of 22.0months and 12.0 months respectively (P=0.16); patients with (n=3) or without (n=4) co-occurring TP53 mutations had a median OS of not up to now and 12.0 months respectively (P=0.23); patients with (n=3) or without (n=4) co-occurring KRAS mutations had a median OS of 3.0 months and 22.0 months respectively (P=0.07); patients with (n=2) or without (n=5) co-occurring SETD2 mutations had a median OS of 3.0 months and 22.0 months respectively (P=0.01).
Conclusion
The present study expanded the database on VHL gene mutations in NSCLC and enriched the spectrum of known somatic mutations of the VHL gene. Chemotherapy may be considered as a possible treatment for carriers of the mutation. SETD2 mutated accompanied mutations might play a poor prognosis in VHL gene mutation NSCLC.
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EP1.03-14 - Clinicopathologic Characteristics and Outcomes of Chinese Patients with Non-Small-Cell Lung Cancer and INPP4B Mutations (ID 109)
08:00 - 18:00 | Author(s): Zhangzhou Huang
- Abstract
Background
Inositol polyphosphate 4-phosphatase B (INPP4B) has been identified as a tumour suppressor in different human cancers. However, the role of INPP4B in the angiogenesis of human non-small cell lung cancer (NSCLC) remains unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring INPP4B mutations.
Method
A total of 750 patients with non-small-cell lung cancer were recruited between July 2012 and December 2016. The status of INPP4B mutations and other genes were detected by next generation sequencing.
Result
INPP4B gene mutation rate was 2.80% (21/750) in non-small cell lung cancer, including p.R623K (2 patients), p.N378S (1 patient), p.G187W (1 patient), p.V117I (1 patient), c.1721-1G>T (1 patient), p.R818* (1 patient), p.T829R (1 patient), p.Q753H (1 patient), p.L542M (1 patient), p.I68M (1 patient), p.Q814E (1 patient), p.K448N (1 patient), p.C617F (1 patient), p.Q600H (1 patient), p.G479* (1 patient), p.L155Q (1 patient), p.P572A (1 patient), p.L16V (1 patient), p.F652Y (1 patient), and p.T671S plus p.N228K (1 patient), and median overall survival (OS) for these patients was 15.0 months. Among them, all patients were INPP4B gene with co-occurring mutations. Briefly, patients with (n=2) or without (n=19) co-occurring EGFR mutations had a median OS of 20.0 months and 5.5 months respectively (P=0.01); patients with (n=17) or without (n=4) co-occurring TP53 mutations had a median OS of 15.0 months and 14.4 months respectively (P=0.68); patients with (n=7) or without (n=14) co-occurring PTPRD mutations had a median OS of not up to now and 15.0 months respectively (P=0.48); patients with (n=8) or without (n=13) co-occurring KRAS mutations had a median OS of 17.0 months and 15.0 months respectively (P=0.68).
Conclusion
INPP4B mutations were observed in 2.80 % of cases of NSCLC. INPP4B-mutated NSCLC can exhibit other driver gene alterations. No clinical characteristics were significantly associated with INPP4B mutation.
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EP1.03-18 - Analysis of IDH1 Mutation Spectrum from Non-Small-Cell Lung Cancer in East Asian Patients (ID 95)
08:00 - 18:00 | Author(s): Zhangzhou Huang
- Abstract
Background
Isocitrate dehydrogenase 1 (IDH1) is a metabolic enzyme that converts isocitrate to alpha-ketoglutarate. IDH1 mutations are associated with the accumulation of the oncometabolite D-2-hydroxyglutarate, which acts as an epigenetic modifier, and the development of multiple malignancies. Previous studies uncovered mutations in IDH1 in several malignancies, with the most frequent mutation being IDH1 R132H. It has been demonstrated that IDH1 expression is induced in non-small-cell lung cancer (NSCLC). The aim of this study is to investigate mutations and prognosis of NSCLC harboring IDH1 mutations.
Method
A total of 893 patients with non-small-cell lung cancer were recruited between July 2012 and December 2016. The status of IDH1 mutations and other genes were detected by next generation sequencing.
Result
IDH1 gene mutation rate was 1.23% (11/893) in non-small cell lung cancer, including Q138S (1 patient), D79V (1 patient), T373N (1 patient), C114* (1 patient), W336L (1 patient), I99M (1 patient), G104R (1 patient), R132C (1 patient), A193S (1 patient), Y34C (1 patient) and H67R (1 patient), and median overall survival (OS) for these patients was 11.0 months. Among them, all patients were IDH1 gene with co-occurring mutations. Briefly, patients with (n=9) or without (n=2) co-occurring TP53 mutations had a median OS of not up to now months and 8.5 months respectively (P=0.32); patients with (n=2) or without (n=9) co-occurring KMT2D mutations had a median OS of 11.5 months and 11.0 months respectively (P=0.80); patients with (n=5) or without (n=6) co-occurring KRAS mutations had a median OS of not up to now months and 8.0 months respectively (P=0.22); patients with (n=2) or without (n=9) co-occurring CREBBP mutations had a median OS of 15.5 months and 8.0 months respectively (P=0.67).
Conclusion
Our results demonstrated that decreased IDH1 gene mutation correlated with poor overall survival in NSCLC patients. IDH1 gene mutation may define a subset of patients with lung cancer appropriate for investigational therapeutic strategies.
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EP1.03-19 - The Frequency and Prognosis of MDM2 Mutations in East Asian Non-Small-Cell Lung Cancer Patients (ID 107)
08:00 - 18:00 | Author(s): Zhangzhou Huang
- Abstract
Background
In neoplasm, the mouse double minute 2 (MDM2) is an oncoprotein that contributes to the promotion of cell growth, survival, invasion, and therapeutic resistance. The aim of this study is to investigate mutations and prognosis of non-small cell lung cancer (NSCLC) harboring MDM2 mutations.
Method
A total of 1152 patients with non-small-cell lung cancer were recruited between July 2012 and December 2016. The status of MDM2 mutations and other genes were detected by next generation sequencing.
Result
MDM2 gene mutation rate was 0.52% (6/1152) in non-small cell lung cancer, including D179N (1 patient), S84L (1 patient), T195M (1 patient), V234L (1 patient), A471S (1 patient) and E184Q (1 patient), and median overall survival (OS) for these patients was 24.0 months. Among them, all patients were MDM2 gene with co-occurring mutations. Briefly, patients with (n=2) or without (n=4) co-occurring EGFR mutations had a median OS of 18.5 months and 24.0 months respectively (P=0.89); patients with (n=4) or without (n=2) co-occurring TP53 mutations had a median OS of 24.0 months and 7.0 months respectively (P=0.05); patients with (n=2) or without (n=4) co-occurring BRCA1 mutations had a median OS of 24.0 months and 13.0 months respectively (P=0.20); patients with (n=2) or without (n=4) co-occurring KEAP1 mutations had a median OS of 15.5 months and 24.0 months respectively (P=0.59).
Conclusion
MDM2 mutations represent a distinct subset of NSCLC. Next generation sequencing showed that MDM2 mutations commonly co-existed with other driver genes. Our results show that MDM2 mutations delineate an aggressive subtype of lung cancer for which a targeted treatment through MDM2 inhibition might offer new opportunities.
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P1.03 - Biology (ID 161)
- Event: WCLC 2019
- Type: Poster Viewing in the Exhibit Hall
- Track: Biology
- Presentations: 2
- Moderators:
- Coordinates: 9/08/2019, 09:45 - 18:00, Exhibit Hall
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P1.03-35 - Analysis of TET2 Gene Aberrations in East Asian Non-Small-Cell Lung Cancer Patients and Evaluation of Their Prognosis (ID 97)
09:45 - 18:00 | Author(s): Zhangzhou Huang
- Abstract
Background
Ten-eleven translocation 2 (TET2) enzymes are frequently deregulated in cancer, but the genetic spectrum of TET2 mutation non-small cell lung cancer patients (NSCLC) patients is unclear. The aim of this study is to investigate mutations and prognosis of NSCLC harboring TET2 mutations.
Method
A total of 895 patients with non-small-cell lung cancer were recruited between July 2012 and December 2016. The status of TET2 mutations and other genes were detected by next generation sequencing.
Result
TET2 gene mutation rate was 1.90% (17/895) in non-small cell lung cancer, including G126W (1 patient), E1477* (1 patient), I1871Nfs*4 (1 patient), T665K (1 patient), Y60F (1 patient), D932H (1 patient), M533I (1 patient), R1262W (1 patient), N71Kfs*5 (1 patient), Q769* (1 patient), W1198C (1 patient), Y1645Ifs*16 (1 patient), Q1532* (1 patient), R369W (1 patient), D648Y (1 patient), G1370V (1 patient) and T344K (1 patient), and median overall survival (OS) for these patients was 19.0 months. Among them, all patients were TET2 gene with co-occurring mutations. Briefly, patients with (n=15) or without (n=2) co-occurring TP53 mutations had a median OS of 19.0 months and 4.0 months respectively (P<0.01); patients with (n=3) or without (n=10) co-occurring CTNNB1 mutations had a median OS of 13.0 months and 19.0 months respectively (P=0.90); patients with (n=3) or without (n=10) co-occurring NF1 mutations had a median OS of not up to now months and 13.0 months respectively (P=0.87), patients with (n=3) or without (n=10) co-occurring KDM5C mutations had a median OS of not up to now months and 13.0 months respectively (P=0.75).
Conclusion
TET2 oncogenic activation through mutation defines a novel and distinct subset of NSCLC. CTNNB1, NF1 and KDM5C gene accompanied may have less correlation with KIT mutation in NSCLC patients. TP53 accompanied mutations might play a good prognosis in TET2 gene mutation non-small cell lung cancer.
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P1.03-47 - KEAP1 Mutations in East Asian Patients with NSCLC: An Investigation of Prevalence, Clinicopathologic Characteristics and Prognosis (ID 104)
09:45 - 18:00 | Author(s): Zhangzhou Huang
- Abstract
Background
The KEAP1/NRF2 pathway is a master regulator of the cellular redox state through the induction of several antioxidant defence genes implicated in chemotherapeutic drugs resistance of tumor cells. Because of the rarity of those mutations, associated clinical features and prognostic significance have not been thoroughly described so far. The aim of this study is to investigate mutations and prognosis of NSCLC harboring KEAP1 mutations.
Method
A total of 317 patients with non-small-cell lung cancer were recruited between July 2012 and December 2016. The status of KEAP1 mutations and other genes were detected by next generation sequencing.
Result
KEAP1 gene mutation rate was 10.09% (32/317) in non-small cell lung cancer, including D618Tfs*54 (2 patients), W252L (1 patient), G158C (1 patient), D618Tfs*54 (1 patient), L237Q (1 patient), R415C (1 patient), K97N (1 patient), C368F (1 patient), A95T (1 patient), C273F (1 patient), S243F (1 patient), E149K (1 patient), H96L (1 patient), L70Q (1 patient), G558W (1 patient), E493K (1 patient), A40P (1 patient), E343V (1 patient), E219* (1 patient), G158C (1 patient), D235Tfs*3 (1 patient), I125T (1 patient), R320L (1 patient), R470H (1 patient), E244* (1 patient), G158V (1 patient), C368F (1 patient), I185F (1 patient), N157_M161del (1 patient), R336* (1 patient) and E219Q plus D526N (1 patient), and median overall survival (OS) for these patients was 13.5 months. Among them, all patients were KEAP1 gene with co-occurring mutations. Briefly, patients with (n=20) or without (n=12) co-occurring TP53 mutations had a median OS of 14.5 months and 13.5 months respectively (P=0.71); patients with (n=15) or without (n=17) co-occurring KRAS mutations had a median OS of 15.0 months and 12.0 months respectively (P=0.79); patients with (n=16) or without (n=16) co-occurring STK11 mutations had a median OS of 13.5 months and 18.0 months respectively (P=0.60); patients with (n=4) or without (n=28) co-occurring PIK3CA mutations had a median OS of not up to now and 12.0 months respectively (P=0.16).
Conclusion
KEAP1 gene mutation coexists with other gene mutation in NSCLC. TP53, KRAS, STK11 and PIK3CA gene accompanied may have less correlation with KEAP1 mutation in NSCLC patients. Analysis of KEAP1 mutations shows promise as a way to refine individual patients with NSCLC, and provides more insight into effective treatment strategies for patients with KEAP1 mutations.
