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Poster display session

3638 - Holistic therapeutic strategy of TNBC necessitates in depth molecular classification: a prospective study

Date

11 Sep 2017

Session

Poster display session

Presenters

Rittwika Bhattacharyya

Citation

Annals of Oncology (2017) 28 (suppl_5): v74-v108. 10.1093/annonc/mdx365

Authors

R. Bhattacharyya1, K. Banerjee2, M. Sen1, A. Mukhopadhyay1

Author affiliations

  • 1 Molecular Biology, Netaji Subhas Chandra Bose Cancer Research Institute, 700016 - Kolkata/IN
  • 2 Molecular Biology, Saroj Gupta Cancer Centre and Research Institute, 700063 - Kolkata/IN
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Resources

Abstract 3638

Background

Triple negative breast cancer (TNBC), the most heterogeneous and aggressive breast cancer has always remained a global burden. To understand the molecular pathogenesis, we stratified the seven subgroups of TNBC propounded by Lehmann et al (2011) as: [1] TNBC with alterations of the DNA damage repair and cell cycle checkpoint pathways (Basal Like 1 & 2 (BL1, BL2)), [2] with upregulation of cell signalling and cell motility pathways (mesenchymal (M), mesemchymal stem like (MSL)), [3] with upregulated cell survival pathways (BL2, M, MSL) [4] With upregulated angiogenesis pathways (BL2, MSL), [5] With upregulation of pathways associated with T cell signalling, [6] With upregulated Androgen receptor signalling pathways. Our objective was to prioritize the basic molecular heterogeneity of TNBC in redefining our choice of drugs.

Methods

Lehmann’s TNBC subgroups showed deregulation of diverse molecular pathways necessitating targeted therapeutics. We conducted a Meta-Analysis on12 randomized reported trial cases (n = 1170), solely under the following classes of drug regimens: [1] DNA destabilizers, [2] PARP inhibitors, [3] Microtubule stabilizers, [4] Angiogenesis inhibitors, [5] Antimetabolite, [6] T cell targeted therapy; as single or combinational therapies. Radiotherapy recipients were excluded.

Results

Best therapeutic efficacies of DNA destabilizers with angiogenesis inhibitors in combination than monotherapy with either (OR: 5.011-7.286; p value< 0.001) indicated a significant prevalence of basal like TNBCs in populations. Statistical significance with antimetabolites as combination therapy (OR: 2.343; p value: 0.018) and not with microtubule stabilizer (OR: 0.377) were remarkable, indicating probability of less predominance of M or MSL type TNBC in a population. PARP inhibitors or T cell targeted therapies were also found promising (OR: 1.120, 1.040 respectively), warranting their targeted usage for BRCA1 deficient and IM type TNBCs respectively.

Conclusions

For TNBC treatment, personalized medicine and not a generalized treatment strategy should be considered.

Clinical trial identification

NA

Legal entity responsible for the study

Netaji Subhas Chandra Bose Cancer Research Institute

Funding

None

Disclosure

All authors have declared no conflicts of interest.

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