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PIK3CA mutations linked to lower pCR rates in women with HER2-positive breast cancer

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No clinical role for this finding yet

Investigators from the German Breast Group have evaluated the association between the presence of PIK3CA mutations and response to anti-HER2 therapy by analyzing specimens collected from patients who participated in three previously conducted prospective neoadjuvant clinical trials. Their data indicate that the presence of PIK3CA mutations is associated with a poorer pathologic complete response (pCR) in patients who received trastuzumab, lapatinib, or a combination of the two. Although intriguing, the exact clinical application of these data requires a thoughtful discussion of their meaning.

Substantial attention has been paid to the development and testing of new therapeutic agents, but less rigor has been applied when identifying and validating tumor biomarkers. Recent efforts to generate the same sense of value for tumor biomarkers that we have for anticancer treatments have gained traction. It is important to understand that a tumor biomarker is an indication of cancer biology and behavior but that there may be one or more tests for that biomarker and they may not provide identical, or even similar, results. In this regard, a tumor biomarker test should not be incorporated into routine clinical care until it has cleared a number of hurdles, best articulated by the Evaluation of Genomic Applications in Practice and Prevention Working Group of the Centers for Disease Control and Prevention.

First, a tumor biomarker must be demonstrated to have analytic validity. In other words, the assay must accurately, reliably, and reproducibly measure what it is intended to measure. Second, the tumor biomarker test must have clinical (or biologic) validity, which implies that it separates one population into two or more groups with distinctly different outcomes. For a tumor biomarker test to be incorporated into standard of care, it also must be shown to have clinical utility. Establishment of clinical utility requires a high level of evidence from either prospective or prospective-retrospective studies demonstrating that application of the marker to direct therapy improves patient outcomes with sufficient magnitude to justify testing all eligible patients.

So, can we apply the intriguing data that were generated by Dr. Loibl and her associates to routine clinical care? Can mutations in PIK3CA be used to withhold anti-HER2 therapy in patients with HER2-positive breast cancer? Our answer is a resounding no, and the authors themselves do not suggest such a use of this assay. Indeed, there was no difference in disease-free survival or overall survival between the cohorts with PIK3CA wild-type versus mutant tumors, although follow-up was relatively short at only 3.5 years. Given the enormous disease-free survival and overall survival benefit of adjuvant trastuzumab, the data need to be much clearer about the lack of benefit of HER2-directed therapies before we would recommend against treatment with these lifesaving and relatively tolerable therapies.

Dr. N. Lynn Henry, Dr. Anne F. Schott, and Dr. Daniel F. Hayes are with the University of Michigan Comprehensive Cancer Center in Ann Arbor. These comments were extracted from an accompanying editorial published online J. Clin. Oncol. 2014 Sept. 8 [doi:10.1200/JCO.2014.57.6132]). Dr. Henry disclosed having received research funding from sanofi-aventis, BioMarin, and Celldex. Dr. Schott disclosed having received research funding from Dompé and Dr. Hayes disclosed having received research funding from Janssen. Dr. Hayes also disclosed a consulting or advisory role with Pfizer as well as stock ownership with Oncimmune and Inbiomotion.


 

FROM THE JOURNAL OF ONCOLOGY

References

Breast cancer patients with newly diagnosed human epidermal growth factor receptor 2–positive tumors with a PIK3CA mutation are less likely to achieve a pathologic complete response after neoadjuvant anthracycline-taxane–based chemotherapy with anti-HER2 treatment, results from a German study demonstrated.

"This effect remains, even if a dual anti-HER2 treatment is given and rates of pCR [pathologic complete response] are lowest in the HR-positive/HER2-positive tumors harboring the PIK3CA mutation," German Breast Group researchers led by Dr. Sibylle Loibl wrote in a study published online Sept. 8 in the Journal of Clinical Oncology. "The PIK3CA mutation data could be combined with downstream markers such as p4EBP1 using class prediction algorithms to improve characterization of the tumors and select appropriate tumors. Our data suggest that investigation of alternative therapies (such as a PI3K inhibitor) in PIK3CA-mutant HER2-positive breast cancers is warranted."

Although mutations of the PIK3CA gene are found in about 20% of all breast cancers, the frequency of such mutations is not equally distributed among the different biologic subtypes. Dr. Loibl and her associates set out to investigate the association between PIK3CA genotype and pCR rates in HER2-positive breast cancer treated with either dual or single anti-HER2 treatments in addition to neoadjuvant chemotherapy. They evaluated 504 tumor samples from participants in the GeparQuattro, GeparQuinto, and GeparSixto studies, in which all HER2-positive patients received either trastuzumab or lapatinib or the combination plus anthracycline-taxane chemotherapy (J. Clin. Oncol. 2014 Sept. 8 [Epub doi:10.1200/JCO.2014.55.7876]). PIK3CA mutations were evaluated in tumor material from formalin-fixed, paraffin-embedded tissue core biopsies taken before therapy with a tumor content of at least 20% determined by using classical Sanger sequencing of hot-spot mutations in exon 9 and exon 20.

Of the 504 patients, 291 had hormone receptor (HR)–positive tumors and 213 had HR-negative tumors. During a median follow-up period of 42 months, the researchers observed no statistically significant differences in disease-free survival or in overall survival between patients with or without a PIK3CA mutation (hazard ratios of 1.07 and 0.59, respectively). More than one in five of the patients (21.4%) harbored a PIK3CA mutation, and detection of a PIK3CA mutation was associated with a significantly lower pCR (19.4%, compared with 32.8% among those in the PIK3CA wild-type group [odds ratio, 0.49; P = .008]), Dr. Loibl, professor at the University of Frankfurt, Germany, and her associates reported.

Among the 291 HR-positive tumors, the pCR rate was 11.3% in patients with a PIK3CA mutation, compared with 27.5% in the PIK3CA wild-type group (OR, 0.34; P = .011). Among the 213 HR-negative tumors, the pCR rate was 30.4% in patients with a PIK3CA mutation, compared with 40.1% in those without the mutation (OR, 0.65; P = .223).

Multivariate analysis adjusted for age, tumor stage, nodal status, histologic type, tumor grade, study, and anti-HER2 treatment revealed that, in patients with a PIK3CA mutation, the pCR rates with lapatinib, trastuzumab, and the combination were 16%, 24.3%, and 17.4%, respectively (P = .654), while those rates in the wild-type group were with 18.2%, 33.8%, and 37.1% (P = .017).

"In this study, it seemed that HER2-positive patients with PIK3CA mutations derived long-term benefit from adjuvant trastuzumab, indicating sensitivity rather than resistance to anti-HER2 treatment, although numbers of patients were small," the researchers wrote.

"In the metastatic setting, data sets are small, conflicting, and without clear treatment effects. Indeed, the lower pCR rate in the HR-positive/HER2-positive PIK3CA mutant cohort could reflect lower chemosensitivity or resistance to anti-HER2 therapy. HR-positive/HER2-positive patients historically had a lower pCR rate with chemotherapy alone. In our data set, patients with PIK3CA mutations had similar pCR rates across all anti-HER2 treatment arms. In past studies, this pCR rate was as low as that of HER2-positive patients receiving chemotherapy without trastuzumab. However, because trastuzumab is now the standard of care, we cannot make any comments based on our data regarding the impact of PIK3CA genotype on patients who did not receive anti-HER2 therapy," they said.

The study was supported by a grant from the RESPONSIFY Consortium. Members of the research team disclosed numerous financial relationships with industry.

dbrunk@frontlinemedcom.com

On Twitter @dougbrunk

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