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Establishing the standard Mexican Female Breast parameters from measurements obtained with this study will aid in obtaining a more predictable and aesthetically pleasing result in our population. Patients subject to breast augmentation, reduction, mastopexy and reconstructive breast surgery, will benefit from this data.

Kuleshov, M. V. et al. Enrichr: a comprehensive gene set enrichment analysis web server 2016 update. Nucleic Acids Res. 44, W90–W97 (2016). Rooney, M. S., Shukla, S. A., Wu, C. J., Getz, G. & Hacohen, N. Molecular and genetic properties of tumors associated with local immune cytolytic activity. Cell 160, 48–61 (2015).To compare associations of the oncogenic alterations between datasets and intrinsic subtypes a Fisher exact test was performed, using the fisher.multcomp function on R, and p-values were controlled for false-discovery rate with the Benjamini & Hochberg method and a multivariate Cox proportional hazards analysis was computed with SAS University Edition Statistical. Two-tailed Kruskal–Wallis or Wilcoxon test were applied to define statistical differences between the conditions evaluated on continuous variables. Statistical significance was set as p = < 0.05. Reporting summary Kim, S. B. et al. Ipatasertib plus paclitaxel versus placebo plus paclitaxel as first-line therapy for metastatic triple-negative breast cancer (LOTUS): a multicentre, randomised, double-blind, placebo-controlled, phase 2 trial. Lancet Oncol. 18, 1360–1372 (2017). Gonzalez-Perez, A. & Lopez-Bigas, N. Functional impact bias reveals cancer drivers. Nucleic Acids Res. 40, e169 (2012).

Ciriello, G., Cerami, E., Sander, C. & Schultz, N. Mutual exclusivity analysis identifies oncogenic network modules. Genome Res. 22, 398–406 (2012).Other potentially novel mutated genes in the HM tumors exhibiting significant mutation prevalence (≥3.0%), non-previously reported in other datasets (Supplementary Data 5), includes MRPL37 and SLC16A8 ( q-value = 2.72E-02 and 1.36E-02, respectively). Although, these novel mutations are predicted to be passenger alterations, most of them have a high deleterious oncogenic capacity and a functional consequence of missense or nonsense change (Supplementary Fig. 7e). Driver and clinically actionable genomic alterations in HM population Parker, J. S. et al. Supervised risk predictor of breast cancer based on intrinsic subtypes. J. Clin. Oncol. 27, 1160–1167 (2009).