Genocea Presents Data at AACR Annual Meeting Further Highlighting Advantages of ATLAS Platform in Identification of Neoantige...
18 April 2018 - 11:01PM
- ATLAS data demonstrate in silico methods miss
most empirically confirmed neoantigens - - ATLAS able to identify
inhibitory neoantigens - - Mouse ATLAS melanoma model developed to
study mechanism of inhibitory antigens -
Genocea Biosciences, Inc. (NASDAQ:GNCA), a
biopharmaceutical company developing neoantigen cancer vaccines,
today announced highlights from its scientific presentations at the
2018 Annual Meeting of the American Association for Cancer Research
(AACR 2018), taking place April 14-18, 2018 in Chicago, IL.
Jessica Flechtner, Ph.D., Genocea’s chief scientific officer
commented on the AACR presentations: “We continue to generate data
that demonstrate the versatility of our ATLAS platform. As the
studies presented at AACR indicate, ATLAS is a differentiator for
Genocea – allowing us to do what in silico approaches cannot – to
both identify and characterize neoantigens for use in personalized
cancer vaccines. We believe that our ability to find stimulatory
and inhibitory antigens during the neoantigen selection process
combined with our capacity to explore mechanisms of inhibitory
antigens in a murine model, may enable us to help cure cancer by
pioneering next-generation cancer vaccines.”
Summary of AACR Poster #730, “Empirical neoantigen
identification using the ATLAS™ platform across thousands of
mutations and multiple tumor types highlights advantages over
algorithmic prediction methods”:
- ATLAS enables identification of biologically relevant CD4+ and
CD8+ T cell neoantigens in subjects in an unbiased manner, by using
subjects’ own antigen-presenting cells (APCs) and T cells rather
than predictive algorithms to identify and characterize T cell
responses to all candidate neoantigens.
- Neoantigen screening was performed on 23 individuals across
eight tumor types with mutational burden ranging from 9 to 319
unique mutations.
- Empiric identification of neoantigens derived from somatic
mutations from each patient's tumor independently of HLA type and
without predictions resulted in the following observations:
- ATLAS identified stimulatory neoantigens of both CD4+ and CD8+
T cells, which Genocea believes confirms the importance of
including antigens of relevance for both T cell subsets in
neoantigen vaccines;
- There is little overlap between CD4+ and CD8+ T cell
neoantigens; fewer than 2% of empirically confirmed neoantigens
were shared between T cell subsets;
- Prediction algorithms missed up to 69% of ATLAS-identified
neoantigens, with only 2% of CD8+ neoantigens and 24% of CD4+
neoantigens accurately predicted;
- The major histocompatibility complex (MHC) class I algorithm
appeared to better predict CD4+, not CD8+, neoantigens;
- ATLAS also identified inhibitory neoantigens of both CD4+ and
CD8+ T cells
- Inhibitory neoantigens outnumbered stimulatory neoantigens more
than three-fold in aggregate in the screened patients;
- Inhibitory antigens currently cannot be identified using in
silico approaches.
Summary of Poster #5718, “ex
vivo ATLASTM identification of neoantigens for
personalized cancer immunotherapy in mouse melanoma”:
- The B16F10 mouse melanoma model was utilized to characterize
neoantigens. More than 1,600 tumor-specific mutations (possible
neoantigens) were interrogated using the ATLAS technology and CD8+
T cells from tumor-bearing C57BL/6 mice.
- Similar to human neoantigen screens, mouse ATLAS (mATLAS)
identified both stimulatory and inhibitory neoantigens:
- 99% of mutations identified using whole exome sequencing were
screened;
- 68 stimulatory (4% of total mutations) and 57 inhibitory (3% of
total mutations) neoantigens were identified.
- NetMHCPan, a MHC-binding prediction algorithm, failed to
identify the majority of mATLAS-identified neoantigens:
- Only 2% of B16F10 neoantigens predicted by algorithms were
empirically confirmed to be stimulatory antigens;
- 91% of stimulatory neoantigens empirically identified with
mATLAS were not predicted;
- 6% of algorithm-predicted neoantigens were inhibitory.
- These data demonstrate that inhibitory antigens can be
identified in mouse models, allowing for future research into the
mechanism of ATLAS-identified inhibitory responses and their
relationship to stimulatory neoantigens in mediating tumor
control.
About Genocea Biosciences, Inc.Genocea's
mission is to help conquer cancer by designing and delivering
targeted vaccines and immunotherapies. While traditional
immunotherapy discovery methods have largely used predictive
methods to propose T cell targets, or antigens, Genocea has
developed ATLAS™, its proprietary technology platform, to identify
clinically relevant antigens of T cells based on actual human
immune responses. Genocea is using ATLAS in immuno-oncology
applications to develop neoantigen cancer vaccines, while also
exploring partnership opportunities for general cancer vaccines and
a vaccine targeting cancers caused by Epstein-Barr Virus. Genocea
expects to begin clinical development of its first neoantigen
cancer vaccine, GEN-009, in 2018. For more information, please
visit www.genocea.com.
Forward-Looking Statements This press release
includes forward-looking statements, including statements relating
to the expected clinical development of GEN-009, within the meaning
of the Private Securities Litigation Reform Act. Such
forward-looking statements are subject to risks and uncertainties
that could cause actual results to differ materially from those
expressed or implied in such statements. Genocea cautions that
these forward-looking statements are subject to numerous
assumptions, risks and uncertainties, which change over time.
Applicable risks and uncertainties include those identified under
the heading "Risk Factors" included in Genocea's Annual Report on
Form 10-K for the year ended December 31, 2017 and any subsequent
SEC filings. These forward-looking statements speak only as of the
date of this press release and Genocea assumes no duty to update
forward-looking statements, except as may be required by law.
Contact: Jennifer LaVin
207-360-0473jennifer.lavin@genocea.com
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