BACKGROUND

Breast cancer remains a leading malignancy among women globally. In addition to established factors like histopathology, hormone receptor status, and lymph node involvement, tools such as immunohistochemistry and molecular tests have been developed to assess tumor behavior and recurrence risk.

OBJECTIVE

This study investigates the concordance between the Ki-67 proliferation index measured by immunohistochemistry and the recurrence risk scores obtained from molecular genomic testing in patients with invasive breast cancer.

METHODOLOGY

This cross-sectional study included patients with invasive breast carcinoma at St. Luke’s Medical Center from 2019 to 2024, who underwent biopsy or mastectomy, with hormone status and Ki-67 index assessed by immunohistochemistry. All patients also had molecular genomic testing using either MammaPrint or OncotypeDX. Concordance between Ki-67 and the genomic recurrence risk score was evaluated using Kappa statistics, and results were further analyzed according to clinical risk and hormone receptor status.

RESULTS

Fifty-eight (58) patients met the study criteria. Most had grade 2, hormone receptor-positive, HER2-negative, and node-negative tumors, with high clinical risk based on Adjuvant! Online criteria (adapted from the MINDACT trial). The agreement between categorical Ki-67 and molecular recurrence risk was only fair: 66.7% for MammaPrint (kappa=0.35) and 60% for OncotypeDX (kappa = 0.29) using a 30% Ki-67 cutoff.

CONCLUSION

There is a fair agreement between Ki-67 and the molecular genomic tests. These findings are consistent with prior studies reporting weak to moderate association. Despite the limited sample size, Ki-67 remains a practical and accessible risk stratification tool, particularly where genomic assays are unavailable. The study supports integrating Ki-67 with clinicopathologic and genomic data to guide therapy, reflecting current best-practice recommendations.

Human ; Female ; Breast Neoplasms

Introduction: With advancements in the understanding of lung cancer biology, targeted therapy has become the rule rather than the exception. Patients with ALK rearrangements are amenable to therapy with Alectinib and other ALK inhibitors, which has been associated with better patient outcomes. While ALK rearrangement should be routinely tested in non-squamous non-small cell lung cancer (NSCLC), the cost and availability of this test is a prohibitive factor, particularly in the Philippine setting. Objectives: This study aimed (1) to determine the prevalence of ALK-rearranged NSCLC among adult Filipino lung cancer patients in St. Luke’s Medical Center (SLMC) from 2016 to 2018 and (2) to determine the clinico-pathologic features of adult Filipinos with ALK-rearranged NSCLC. Methodology: This is a retrospective cross-sectional descriptive study wherein the prevalence of ALK-rearranged NSCLC, detected using fluorescence in-situ hybridization (FISH) or immunohistochemistry (IHC), was determined. Clinical data of patients for whom ALK testing was performed were collected. Hematoxylin and Eosin (H&E) slides were retrieved and reviewed for the presence of certain morphologic features. Patients whose H&E slides cannot be retrieved were excluded from the study. Results: ALK rearrangement was seen in 7.8% (8/103) of tumors submitted for ALK testing. Patients with ALK-rearranged tumors were generally young, light smokers, and presented with advanced clinical stage. Clear cell features and solid pattern were noted in one case and three cases, respectively. However, due to small sample size, further statistical analysis could not be performed to analyze the association of these features with the presence of ALK rearrangement. Conclusion Despite a small sample size, the prevalence and clinical profile of ALK-rearranged NSCLC in our institution are congruent with those previously described in Western populations. The association of clinical profile and morphologic features with the presence of ALK rearrangement can be further explored in future studies.
Lung Neoplasms ; Anaplastic Lymphoma Kinase