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Mini Oral session

98O - The immunomodulatory (IM) signature enhances prediction of pathologic complete response (pCR) to neoadjuvant therapy (NAT) in triple negative breast cancers (TNBC) with moderate stromal tumour infiltrating lymphocytes (sTIL)

Date

23 May 2020

Session

Mini Oral session

Presenters

Nour Abuhadra

Citation

Annals of Oncology (2020) 31 (suppl_2): S48-S53. 10.1016/annonc/annonc119

Authors

N. Abuhadra1, R. Sun2, J.K. Litton3, G. Rauch4, A.M. Thompson5, B. Lim1, B. Adrada4, E. Mittendorf6, S. Damodaran7, R. Pitpitan4, B. Arun8, J. White1, E. Ravenberg1, L. Santiago4, A. Sahin9, R. Murthy10, N.T. Ueno11, N. Ibrahim1, S. Moulder3, L. Huo9

Author affiliations

  • 1 Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, 77030 - Houston/US
  • 2 Department Of Biostatistics, MD Anderson Cancer Center, 77030 - Houston/US
  • 3 Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, 77030-4095 - Houston/US
  • 4 Department Of Diagnostic Radiology, Division Of Diagnostic Imaging, The University of Texas MD Anderson Cancer Center, 77030-4095 - Houston/US
  • 5 Breast Surgical Oncology, Baylor College of Medicine, 77030 - Houston/US
  • 6 Surgery, Brigham and Women's Hospital, 2115 - Boston/US
  • 7 Breast Medical Oncology, The M. D. Anderson Cancer Center, 77030 - Houston/US
  • 8 Breast Medical Oncology And Clinical Cancer Genetics, The M. D. Anderson Cancer Center, 77030 - Houston/US
  • 9 Department Of Pathology, The University of Texas MD Anderson Cancer Center, 77030 - Houston/US
  • 10 Breast Medical Oncology, MD Anderson Cancer Center, 77030 - Houston/US
  • 11 Department Of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, 77030 - Houston/US
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Resources

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Abstract 98O

Background

In TNBC, the IM signature is highly enriched in immune cell markers and signaling which likely represents gene expression from both the tumor cells and infiltrating lymphocytes. High sTIL is independently associated with improved pCR rates in TNBC. The association between the IM subtype and sTIL in predicting pCR is not known.

Methods

Pretreatment core biopsies from 181 patients with early-stage TNBC enrolled on the ARTEMIS trial (NCT02276443) were evaluated for sTIL by H&E and Vanderbilt subtype using Affymetrix arrays and TNBCtype. sTIL was graded as low (<10%), moderate (10-30%) and high (>30%) using cut-points previously established to correlate with pCR. We calculated a point estimate and 95% confidence interval for the probability that a subject with given IM and TIL status will achieve pCR.

Results

The IM subtype was identified in fewer TNBCs with low or moderate sTIL (4 and 27%, respectively) than in those with high sTIL (62%, p<0.05). Independently, IM subtype and high sTIL subgroups achieved pCR at similar rates (62% and 76% respectively). We observed the largest difference in pCR rates between IM and non-IM subtype patients in the Moderate sTIL group. (58% vs 33%, p=0.051). Table: 98O

sTIL and pCR rates according to IM status

IM
sTIL Group N # pCR %pCR CI
Low 3 1 33 (0.01-0.91)
Moderate 24 14 58 (0.37-0.78)
High 13 10 77 (0.46-0.95)
Total 40 25 62
Other Subtypes
sTIL Group N # pCR %pCR CI
Low 67 21 31 (0.21-0.44)
Moderate 66 22 33 (0.22-0.46)
High 8 6 75 (0.35-0.97)
Total 141 49 34

Conclusions

High TIL and IM subtype are associated with similar rates of pCR and the addition of the IM signature to sTIL high or sTIL low TNBCs did not impact prediction of pCR. In patients with moderate TIL, the IM subtype was associated with higher rates of pCR (58%) as compared to other subtypes (33%). Larger numbers of patients are needed to confirm the predictive value of the IM signature in TIL moderate TNBC.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

MD Anderson Moon Shots Program, CPRIT Multi-Investigator Research Award (MIRA).

Disclosure

B. Lim: Research grant/Funding (institution): Pfizer; Research grant/Funding (institution): Amgen. B. Arun: Research grant/Funding (institution): AbbVie; Research grant/Funding (institution): AstraZeneca; Research grant/Funding (institution): Invitae. S. Moulder: Research grant/Funding (institution): Pfizer; Research grant/Funding (institution): Genentech; Research grant/Funding (institution): Novartis; Research grant/Funding (institution): Seattle Genetics; Research grant/Funding (institution): EMD Serono; Research grant/Funding (institution): Bayer; Research grant/Funding (institution): AstraZeneca. All other authors have declared no conflicts of interest.

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