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  • 1
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    Online Resource
    Sa1231 TUMOR SIZE INCREASES THE RISK FOR LYMPH NODE METASTASES IN T1B ESOPHAGEAL ADENOCARCINOMA
    Elsevier BV ; 2019
    In:  Gastrointestinal Endoscopy Vol. 89, No. 6 ( 2019-06), p. AB178-AB179
    Details
    In: Gastrointestinal Endoscopy, Elsevier BV, Vol. 89, No. 6 ( 2019-06), p. AB178-AB179
    Type of Medium: Online Resource
    ISSN: 0016-5107
    URL: Article
    DOI: 10.1016/j.gie.2019.03.122
    RVK:
    XA 44545
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
    detail.hit.zdb_id: 2006253-9
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  • 2
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    Molecular testing in metastatic colorectal adenocarcinoma cytology cell pellets
    Wiley ; 2019
    In:  Diagnostic Cytopathology Vol. 47, No. 11 ( 2019-11), p. 1132-1137
    Details
    In: Diagnostic Cytopathology, Wiley, Vol. 47, No. 11 ( 2019-11), p. 1132-1137
    Abstract: Mutational status for KRAS , NRAS , and BRAF genes should be performed on all colorectal carcinoma (CRC) specimens in order to guide targeted therapy selection for metastatic disease. Mutations are typically assessed via polymerase chain reaction and/or next generation sequencing (NGS) on formalin‐fixed paraffin‐embedded tissues. With minimally invasive diagnostic methodologies, the cytology cell pellet obtained by fine‐needle aspiration (FNA) can serve as an alternative source of tumor deoxyribonucleic acid. Methods An electronic record review of the cytopathology files (CoPathPlus, Cerner Corp., North Kansas City, Missouri) from September 1, 2015 through December 31, 2018 was conducted. All cytology specimens obtained via FNA and diagnosed as metastatic CRC on which NGS was performed were included. NGS for KRAS , NRAS , and BRAF mutations using the AmpliSeq Cancer Hotspot Panel v2.0 kit (Thermo Fisher Scientific, Waltham, Massachusetts) was performed on cytology cell pellets. Results Forty‐eight cases were identified. Forty‐six of 48 specimens (96%) were adequate for molecular testing. Of those adequate specimens, proportion of malignant cells in the sample ranged from 5% to 95% (mean 46%). Twenty‐seven of 48 cases (56%) were positive for clinically relevant mutations. Twenty‐four of 27 cases (89%) were positive for KRAS mutations, with exon 2 most frequently involved (22/24 cases, 92%). Two of 27 cases (7%) were positive for NRAS mutations and one case (1/27, 4%) was positive for a BRAF mutation involving codon 594. Conclusion Mutational analysis performed on cytology cell pellets serves as a useful means of gathering clinically actionable information on tumor mutation status in metastatic CRC.
    Type of Medium: Online Resource
    ISSN: 8755-1039 , 1097-0339
    URL: Issue
    URL: Article
    DOI: 10.1002/dc.v47.11
    DOI: 10.1002/dc.24275
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2001251-2
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  • 3
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    Targeted Next-Generation Sequencing in Men with Metastatic Prostate Cancer: a Pilot Study
    Springer Science and Business Media LLC ; 2018
    In:  Targeted Oncology Vol. 13, No. 4 ( 2018-8), p. 495-500
    Details
    In: Targeted Oncology, Springer Science and Business Media LLC, Vol. 13, No. 4 ( 2018-8), p. 495-500
    Type of Medium: Online Resource
    ISSN: 1776-2596 , 1776-260X
    URL: Article
    DOI: 10.1007/s11523-018-0576-z
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2018
    detail.hit.zdb_id: 2222136-0
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  • 4
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    Immune checkpoint inhibitors in liver transplant: a case series
    AME Publishing Company ; 2023
    In:  Journal of Gastrointestinal Oncology Vol. 14, No. 2 ( 2023-4), p. 1141-1148
    Details
    In: Journal of Gastrointestinal Oncology, AME Publishing Company, Vol. 14, No. 2 ( 2023-4), p. 1141-1148
    Type of Medium: Online Resource
    ISSN: 2078-6891 , 2219-679X
    URL: Journal
    URL: Article
    DOI: 10.21037/jgo
    DOI: 10.21037/jgo-22-922
    Language: Unknown
    Publisher: AME Publishing Company
    Publication Date: 2023
    detail.hit.zdb_id: 2594644-4
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  • 5
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    Outcomes in Patients With Pancreatic Adenocarcinoma With Genetic Mutations in DNA Damage Response Pathways: Results From the Know Your Tumor Program
    American Society of Clinical Oncology (ASCO) ; 2019
    In:  JCO Precision Oncology , No. 3 ( 2019-12), p. 1-10
    Details
    In: JCO Precision Oncology, American Society of Clinical Oncology (ASCO), , No. 3 ( 2019-12), p. 1-10
    Abstract: Up to 25% of pancreatic adenocarcinomas (PDACs) harbor mutations in the homologous recombination DNA damage response (HR-DDR) pathway. Although known to affect responsiveness to DNA-damaging chemotherapy, the prognostic relevance of these mutations is unclear and outcomes in patients with PDAC who harbor HR-DDR mutations beyond BRCA1/2 remain unexplored. METHODS We evaluated 820 patients with PDAC enrolled in the Know Your Tumor program for whom we had collected comprehensive genomic testing results and longitudinal clinical outcomes. Patients were categorized as having resected versus advanced disease, and as having received platinum-based therapy versus being platinum naïve. Tumor genomic profiles were categorized as HR-DDR mutated (HR-DDR mut ) or proficient (pHR-DDR) on the basis of the presence of pathogenic mutations of somatic or germline origin in BRCA1/2 or PALB2 (group 1); ATM/ATR/ATRX (group 2); or BAP1, BARD1, BRIP1, CHEK1/2, RAD50/51/51B, or FANCA/C/D2/E/F/G/L (group 3). Overall survival was measured from the date of diagnosis until death. RESULTS Median overall survival (mOS) was similar in all resected patients irrespective of exposure to platinum-based therapy, whereas for platinum-treated patients with advanced disease, mOS was significantly longer for HR-DDR mut versus pHR-DDR (2.37 years v 1.45 years, respectively). Of importance, no difference was identified in platinum-naïve patients. mOS in patients with mutations in all three HR-DDR mut groups was greater than that for pHR-DDR patients, but this difference was lost in platinum-naïve patients. CONCLUSION Patients with advanced HR-DDR mut have improved mOS when treated with platinum-based therapy compared with pHR-DDR patients. In platinum-naïve patients, there is no mOS difference, which suggests that HR-DDR status has no pure prognostic value. These findings support the need to test all patients with advanced PDAC to ensure that HR-DDR mut patients receive the benefit of treatment with platinum-based therapy.
    Type of Medium: Online Resource
    ISSN: 2473-4284
    URL: Article
    DOI: 10.1200/PO.19.00115
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2019
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  • 6
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    CTNI-04. ACTIVITY OF LAROTRECTINIB IN TROPOMYOSIN RECEPTOR KINASE (TRK) FUSION CANCER PATIENTS WITH CENTRAL NERVOUS SYSTEM (CNS) METASTASES
    Oxford University Press (OUP) ; 2020
    In:  Neuro-Oncology Vol. 22, No. Supplement_2 ( 2020-11-09), p. ii41-ii42
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 22, No. Supplement_2 ( 2020-11-09), p. ii41-ii42
    Abstract: NTRK gene fusions occur in a range of tumor types, including those with CNS metastases. Larotrectinib, a highly selective FDA- and EMA- approved TRK inhibitor, demonstrated an objective response rate (ORR) of 79% across various cancers (Hong et al. Lancet Oncol. 2020). We report data on patients with TRK fusion cancer with CNS metastases treated with larotrectinib. METHODS Patients with solid tumors with CNS metastases at baseline harboring an NTRK gene fusion enrolled in two clinical trials (NCT02122913 and NCT02576431) were identified. Response was assessed by the investigator per RECIST v1.1. RESULTS As of July 15, 2019, 14 patients with CNS-metastases were enrolled: lung cancer (n=7), thyroid cancer (n=4), melanoma (n=2), and non-secretory breast cancer (n=1). Median age was 53 years (range 25–76). Including all sites of disease, the ORR was 71% (95% CI 42–92%): ten patients had a partial response (PR), two had stable disease (SD), and two had progressive disease (lung and melanoma). Of the three patients with measurable intracranial disease at baseline, the best intracranial response was 1 complete response, 1 PR, and 1 SD. Median duration of response for all patients was 14.8 months (range 1.9+ to 17.4+), median progression-free survival was 9.9 months (range 1.4 to 19.3+), and median overall survival was 27.8 months (range 1.4+ to 27.8). Treatment duration ranged from 1.4 to 25.0 months; six patients continued treatment beyond progression (lasting between 0.1+ and 8.5 months). Treatment-emergent adverse events (TEAEs) were mainly Grade 1 and 2; Grade 3 TEAEs occurred in seven patients (50%), with one (myalgia) attributed to larotrectinib (7%). There were no Grade 4 TEAEs. CONCLUSIONS Larotrectinib was highly active and well tolerated in TRK fusion cancer patients with CNS metastases. These results support testing for NTRK gene fusions across all cancers, including in patients with CNS metastases.
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/noaa215.171
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
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  • 7
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    Downregulation of Ribosomal Proteins Is Seen in Non 5q- MDS
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 854-854
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 854-854
    Abstract: Recent work (Ebert et al, Nature 2008, Jan 17:335-9) has shown that ribosomal protein S14 (RPS14) is underexpressed in myelodysplasia (MDS) with deletion of chromosome 5q and plays a role in its pathogenesis. The role of ribosomal proteins in other more common subtypes of MDS is unknown. We conducted a meta-analytical comparison of gene expression profiles of 60 cases of non 5q- MDS CD34+ cells with 52 normal CD34+ profiles. These datasets were obtained from seven independent studies from NCBI’s GEO database. The data was integrated based on UniGene IDs and were quantile normalized to ensure cross-study comparability. (Based on our previous approach; Sohal et al PLOS One, 2008, Zhou et al, Blood, 2008). Using significance analysis of microarrays (SAM) and a false discovery rate (FDR) of just 0.04%, we found that ribosomal protein were the class of genes that were most significantly altered in MDS. We observed that RPL35a, RPS9, RPL10, RPL22, RPS14, RPS10, RPS15a, RPS24, RPL24, RPL36, RPL21, RPL23 were strikingly downregulated in non-5q- MDS CD34+ cells. To determine if these alterations were a result of changes in DNA copy numbers of these genes, we examined 20 MDS samples by high resolution array comparative genome hybridization (aCGH) performed on Nimblegen whole genome tiling arrays. aCGH at 6kb resolution revealed deletions in RPL14, RPL22, RPL36, RPS10, RPS5 and even RPS14 in distinct selected cases of non 5q- MDS. These small deletions, which were not identifiable by traditional karyotyping methods, may be putative mechanisms of ribosomal protein downregulation and ultimately, in MDS development and/or progression. Since MDS is also characterized by aberrant epigenetic silencing of genes, we next examined the methylation status of ribosomal gene promoters by high resolution global DNA methylation profiling by using the HELP assay (HpaII tiny fragment Enrichment by Ligation-mediated PCR; Khulan et al, Genome Res. 2006 Aug;16(8)). This assay uses differential methylation-specific digestion by HpaII and MspI followed by amplification, two color labeling and hybridization to quantitatively determine individual promoter CpG island methylation. While there were sporadic changes in some patients, we did not observe any consistently significant changes in methylation of these ribosomal gene promoters on comparison with normal anemic controls. In summary, we show novel widespread alterations in ribosomal protein expression in MDS, at least some of which are associated with genomic deletions. These findings illustrate the applicability of meta-analytical genomic approaches in a heterogeneous disease such as MDS. Most importantly, our data points to the dramatic role of alteration in the protein translational machinery in pathogenesis of MDS.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.854.854
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
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  • 8
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    Incidence of Venous Thromboembolism in Patients with Resected Biliary Tract Cancers
    American Society of Hematology ; 2016
    In:  Blood Vol. 128, No. 22 ( 2016-12-02), p. 5004-5004
    Details
    In: Blood, American Society of Hematology, Vol. 128, No. 22 ( 2016-12-02), p. 5004-5004
    Abstract: Background: Venous thromboembolism (VTE) is an important complication of cancer, with adverse impact on morbidity and mortality. In biliary tract cancer (BTC), there is a paucity of data on incidence of VTE and any prognostic markers that may correlate with VTE. Objectives: To determine the incidence of VTE events in patients with resected BTC, as well as identify predictors of VTE. Methods: We conducted a retrospective cohort study of consecutive patients with BTC undergoing surgical resection with a curative intent at the Cleveland Clinic between 1/1/2006-6/30/2014. Electronic medical records and tumor registry were reviewed for baseline demographic and laboratory data, the incidence of VTE after initial diagnosis, including deep venous thrombosis (DVT) of the extremities, pulmonary emboli (PE), or intra-abdominal thrombi. Rates of VTE are reported. Results: The study population comprised 142 patients with a median age of 62 (range 31-84) years; 53% were women. Location of the tumors included extrahepatic (21%), intrahepatic (45%), hilar (9%), and gallbladder (25%). During follow-up, 33 (23.2%) patients had documented VTE. Twenty-five patients had 1 event each, 6 had 2 events each, 1 had 3 events, and 1 patient had 4 events, for a total of 44 events. Of these 44 events, 19 (43.2%) were lower extremity DVTs, 9 (20.4%) were upper extremity DVTs, 7 (16%) were PE, and 9 (20.4%) were visceral (intra-abdominal) thrombi. Four (12.1%) of the 33 patients experienced VTE prior to surgical resection. Univariable analyses did not reveal any association with clinical variables - including age, sex, race, baseline hemoglobin, white blood cell or platelet counts, albumin, location of the tumor, chemotherapy or radiation, and smoking. Conclusion: Nearly one in four patients with biliary tract cancers who have undergone surgical resection develop VTE. Larger prospective studies focusing on risk factors and novel biomarkers are warranted. Disclosures Khorana: Sanofi: Consultancy, Honoraria; Leo: Consultancy, Honoraria, Research Funding; Amgen: Consultancy, Honoraria, Research Funding; Bayer: Consultancy, Honoraria; Halozyme: Consultancy, Honoraria; Pfizer: Consultancy, Honoraria; Roche: Consultancy, Honoraria; Janssen Scientific Affairs, LLC: Consultancy, Honoraria, Research Funding.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V128.22.5004.5004
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2016
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 9
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    A High Resolution Epigenomic Map of Myelofibrosis Reveals Multiple Chromosomal Deletions and Amplifications Accompanied by a High Level of Functionally Important Methylation.
    American Society of Hematology ; 2006
    In:  Blood Vol. 108, No. 11 ( 2006-11-16), p. 2684-2684
    Details
    In: Blood, American Society of Hematology, Vol. 108, No. 11 ( 2006-11-16), p. 2684-2684
    Abstract: Chronic idiopathic myelofibrosis (MF) is a clonal hematopoietic disorder that leads to progressive marrow fibrosis and peripheral cytopenias. Very little is known about the role of chromosomal alterations and DNA methylation in the pathobiology of this disease. We used a combination of gene expression analysis, high density array based comparative genomic hybridization (aCGH) and genome wide methylation analysis to perform an integrated genomic analysis of MF. Gene expression analysis was performed using 37K oligo maskless arrays and high density aCGH was performed at 6Kb resolution using Nimblegen platform. Whole genome methylation was analyzed by a recently described novel method ( Khulan et al, Genome Res. 2006 Aug;16(8)) that uses differential methylation specific digestion by HpaII and MspI followed by pcr amplification, two color labeling and hybridization to quantitatively determine individual promoter CpG island methylation. aCGH revealed a very high number of microdeletions (range 622–1148, mean ± SD 555±144 ) and amplifications (range 463–770, mean ± SD 781±246) in a pilot study conducted in 4 patients with MF. Twenty three common regions were found to amplified in all patients which included regions of chr3p25, chr8p21, chr12q24, chr14q32, chr17p13 and chr17q12, which code for a novel set of genes including B-cell CLL/lymphoma 7A, GTPase activating Rap, BRF1 and others. Five regions were found to be commonly deleted in all samples (chr1q31, chr5q12, chr20p13, chrXq21, chrXq28). Thirty eight DNA segments were found to be deleted and 142 amplified in 75% of the samples. Several potential pathogenic genes encoding for transcription factors, cytokines and cytokine receptors were found to be coded by these segments. A custom human oligo array was used to determine methylation by calculating HpaII/MspI cut fragment intensity ratio. All patient samples had a very high level of methylation (range 64–82%, mean 72% ± 8.6%). Expression was found to be significantly decreased for the genes that were methylated (p 〈 .0001, T test) demonstrating the functional relevance of this assay. Analysis of common differentially methylated genes (when compared to normal samples) and their validation are ongoing. Microdeletions and amplifications seen on aCGH did not correlate with changes in global expression of the involved genes. Interestingly, when data from all platforms were combined, methylation of the genes with altered copy number led to significant decreases in gene expression (p=.03, T test). This result suggests pathogenic changes in gene expression in MF result from an interplay between DNA copy number alterations and methylation of the remaining alleles. The high rate of methylation demonstrated in MF suggests that epigenetic silencing of genes may play an important role in pathogenesis and points to the potential utility of hypomethylating agents in this disease.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V108.11.2684.2684
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2006
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 10
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    Neoadjuvant treatment of pancreatic adenocarcinoma: a systematic review and meta-analysis of 5520 patients
    Springer Science and Business Media LLC ; 2017
    In:  World Journal of Surgical Oncology Vol. 15, No. 1 ( 2017-12)
    Details
    In: World Journal of Surgical Oncology, Springer Science and Business Media LLC, Vol. 15, No. 1 ( 2017-12)
    Type of Medium: Online Resource
    ISSN: 1477-7819
    URL: Article
    DOI: 10.1186/s12957-017-1240-2
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2017
    detail.hit.zdb_id: 2118383-1
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