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  • American Society of Clinical Oncology (ASCO)  (20)
  • Tan, Eng-Huat  (20)
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  • American Society of Clinical Oncology (ASCO)  (20)
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  • 1
    Online Resource
    Online Resource
    A phase Ib proof-of-concept study of LBH589 (LBH) and everolimus (EVE) in advanced solid tumors enriched for Epstein-Barr virus (EBV)-related cancers.
    American Society of Clinical Oncology (ASCO) ; 2012
    In:  Journal of Clinical Oncology Vol. 30, No. 15_suppl ( 2012-05-20), p. 3098-3098
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 30, No. 15_suppl ( 2012-05-20), p. 3098-3098
    Abstract: 3098 Background: Histone deacetylase and mTOR inhibition circumvent critical EBV-oncogenic pathways with preclinical studies demonstrating lytic induction in EBV infected cells, as well as immunomodulatory and antiangiogenic effects. Methods: Patients (Pt) with advanced solid tumors enriched for EBV–related cancers were enrolled to determine safety, tolerability, maximum tolerated dose (MTD), pharmacokinetics (PK), pharmacodynamics and preliminary antitumor activity. LBH was instituted 7-days prior to combination treatment. NPC pt received antiviral prophylaxis of either acyclovir (Ac) or valaciclovir (Vc). Serum EBV DNA levels (EBNA-1) were measured weekly and plasma cytokines profiled using a 31-plex Luminex panel. Results: 15 pt have been treated (M:F 13:2, median age 50, R: 38-63) 10 NPC, 5 non-NPC (colon, RCC, breast, gastric, sarcoma) at 3 dose levels – LBH (3x/wk)-EVE (daily):10-2.5, 10-5, 15-5. Two dose limiting toxicities of G4 (grade) thrombocytopenia were observed at LBH15-RAD5. Significant adverse events (AE) (G≥3) were dysphagia (1) and thrombocytopenia (3). Common AEs (G1/2) included fatigue (80%), anorexia (60%), mucositis (53%), xerostomia (26%), dysphagia (26%). Two minor responses were seen (1 NPC, 1 breast) and 2 pt (1 NPC, 1 RCC) had prolonged stable disease ( 〉 16 weeks). Modulation of EBV DNA titres was seen only in NPC pt, with median fold-change from baseline of 10.9 (0.05-174). Pt on Ac prophylaxis (n=5) had significant increases in DNA titres (9-174 fold), while those on Vc (n=4) were less pronounced (0.05-11 fold, p 〈 0.03), with one pt (with minor response) having persistent decline in EBV titres. In a limited pt subset (n=9, 30 timepoints), plasma cytokine profiles were consistent with a T-cell response, specifically, elevated levels of FLT3L, IFN-gamma, IL-13 and IL-17. PK and PBMC target modulation studies are being analysed. Conclusions: LBH-EVE results in induction of EBV DNA titres with an associated host T cell response. MTD is LBH10-EVE5 in Asian pt, majority of whom had NPC. A pre-planned expansion cohort that incorporates multi-parametric functional imaging exploring two schedules of LBH in combination with EVE5 is ongoing.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2012.30.15_suppl.3098
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2012
    detail.hit.zdb_id: 2005181-5
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  • 2
    Online Resource
    Online Resource
    Clonal MET Amplification as a Determinant of Tyrosine Kinase Inhibitor Resistance in Epidermal Growth Factor Receptor–Mutant Non–Small-Cell Lung Cancer
    American Society of Clinical Oncology (ASCO) ; 2019
    In:  Journal of Clinical Oncology Vol. 37, No. 11 ( 2019-04-10), p. 876-884
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 37, No. 11 ( 2019-04-10), p. 876-884
    Abstract: Mesenchymal epithelial transition factor ( MET) activation has been implicated as an oncogenic driver in epidermal growth factor receptor ( EGFR)–mutant non–small-cell lung cancer (NSCLC) and can mediate primary and secondary resistance to EGFR tyrosine kinase inhibitors (TKI). High copy number thresholds have been suggested to enrich for response to MET inhibitors. We examined the clinical relevance of MET copy number gain (CNG) in the setting of treatment-naive metastatic EGFR-mutant–positive NSCLC. Patients and Methods MET fluorescence in situ hybridization was performed in 200 consecutive patients identified as metastatic treatment-naïve EGFR-mutant–positive. We defined MET-high as CNG greater than or equal to 5, with an additional criterion of MET/centromeric portion of chromosome 7 ratiο greater than or equal to 2 for amplification. Time-to-treatment failure (TTF) to EGFR TKI in patients identified as MET-high and -low was estimated by Kaplan-Meier method and compared using log-rank test. Multiregion single-nucleotide polymorphism array analysis was performed on 13 early-stage resected EGFR-mutant–positive NSCLC across 59 sectors to investigate intratumoral heterogeneity of MET CNG. Results Fifty-two (26%) of 200 patients in the metastatic cohort were MET-high at diagnosis; 46 (23%) had polysomy and six (3%) had amplification. Median TTF was 12.2 months (95% CI, 5.7 to 22.6 months) versus 13.1 months (95% CI, 10.6 to 15.0 months) for MET-high and -low, respectively ( P = .566), with no significant difference in response rate regardless of copy number thresholds. Loss of MET was observed in three of six patients identified as MET-high who underwent postprogression biopsies, which is consistent with marked intratumoral heterogeneity in MET CNG observed in early-stage tumors. Suboptimal response (TTF, 1.0 to 6.4 months) to EGFR TKI was observed in patients with coexisting MET amplification (five [3.2%] of 154). Conclusion Although up to 26% of TKI-naïve EGFR-mutant–positive NSCLC harbor high MET CNG by fluorescence in situ hybridization, this did not significantly affect response to TKI, except in patients identified as MET-amplified. Our data underscore the limitations of adopting arbitrary copy number thresholds and the need for cross-assay validation to define therapeutically tractable MET pathway dysregulation in EGFR-mutant–positive NSCLC.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.18.00177
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2019
    detail.hit.zdb_id: 2005181-5
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  • 3
    Online Resource
    Online Resource
    Safety profile of 152 consecutive image-guided lung and liver tumor biopsies for molecular profiling (IMPACT-SG).
    American Society of Clinical Oncology (ASCO) ; 2015
    In:  Journal of Clinical Oncology Vol. 33, No. 15_suppl ( 2015-05-20), p. e22134-e22134
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 33, No. 15_suppl ( 2015-05-20), p. e22134-e22134
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2015.33.15_suppl.e22134
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2015
    detail.hit.zdb_id: 2005181-5
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  • 4
    Online Resource
    Online Resource
    Association of smoking status with p16 and cyclin D1 (CCND1) expression with clinical characteristics and overall survival (OS) in oropharyngeal squamous cell carcinoma (OSC).
    American Society of Clinical Oncology (ASCO) ; 2012
    In:  Journal of Clinical Oncology Vol. 30, No. 15_suppl ( 2012-05-20), p. 5551-5551
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 30, No. 15_suppl ( 2012-05-20), p. 5551-5551
    Abstract: 5551 Background: Smoking-related head and neck cancer (HNC) is genetically different, with higher mutation rates compared with non-smokers (NS). Human papillomavirus (HPV)-positive (+) OSC has a superior prognosis independent of treatment. Among HPV+ patients (pt), current or prior smokers (CS) have poor OS compared with NS. Expression of p16, a known HPV surrogate, and CYD1, a cell cycle marker often dysregulated in HNC, was evaluated with respect to smoking status and OS. Methods: Expression of p16 and CYD1 was assessed by immunohistochemistry in 108 OSC pt treated between 1999-2009, using cutoffs of ≥70% (p16+) and ≥10% (CYD1+) stained tumor cells. Associations between expression, clinical characteristics and OS were evaluated by Kaplan-Meier method and compared by log rank test. Hazard ratio (HR) for death was estimated using Cox models. Results: 31 pt (28.7%) were p16+ and 80 pt (75.5%) were CYD1 negative(-). p16+ pt were younger (median age 57 v 66 yrs, p=0.002), more likely female (35.5% v 15.2%, p=0.035), NS (51.6% v 13.9%, p 〈 0.001) with lower combined age-comorbidity score (ageCS) (p=0.003). CYD1+ pt were older (median 66 v 57 yrs, p=0.015), more likely CS (81.5% v 48.1%, p=0.002) with higher ageCS (p=0.018). At a median f/u of 65.7 months, median OS was 57.3 months. p16+ pt had better OS than p16- pt (median OS not reached (NR) v 22.3 mths, p 〈 0.001). CYD1+ pt had poorer OS than CYD1- pt (median OS NR v 17.7 mths, p 〈 0.001). On multivariable analysis p16 and CYD1 status were independently associated with OS (HR 0.412, p=0.045 and HR 4.06, p=0.011 respectively), independent of smoking status (HR 5.01, p=0.008), ageCS (HR 1.32 per 1 point increase, p 〈 0.001) and stage. Strikingly, among NS, 5-year OS in p16+ compared with p16- pt was 100% vs 67% (p 〈 0.001). In contrast, among CS, p16 status had no association with OS (HR 0.97, p=0.943), while CYD1 status and ageCS were independent predictors of death (HR 4.70, p=0.025 and HR 1.28, p 〈 0.001 respectively). Conclusions: In OSC, NS with high p16 expression have excellent prognosis. Among CS, pt with fewer comorbidities and low CYD1 expression have better OS. p16 status was not prognostic in the latter group of patients.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2012.30.15_suppl.5551
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2012
    detail.hit.zdb_id: 2005181-5
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  • 5
    Online Resource
    Online Resource
    A phase Ib safety and tolerability study of a pan class I PI3K inhibitor buparlisib (BKM120) and gefitinib (gef) in EGFR TKI-resistant NSCLC.
    American Society of Clinical Oncology (ASCO) ; 2013
    In:  Journal of Clinical Oncology Vol. 31, No. 15_suppl ( 2013-05-20), p. 8107-8107
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 31, No. 15_suppl ( 2013-05-20), p. 8107-8107
    Abstract: 8107 Background: Overcoming EGFR TKI resistance (R) is a major clinical challenge; reported mechanisms include EGFR T790M mutation (mt), MET amplification (amp) and PIK3CA mt. As the PI3K pathway is a central convergent signaling node, we hypothesized that addition of buparlisib (BKM) could overcome EGFR TKI-R. Methods: Patients (pt) resistant to EGFR TKI (Jackman JCO 2010) were enrolled to determine safety, tolerability, pharmacokinetics (PK) and pharmacodynamics of BKM-gef. Using a “3+3” design, escalating doses of BKM were added to pt progressing on gef (Gp A). Pt not on gef preceding enrolment received a 2 wk run in (Gp B). Given the favorable CNS penetration of BKM, a CNS gp with brain metastases only was included. Pt had pretreatment biopsies and sequential PET-CT scans (baseline & d28). Results: 15 pt have been treated at 3 dose levels: BKM 80 mg/d (n=6), 100 mg/d (n=6), 80 mg 5d on 2d off (5/2, n=3), with gef 250 mg/d. Gp A (n=9, 1 CNS), B (n=6, 1 CNS), F:M (9:6), median age 63 (47-73) and majority 〉 3 lines of therapy. DLT was G3 diarrhea observed in 2/6 pt at BKM100. Common adverse events (AE, all grades) include rash (80%), diarrhea (73%), fatigue (60%), anorexia (47%), mucositis (40%). Notably, 40% of pt had late (beyond DLT period) G3 toxicities such as rash and diarrhea. MTD is BKM 80/d and gef 250/d. To improve the overall safety profile, an intermittent schedule of BKM80 5/2 was also found to be feasible. In gp B, PET-CT done after 2 wk run-in of gef, 3/4 evaluable pt demonstrated reduction in SUV max of which 1 had PR. With addition of BKM, reduction in SUV max ( 〉 25%) was seen in 4/10 pt (gp A & B). Median PFS 2.8 m (95%CI 2.3 – 8.1), two pt in CNS gp had PFS of 2.8 and 10.7 m. Molecular analyses revealed 6/12 (50%) harbored T790M mt, 2/5 (40%) MET amp, 0/12 PI3KCA mt. In gp A, 4/9 pt (2 T790M; 1 MET amp) had clinical responses, including slight tumor shrinkage and reduced pleural effusion, but required dose reductions due to AE. PK profiles are being analyzed. Conclusions: MTD is gef 250-BKM 80/d. Antitumor activity has been observed with addition of BKM in EGFR TKI-R pt. In view of late toxicities and long t½ of BKM, exploring alternative schedules is warranted. A dose expansion cohort at MTD is currently ongoing. Clinical trial information: NCT01570296.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2013.31.15_suppl.8107
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2013
    detail.hit.zdb_id: 2005181-5
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  • 6
    Online Resource
    Online Resource
    Fanconi's Anemia in Adulthood: Chemoradiation-Induced Bone Marrow Failure and a Novel FANCA Mutation Identified by Targeted Deep Sequencing
    American Society of Clinical Oncology (ASCO) ; 2011
    In:  Journal of Clinical Oncology Vol. 29, No. 20 ( 2011-07-10), p. e591-e594
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 29, No. 20 ( 2011-07-10), p. e591-e594
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2011.35.1064
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2011
    detail.hit.zdb_id: 2005181-5
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  • 7
    Online Resource
    Online Resource
    Never-Smokers With Lung Cancer: Epidemiologic Evidence of a Distinct Disease Entity
    American Society of Clinical Oncology (ASCO) ; 2006
    In:  Journal of Clinical Oncology Vol. 24, No. 15 ( 2006-05-20), p. 2245-2251
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 24, No. 15 ( 2006-05-20), p. 2245-2251
    Abstract: Tobacco smoke is a definite causative agent for lung cancer. It is increasingly being recognized that never-smokers can be afflicted with non–small-cell lung cancer (NSCLC). We aim to assess survival differences between smokers and never-smokers with NSCLC. Patients and Methods We analyzed 975 NSCLC patients who presented from January 1999 to December 2002. Clinical characteristics among current-, former- and never-smokers were tested using χ 2 or Kruskal-Wallis test. The hazard ratio (HR) for death and its 95% CI were calculated by Cox regression. Results Of 975 patients, 59 had no smoking history and 33 had no quit time recorded. Of 883 patients analyzed, 286 patients (32.4%) were never-smokers. One hundred ninety-six never-smokers (68.5%) were females compared with 12% among current- and 13% among former-smokers (P 〈 .001). There was a significant difference in histologic subtype between never-smokers and smokers: 69.9% with adenocarcinoma versus 39.9% (current-smokers) versus 47.3% (former-smokers); 5.9% with squamous cell carcinoma versus 35.7% (current-smokers) versus 28% (former-smokers; P 〈 .001). Smokers had significantly poorer performance status (P = .002) and higher median age at diagnosis (P 〈 .001) while more never-smokers presented with advanced disease (P = .002). Eight hundred and five patients (82.6%) died by May 30, 2005. The HR for smokers was significantly higher on both univariate and multivariate analysis (HR, 1.297; 95% CI, 1.040 to 1.619). Conclusion Never-smokers comprised a high proportion of NSCLC patients in Singapore. Definite epidemiologic differences exist between never-smokers and smokers. Differences in survival outcome further suggest that the biology underlying the pathogenesis and behavior of the disease may be different for never-smokers.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2005.04.8033
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2006
    detail.hit.zdb_id: 2005181-5
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  • 8
    Online Resource
    Online Resource
    Differences in clinical characteristics and overall survival in never-smokers with lung squamous cell carcinoma.
    American Society of Clinical Oncology (ASCO) ; 2014
    In:  Journal of Clinical Oncology Vol. 32, No. 15_suppl ( 2014-05-20), p. e12527-e12527
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 32, No. 15_suppl ( 2014-05-20), p. e12527-e12527
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2014.32.15_suppl.e12527
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2014
    detail.hit.zdb_id: 2005181-5
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  • 9
    Online Resource
    Online Resource
    A phase II study of nimotuzumab and CDDP concurrent with radiation in locally advanced squamous cell carcinoma of the head and neck (SCCHN).
    American Society of Clinical Oncology (ASCO) ; 2012
    In:  Journal of Clinical Oncology Vol. 30, No. 15_suppl ( 2012-05-20), p. e16024-e16024
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 30, No. 15_suppl ( 2012-05-20), p. e16024-e16024
    Abstract: e16024 Background: Nimotuzumab is a humanized monoclonal antibody (MAb) to EGFR. Concurrent cisplatin with radical radiotherapy (RT) is standard treatment for locally advanced SCCHN where it is unresectable or for organ-preservation. We explored the combination of nimotuzumab with concurrent CDDP and RT in these patients (pts). Methods: Pts with locally advanced stage III/IV SCCHN were eligible for study if: age 〉 18, ECOG 0-1, SCC, normal organ function. Analysis was by intention-to-treat (ITT). CDDP 100 mg/m 2 on days 1, 22, and 43 was given with RT (70 Gy over 35 fractions). Nimotuzumab was given as a flat dose of 200 mg weekly on weeks 1 to 8 of treatment. Pts were followed up for RECIST response, progression free survival and toxicity. Results: Twenty-eight pts were available for analysis at the time of report. The median age was 58 (30-69). Most were Chinese (90%) and all ECOG 0-1. Twelve pts had oropharynx Ca, 16 had non-oropharyx Ca. Twenty-five pts were evaluable for response, 2 pts withdrew consent after 2 weeks, 1 pt died of undiagnosed Fanconi anemia. By ITT, the best overall response rate (CR/PR) was 78.6% (12 CR/10 PR), SD 3.6% (1), PD 7.2% (2). Pts with oropharynx Ca had higher PFS rate at 1 year than non-oropharynx (80% vs 48%). Major grade 3/4 toxicities were limited to mucositis, dysphagia, and fatigue. Grade 5 toxicity due to febrile pancytopenia occurred in 1 pt with undiagnosed Fanconi’s. Acneiform rash typical of EGFR inhibitors occurred in 1 pt. Conclusions: Nimotuzumab with concurrent CDDP/RT is feasible and there was minimal additional toxicity encountered. Final results will be updated at the meeting.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2012.30.15_suppl.e16024
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2012
    detail.hit.zdb_id: 2005181-5
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  • 10
    Online Resource
    Online Resource
    Do elderly patients benefit from enrollment in phase I clinical trials?
    American Society of Clinical Oncology (ASCO) ; 2013
    In:  Journal of Clinical Oncology Vol. 31, No. 15_suppl ( 2013-05-20), p. 9509-9509
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 31, No. 15_suppl ( 2013-05-20), p. 9509-9509
    Abstract: 9509 Background: Despite the significant burden of cancer in the older population, their outcomes in the context of phase I studies have been poorly studied. We evaluated the clinical characteristics and outcomes of elderly pts enrolled in phase 1 clinical trials in our centre and evaluate the performance of Royal Marsden Hospital (RMH) prognostic score (albumin, LDH, no of met sites) in this pt population. Methods: 296 consecutive pts who were treated in 20 phase 1 trials from 2005-2012 in our unit were analysed. Clinical characteristics and outcomes between young pts ( 〈 65, n=202) and older pts (≥65, n=94) were compared. Results: The median age of the older pts was 69 (65-84), 71% were males. 51% of the pts received chemotherapy based treatment with or w/out biological agents. 61% of the pts had lung cancers and 32% had gastrointestinal cancers. 52% of pts had ≥2 co-morbidities. After median follow up of 7.5 mths (0.36-50.6 mths), the median progression free survival (PFS) and overall survival (OS) were 5.8 and 8.8 mths respectively. Although elderly pts had more co-morbidities and lower albumin levels at baseline, there was no significant difference in survival (8.8 vs 9.9 mths), p=0.68) compared to younger pts. The prognostic factors for OS identified in multivariate analysis were prior lines of chemotherapy (0-2 vs ≥3), baseline sodium levels (≥135 vs 〈 135mmol/L) and platelet levels (≤400 vs 〉 400×10⁹). We developed a risk nomogram based on the factors identified prognostic of OS with concordance(c)-index of 0.65. RMH score (2-3 vs 0-1) predicted for OS with hazard ratio of 2.1, p=0.03 and c- index of 0.63. 26% of elderly pts experienced grade 3/4 toxicities in the first cycle of treatment. Common grade 3/4 toxicities were dermatological (25%), haematological (17%) and gastrointestinal (13%). Both age of pts (p=0.70) and dose levels (p=0.18) did not have any bearing on occurrence of grade 3/4 toxicities. Conclusions: Elderly pts (≥65) enrolled into phase 1 clinical trials had similar survival outcomes and toxicity profiles compared to younger pts. Risk scoring models to aid patient selection need further clarification in this population.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2013.31.15_suppl.9509
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2013
    detail.hit.zdb_id: 2005181-5
    Location Call Number Limitation Availability
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