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View Full Version : serious adverse liver effects of lapatinib seem to be predicted by patient's genetic


Lani
05-18-2011, 11:44 PM
status (and therefore predictable)


HLA-DRB1*07:01-DQA1*02:01 and UGT1A1*28 allele carriage in hepatic serious adverse event cases identified during lapatinib clinical trials.


Sub-category:
HER2+

Category:
Breast Cancer - HER2/ER

Meeting:
2011 ASCO Annual Meeting

Abstract No:
547

Citation:
J Clin Oncol 29: 2011 (suppl; abstr 547)


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ASCO Annual Meeting!
Session: Breast Cancer - HER2/ER

Type: General Poster Session

Time: Monday June 6, 1:00 PM to 5:00 PM

Location: McCormick Place Hall A

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Author(s): C. F. Spraggs, L. R. Budde, L. P. Briley, C. Cox, E. Rappold, G. Aktan, L. S. Williams, V. E. Mooser, L. R. Cardon; GlaxoSmithKline, Harlow, United Kingdom; GlaxoSmithKline, Research Triangle Park, NC; GlaxoSmithKline, Stevenage, United Kingdom; GlaxoSmithKline, Collegeville, PA; GlaxoSmithKline Upper Providence, Uxbridge, United Kingdom; GlaxoSmithKline, King of Prussia, PA


Abstract Disclosures


Abstract:

Background: Previous pharmacogenetic experiments evaluating lapatinib associated liver safety signals identified and confirmed associations for HLA-DRB1*07:01 and DQA1*02:01 with alanine-amino transferase (ALT) elevation during treatment and UGT1A1*28 with baseline and on-treatment total bilirubin (TBL) elevation, consistent with underlying Gilbert’s syndrome.The carriage of these alleles was investigated in 20 hepatic serious adverse events (SAE) identified during the conduct of lapatinib clinical trials in adjuvant (3 studies), metastatic breast cancer (3 studies) and head and neck cancer (one study). Methods: Twenty hepatic SAE cases that met criteria of concurrent ALT >3x, alkaline phosphatase (ALP) <2x (or missing) and TBL >2x ULN elevations, plus hepatic expert panel adjudication as “probable or possible drug induced liver injury” were selected. Five of these cases are currently treatment blinded due to participation in ongoing clinical trials. Germline DNA was extracted from peripheral blood and genotypes were determined by standard methods. Results: Of the 20 concurrent ALT/TBL elevation cases 14 (70%) were positive for both HLA-DRB1*07:01 and DQA1*02:01 allele carriage, six (30%) were negative for either. Population frequencies are reported between 15% to 25% across major ethnicities. Stratifying these subjects by HLA allele carriage suggested different phenotype characteristics, with a higher mean/median maximum ALT for the HLA-DRB1*07:01/DQA1*02:01 positive group (13.4x/8.0x ULN, n=14), than for the negative group (4.2x/4.2x ULN, n=6). Furthermore, the HLA allele positive group had carriage of the Gilbert’s syndrome UGT1A1*28 genotype (TA7/TA7) in 3/14 (21%) of cases, whilst TA7/TA7 carriage was higher in the HLA allele negative group (5/6, 83%). Conclusions: The previously confirmed lapatinib-associated hepatotoxicity markers HLA-DRB1*07:01/DQA1*02:01 were carried by 70% of these hepatic SAE cases. For the six concurrent ALT/TBL cases that were HLA allele negative, there appeared to be an excess carriage of the Gilbert’s syndrome UGT1A1*28 genotype TA7/TA7, which may contribute to their TBL elevation safety signal.