Immunosign® CR Immune gene expression signatures

Tumor sensitivity to immune effectors

Investigate immune response within the TME

IMMUNOSIGN®CR consists in two different immune genes expression signatures: IMMUNOSIGN®CR 15 and IMMUNOSIGN®CR 21.

IMMUNOSIGN®CR enables the measurement of the naturally occurring immune activity in and around the tumor.

This assay has been designed to assess particularly the adaptive immunity and the immune suppression within the tumor microenvironment (TME).

In clinical trials, IMMUNOSIGN®CR can provide prognostic and predictive information for immunotherapies development and guide for combination strategies.

Prognostic and predictive proof-of-concept of IMMUNOSIGN®CR has been obtained on retrospective cohorts (10 tumor types) (Galon et al. Immunity 2013, and personal communication, Spicer J.F. et al., 2017, Marabelle A. et al., 2017).

Scientific data

Posters presented by our partners at ASCO, AACR, ESMO and SITC congresses:

Characterization of anti‑CD19 chimeric antigen receptor (CAR) T cell‑mediated tumor microenvironment immune gene profile in a multicenter trial (ZUMA‑1) with axica btagene ciloleucel (axi‑cel, KTE‑C19) (J.Galon et al)

  • Evaluation of Key Immune Pathways Within the Tumor Microenvironment
  • Characterizations of top Immunosign Genes Upregulated in Tumor Tissue Early Post–axi‑cel
  • Characterization of an immune gene signature in the tumor microenvironment early after
    Anti CD19 CAR T cell treatment
  • Co‑upregulation of immune checkpoints within the tumor microenvironment resulted from CAR T Cell treatment
  • Interplay between multiple complementary immune programs deployed by CAR T cells and the innate immunity (IL‑15) within the tumor environment to induce tumor responses

ESMO 2019: Phase Ib/II trial of TG4001 by Transgene.

In this study, HalioDx Immunoscore®, Immunosign® and others clinical research service have been performed to assess Immune contexture of patients.
The treatment is associated with changes in tumor microenvironment that are likely to change the course of the pathology by shifting tumor from a cold state to a hotter immune status even in heavily pretreated patients. This may be particularly useful in patient with “immune-excluded” tumor phenotype as shown on the individual study case.




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