br Authors would like to thank
Authors would like to thank Dr. Rémi Safi for her technical support and Dr. Najla Fakhruddin for providing the paraffin blocks of breast carcinoma tissues. This work was supported by grants from Lebanese National Council for Scientific Research, and from the Medical Practice Plan and University Research Board grants at the American University of Beirut (MES).
Author contributions
Conceived and designed the experiments: MES. Performed the ex-
periments: LEH NJ JK. Analyzed the data: LEH NJ AS MES. Contributed
reagents/materials/analysis tools: KZ JK. The manuscript was written
by: LEH, critically reviewed by: AS JS and approved by MES.
Conflicts of interest
The authors declare no competing financial interests.
References
L.A. Lickley, E. Rawlinson, P. Sun, S.A. Narod, Triple-negative breast cancer: clin-ical features and patterns of recurrence, Clin. Cancer Res. 13 (2007) 4429–4434.
[2] B.G. Haffty, Q. Yang, M. Reiss, T. Kearney, S.A. Higgins, J. Weidhaas, L. Harris, W. Hait, D. Toppmeyer, Locoregional relapse and distant NPS-2143 in con-servatively managed triple negative early-stage breast cancer, J. Clin. Oncol. 24
[6] A. Ishihara, H. Tsuda, K. Kitagawa, M. Yoneda, T. Shiraishi, Morphological char-acteristics of basal-like subtype of breast carcinoma with special reference to cy-topathological features, Breast Cancer 16 (2009) 179–185.
[7] L. Fulford, D. Easton, J. Reis-Filho, A. Sofronis, C. Gillett, S. Lakhani, A. Hanby, Specific morphological features predictive for the basal phenotype in grade 3 in-vasive ductal carcinoma of breast, Histopathology 49 (2006) 22–34.
[8] H.-P. Gerber, T.H. Vu, A.M. Ryan, J. Kowalski, Z. Werb, N. Ferrara, VEGF couples hypertrophic cartilage remodeling, ossification and angiogenesis during
J. Daubriac, I. Chen, Anti-VEGF therapy induces ECM remodeling and mechanical barriers to therapy in colorectal cancer liver metastases, Sci. Transl. Med. 8 (2016) 360ra135.
[14] J. Waltenberger, VEGF Resistance as a Molecular Basis to Explain the Angiogenesis Paradox in Diabetes Mellitus, Portland Press Limited, 2009.
[15] J. Rius, M. Guma, C. Schachtrup, K. Akassoglou, A.S. Zinkernagel, V. Nizet,
J. Nijmeh, O. Hermine, A. Bazarbachi, Human T-cell lymphotropic virus type
1–transformed cells induce angiogenesis and 
establish functional gap junctions with endothelial cells, Blood 99 (2002) 3383–3389.
[21] A. Bazarbachi, R.A. Merhi, A. Gessain, R. Talhouk, H. El-Khoury, R. Nasr, O. Gout, R. Sulahian, F. Homaidan, O. Hermine, Human T-cell lymphotropic virus type I-infected cells extravasate through the endothelial barrier by a local angiogenesis-like mechanism, Cancer Res. 64 (2004) 2039–2046.
[22] Y. Kanno, W.R. Loewenstein, Low-resistance coupling between gland cells. Some observations on intercellular contact membranes and intercellular space, Nature 201 (1964) 194–195.
S.E. Shackney, Response to trastuzumab, erlotinib, and bevacizumab, alone and in combination, is correlated with the level of human epidermal growth factor re-ceptor-2 expression in human breast cancer cell lines, Mol. Cancer Ther. 6 (2007) 2664–2674.
B. Thompson, C. Spaulding, S. Macaroun, M.-L. Alegre, Targeting the NF-κB sig-naling pathway in Notch1-induced T-cell leukemia, Nat. Med. 13 (2007) 70–77.
[42] R.E. Brown, A. Law, Morphoproteomic demonstration of constitutive nuclear factor-kappaB activation in glioblastoma multiforme with genomic correlates and ther-apeutic implications, Ann. Clin. Lab. Sci. 36 (2006) 421–426.