PIK3CA mutations in Peruvian patients with HER2-amplified and triple negative non-metastatic breast cancers

Carlos A. Castaneda; Marco Lopez-Ilasaca; Joseph A. Pinto; Michelle Chirinos-Arias; Franco Doimi; Silvia P. Neciosup; Katerin I. Rojas; Tatiana Vidaurre; Justin M. Balko; Carlos L. Arteaga; Henry L. Gomez

doi:10.1016/j.hemonc.2014.09.007

PIK3CA mutations in Peruvian patients with HER2-amplified and triple negative non-metastatic breast cancers

Carlos A. Castaneda, Marco Lopez-Ilasaca, Joseph A. Pinto, Michelle Chirinos-Arias, Franco Doimi, Silvia P. Neciosup, Katerin I. Rojas, Tatiana Vidaurre, Justin M. Balko, Carlos L. Arteaga, Henry L. Gomez

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19 Citas (Scopus)

Resumen

Purpose To determine the frequency of PIK3CA mutations in a Peruvian cohort with HER2-amplified and triple negative breast cancers (TNBC).

Methods We analyzed two cohorts of 134 primary non-metastatic breast cancer patients from Peru. Cohorts consisted of 51 hormone receptors (+)/HER2-amplified breast tumor patients surgically resected as first treatment included in the ALTTO trial (ALTTO cohort) and 81 TNBC patients with residual disease after neoadjuvant treatment (neoadjuvant cohort). Genomic DNA was extracted from paraffin-embedded tumor samples. Samples from the ALTTO and neoadjuvant cohorts were taken at biopsies and from residual tumors, respectively. PIK3CA mutations were detected by sequencing DNA fragments obtained by PCR amplification of exons and their flanking introns. All of the detected PIK3CA mutations were confirmed in a second independent run of sample testing.

Conclusions We found a similar frequency of PIK3CA mutations to that reported in other series. Although we did not include HR+/HER2 patients, those with HER2-amplified tumors were more likely to present PIK3CA mutations compared to patients with triple negative tumors.

Results PIK3CA mutations were present in 21/134 cases (15.7%). Mutations in exon 9 and 20 were present in 10/134 (7.5%) and 11/134 (8.2%), respectively. No cases had mutations in both exons. Mutations in exon 9 consisted of E545A (seven cases), E545K (two cases) and E545Q (one case); while in exon 20, mutations consisted of H1047R (10 cases) and H1047L (one case). Compared to TNBC patients, HER2-amplified patients were more likely to have PIK3CA mutated (23% vs 9.6%; P = 0.034). There were no associations between mutational status of PIK3CA with estrogen receptor status (P = 0.731), progesterone receptor status (P = 0.921), age (P = 0.646), nodal status (P = 0.240) or histological grade (P = 1.00). No significant associations were found between PIK3CA mutational status and clinicopathological features.

Idioma original	Inglés
Páginas (desde-hasta)	142-148
Número de páginas	7
Publicación	Hematology/ Oncology and Stem Cell Therapy
Volumen	7
N.º	4
DOI	https://doi.org/10.1016/j.hemonc.2014.09.007
Estado	Publicada - 1 dic. 2014

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Publisher Copyright:
© 2014 King Faisal Specialist Hospital & Research Centre.

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10.1016/j.hemonc.2014.09.007

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Castaneda, C. A., Lopez-Ilasaca, M., Pinto, J. A., Chirinos-Arias, M., Doimi, F., Neciosup, S. P., Rojas, K. I., Vidaurre, T., Balko, J. M., Arteaga, C. L., & Gomez, H. L. (2014). PIK3CA mutations in Peruvian patients with HER2-amplified and triple negative non-metastatic breast cancers. Hematology/ Oncology and Stem Cell Therapy, 7(4), 142-148. https://doi.org/10.1016/j.hemonc.2014.09.007

@article{bbcaf34d9b234bf08896c7eb85d02af9,

title = "PIK3CA mutations in Peruvian patients with HER2-amplified and triple negative non-metastatic breast cancers",

abstract = "Purpose To determine the frequency of PIK3CA mutations in a Peruvian cohort with HER2-amplified and triple negative breast cancers (TNBC).Methods We analyzed two cohorts of 134 primary non-metastatic breast cancer patients from Peru. Cohorts consisted of 51 hormone receptors (+)/HER2-amplified breast tumor patients surgically resected as first treatment included in the ALTTO trial (ALTTO cohort) and 81 TNBC patients with residual disease after neoadjuvant treatment (neoadjuvant cohort). Genomic DNA was extracted from paraffin-embedded tumor samples. Samples from the ALTTO and neoadjuvant cohorts were taken at biopsies and from residual tumors, respectively. PIK3CA mutations were detected by sequencing DNA fragments obtained by PCR amplification of exons and their flanking introns. All of the detected PIK3CA mutations were confirmed in a second independent run of sample testing.Conclusions We found a similar frequency of PIK3CA mutations to that reported in other series. Although we did not include HR+/HER2 patients, those with HER2-amplified tumors were more likely to present PIK3CA mutations compared to patients with triple negative tumors.Results PIK3CA mutations were present in 21/134 cases (15.7%). Mutations in exon 9 and 20 were present in 10/134 (7.5%) and 11/134 (8.2%), respectively. No cases had mutations in both exons. Mutations in exon 9 consisted of E545A (seven cases), E545K (two cases) and E545Q (one case); while in exon 20, mutations consisted of H1047R (10 cases) and H1047L (one case). Compared to TNBC patients, HER2-amplified patients were more likely to have PIK3CA mutated (23% vs 9.6%; P = 0.034). There were no associations between mutational status of PIK3CA with estrogen receptor status (P = 0.731), progesterone receptor status (P = 0.921), age (P = 0.646), nodal status (P = 0.240) or histological grade (P = 1.00). No significant associations were found between PIK3CA mutational status and clinicopathological features.",

keywords = "Breast cancer, HER2, PIK3CA, Triple negative",

author = "Castaneda, {Carlos A.} and Marco Lopez-Ilasaca and Pinto, {Joseph A.} and Michelle Chirinos-Arias and Franco Doimi and Neciosup, {Silvia P.} and Rojas, {Katerin I.} and Tatiana Vidaurre and Balko, {Justin M.} and Arteaga, {Carlos L.} and Gomez, {Henry L.}",

note = "Publisher Copyright: {\textcopyright} 2014 King Faisal Specialist Hospital & Research Centre.",

year = "2014",

month = dec,

day = "1",

doi = "10.1016/j.hemonc.2014.09.007",

language = "Ingl{\'e}s",

volume = "7",

pages = "142--148",

journal = "Hematology/ Oncology and Stem Cell Therapy",

issn = "1658-3876",

publisher = "King Faisal Specialist Hospital and Research Centre",

number = "4",

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Castaneda, CA, Lopez-Ilasaca, M, Pinto, JA, Chirinos-Arias, M, Doimi, F, Neciosup, SP, Rojas, KI, Vidaurre, T, Balko, JM, Arteaga, CL & Gomez, HL 2014, 'PIK3CA mutations in Peruvian patients with HER2-amplified and triple negative non-metastatic breast cancers', Hematology/ Oncology and Stem Cell Therapy, vol. 7, n.º 4, pp. 142-148. https://doi.org/10.1016/j.hemonc.2014.09.007

TY - JOUR

T1 - PIK3CA mutations in Peruvian patients with HER2-amplified and triple negative non-metastatic breast cancers

AU - Castaneda, Carlos A.

AU - Lopez-Ilasaca, Marco

AU - Pinto, Joseph A.

AU - Chirinos-Arias, Michelle

AU - Doimi, Franco

AU - Neciosup, Silvia P.

AU - Rojas, Katerin I.

AU - Vidaurre, Tatiana

AU - Balko, Justin M.

AU - Arteaga, Carlos L.

AU - Gomez, Henry L.

PY - 2014/12/1

Y1 - 2014/12/1

N2 - Purpose To determine the frequency of PIK3CA mutations in a Peruvian cohort with HER2-amplified and triple negative breast cancers (TNBC).Methods We analyzed two cohorts of 134 primary non-metastatic breast cancer patients from Peru. Cohorts consisted of 51 hormone receptors (+)/HER2-amplified breast tumor patients surgically resected as first treatment included in the ALTTO trial (ALTTO cohort) and 81 TNBC patients with residual disease after neoadjuvant treatment (neoadjuvant cohort). Genomic DNA was extracted from paraffin-embedded tumor samples. Samples from the ALTTO and neoadjuvant cohorts were taken at biopsies and from residual tumors, respectively. PIK3CA mutations were detected by sequencing DNA fragments obtained by PCR amplification of exons and their flanking introns. All of the detected PIK3CA mutations were confirmed in a second independent run of sample testing.Conclusions We found a similar frequency of PIK3CA mutations to that reported in other series. Although we did not include HR+/HER2 patients, those with HER2-amplified tumors were more likely to present PIK3CA mutations compared to patients with triple negative tumors.Results PIK3CA mutations were present in 21/134 cases (15.7%). Mutations in exon 9 and 20 were present in 10/134 (7.5%) and 11/134 (8.2%), respectively. No cases had mutations in both exons. Mutations in exon 9 consisted of E545A (seven cases), E545K (two cases) and E545Q (one case); while in exon 20, mutations consisted of H1047R (10 cases) and H1047L (one case). Compared to TNBC patients, HER2-amplified patients were more likely to have PIK3CA mutated (23% vs 9.6%; P = 0.034). There were no associations between mutational status of PIK3CA with estrogen receptor status (P = 0.731), progesterone receptor status (P = 0.921), age (P = 0.646), nodal status (P = 0.240) or histological grade (P = 1.00). No significant associations were found between PIK3CA mutational status and clinicopathological features.

AB - Purpose To determine the frequency of PIK3CA mutations in a Peruvian cohort with HER2-amplified and triple negative breast cancers (TNBC).Methods We analyzed two cohorts of 134 primary non-metastatic breast cancer patients from Peru. Cohorts consisted of 51 hormone receptors (+)/HER2-amplified breast tumor patients surgically resected as first treatment included in the ALTTO trial (ALTTO cohort) and 81 TNBC patients with residual disease after neoadjuvant treatment (neoadjuvant cohort). Genomic DNA was extracted from paraffin-embedded tumor samples. Samples from the ALTTO and neoadjuvant cohorts were taken at biopsies and from residual tumors, respectively. PIK3CA mutations were detected by sequencing DNA fragments obtained by PCR amplification of exons and their flanking introns. All of the detected PIK3CA mutations were confirmed in a second independent run of sample testing.Conclusions We found a similar frequency of PIK3CA mutations to that reported in other series. Although we did not include HR+/HER2 patients, those with HER2-amplified tumors were more likely to present PIK3CA mutations compared to patients with triple negative tumors.Results PIK3CA mutations were present in 21/134 cases (15.7%). Mutations in exon 9 and 20 were present in 10/134 (7.5%) and 11/134 (8.2%), respectively. No cases had mutations in both exons. Mutations in exon 9 consisted of E545A (seven cases), E545K (two cases) and E545Q (one case); while in exon 20, mutations consisted of H1047R (10 cases) and H1047L (one case). Compared to TNBC patients, HER2-amplified patients were more likely to have PIK3CA mutated (23% vs 9.6%; P = 0.034). There were no associations between mutational status of PIK3CA with estrogen receptor status (P = 0.731), progesterone receptor status (P = 0.921), age (P = 0.646), nodal status (P = 0.240) or histological grade (P = 1.00). No significant associations were found between PIK3CA mutational status and clinicopathological features.

KW - Breast cancer

KW - HER2

KW - PIK3CA

KW - Triple negative

UR - http://www.scopus.com/inward/record.url?scp=84919875519&partnerID=8YFLogxK

U2 - 10.1016/j.hemonc.2014.09.007

DO - 10.1016/j.hemonc.2014.09.007

M3 - Artículo

AN - SCOPUS:84919875519

SN - 1658-3876

VL - 7

SP - 142

EP - 148

JO - Hematology/ Oncology and Stem Cell Therapy

JF - Hematology/ Oncology and Stem Cell Therapy

IS - 4

ER -

PIK3CA mutations in Peruvian patients with HER2-amplified and triple negative non-metastatic breast cancers

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