DetermaIO™ Test for Immunotherapy Response in Triple

DetermaIO™ Test for Immunotherapy Response in Triple-Negative Breast Cancer

KOL Call hosted by Oncocyte09/28/2021

Forward Looking Statement

Any statements that are not historical fact (including, but not limited to statements that contain words such as “will,” “believes,”“plans,” “anticipates,” “expects,” “estimates,” “may,” and similar expressions) are forward-looking statements. These statementsinclude those pertaining to the commercial launch of DetermaRx, development and clinical use of DetermaIO and planned newdiagnostic tests, clinical trials and studies, commercialization plans, future financial and/or operating results, and futureopportunities for Oncocyte, along with other statements about the future expectations, beliefs, goals, plans, or prospectsexpressed by management. Forward-looking statements involve risks and uncertainties, including, without limitation, the potentialimpact of COVID-19 on our financial and operational results, risks inherent in the development and/or commercialization ofdiagnostic tests or products, uncertainty in the results of clinical trials or regulatory approvals, potential interruptions to our supplychain, the need and ability to obtain future capital, maintenance of intellectual property rights, and the need to obtain third partyreimbursement for patients’ use of any diagnostic tests we commercialize, and risks inherent in acquisitions such as failure torealize anticipated benefits, unexpected expenditures or assumed liabilities, unanticipated difficulties in conforming businesspractices including accounting policies, procedures and internal controls, greater than estimated allocations of resources todevelop and commercialize technologies, or failure to maintain any laboratory accreditation or certification. Actual results maydiffer materially from the results anticipated in these forward-looking statements and accordingly such statements should beevaluated together with the many uncertainties that affect the business of Oncocyte, particularly those mentioned in the “RiskFactors” and other cautionary statements found in Oncocyte’s Securities and Exchange Commission filings, which are availablefrom the SEC’s website. You are cautioned not to place undue reliance on forward-looking statements, which speak only as of thedate on which they were made. Oncocyte undertakes no obligation to update such statements to reflect events that occur orcircumstances that exist after the date on which they were made, except as required by law.

2

Mission Statement

3

Oncocyte is a molecular diagnostics company whose mission is to provide actionable answers at critical decision

points across the cancer care continuum, with the goal of improving patient

outcomes by accelerating and optimizing diagnosis and treatment.

4

Oncocyte’s Determa Platform StrategyDelivers Critical Information Throughout the Patient Journey Improving Outcomes and Reducing Costs

Treatment Stratification

Treatment Selection

Therapy Monitoring

Diagnosis of Cancer

Should I give adjuvant chemo?

Should I give immunotherapy?

Is the therapy working?

Treatment Decision

Is the cancercoming back?

Targeted Therapy Selection

Should I give targeted therapy?

Screening

Does patient have cancer?

Patient Monitoring

Available for Research Use Only Clinical Launch 2H21Tx

Tx

TxMRDFor Research Use Only in 2H21 In DevelopmentClinical Launch 2H21Available for Clinical Use

Recurrence Detection

Differentiated Tests To Address Unmet Needs Across All Stages Of Cancer.

Intro to DetermaIO

Clinical validation data presented in multiple tumor types to date

6

Data Summary Recap

REFERENCES1. Nielsen et al. Heliyon2. Ranganath et al. SITC 2019 Poster3. Bianchini et al. ESMO 2021 Podium Presentation4. Seitz et al. AACR 2021 Podium Presentation5. Seitz et al. ASCO 2021 Poster

Non small cell lung cancer (NSCLC)Multiple cohorts (100+ patients) showing improved response rates to ICI among DetermaIO+ patients and better predictive ability than PD-L1 and TMB 1,2

Triple Negative Breast Cancer (TNBC)Randomized clinical trial (241 patients) treated with standard chemo +/-atezolizumab in neoadjuvant setting. Study showed DetermaIO was predictive of response to ICI in Atezo arm only.3

Metastatic Urothelial CancerAnalysis of IMvigor210 study (348 patients) showed that IO+ patients had significantly better median OS, 2-yr OS, and ORR than IO-. DetermaIO was independent of all other biomarkers studied (incl. PD-L1 and TMB) 4

Renal Cell CarcinomaInitial data in 43 patients showed that IO+ patients had significantly better 1yr PFS and extended median PFS as compared to IO- 5

Validated in:900+ Patients

Across 4Tumor Types

Against all 4Approved Immune

Checkpoint Inhibitors

Shown to be predictive of ICI response, not

chemotherapy response

Determine Sensitivity to IO Therapies

7

Test Results Stratification

RNA Expression via qPCR

Proprietary Algorithm

Patients likely to respond to current Immune Checkpoint Inhibitor therapies

Patients unlikely to respond to ICIs and should be considered for other treatment opportunities

IO+IO-• Real-time PCR test on FFPE

biopsy or resection specimen• Measures 27 genes• Pan-cancer application

Shown to be a successful predictor of response in all indications tested to date

Based on an algorithm and threshold that have been

locked down & unchanged among all studies performed

Measures both tumor gene expression and the immunemicroenvironment (TIME)

DetermaIO has its origins in a refined molecular classification of

Triple Negative Breast Cancer (TNBC)

8

Basal-Like 1

Basal-Like 2

Mesenchymal

Luminal AR

Immunomodulatory

MesenchymalStem-Like

BL1

BL2

M

MSL

LAR

IM

-Lehmann BD Identification of human triple-negative breast cancer subtypes and preclinical models for selection of targeted therapies. J Clin Invest. 2011-Ring BZ Generation of an algorithm based on minimal gene sets to clinically subtype triple negative breast cancer patients. BMC Cancer. 2016-Lehmann BD Refinement of Triple-Negative Breast Cancer Molecular Subtypes: Implications for Neoadjuvant Chemotherapy Selection. PLoS One. 2016

2188Genes

Tumor-ImmuneMicro-Environment Signatures

TNBC Tumor Subtypes

BL1 BL2 LAR

M

MSLIM

2011: Lehmann TNBC Classification SystemSix Subtypes of TNBC tumors;1800+ Literature References to date

2016: Lehmann & Ring RefinementsDistinction between native TNBCtumor subtypes and TME components

2018: Stand-alone IO TME SignatureMeasures components of tumor and immune micro-environment to determine sensitivity to IO therapies

101Genes

27Genes

NON-CONFIDENTIAL

Physiology of a tumor in an immune environment

9

Tumor-Immune

homeostasis

Immune Attack

PD-L1 Expression

15-40%

Anti-PD-(L)/PD1 Immunotherapy

60-85%

Tumor selection / Secondary Escape

Immune system keeps tumorsin check

Cancer breaks through immune surveillance

Immune Surveillancere-established

Oncogene mutation and

neoantigen generation

CheckpointTx resistant

Immune Resistant

CheckpointTx sensitiveHOT

Cancer breaks throughImmune surveillance

Immune Fortification

CAF - COLD

Immune Desert

EMT - COLD

Immune Suppressionand Tumor Growth

Primary Response

Immune Attack

Immune Cloaked

Targetable by 2nd Generation Agents

(e.g. Immune stimulants, IL-12, VEGF, TGF-β)

+/- Checkpoint Inhibitors

Advanced NSCLC Clinical Cohort

10

• DetermaIO+ patients were significantly associated with improved PFS

• DetermaIO outperformed PD-L1 and TMB (and was significantly independent of either test)

• Also independent of pembrolizumab vs nivolumab (~1:1), adenocarcinoma vs squamous cell, primary site biopsy vs metastatic Presented at SITC 2019

Submitted for Peer-Reviewed Publication

n = 59 p = 0.60

n = 36 p = 0.50

n = 67 p < 0.001

In Collaboration with the West Cancer Center

Metastatic Urothelial Carcinoma

11

• DetermaIO+ was significantly associated with response to Atezo in Pt progression arm

• DetermaIO was significant in multivariate analysis with PD-L1 and TMB

• DetermaIO was independent of all other biomarkers and molecular signatures in the study

Podium Presentation at AACR 2021Preparing manuscript for submission

IMvigor210 Clinical Trial

N = 348, HR = 0.61295%CI (0.466, 0.803) p<0.001

Applying DetermaIO to Triple Negative Breast CancerMD Anderson / Yale Collaboration

12

Study Design (Phase I/II trial - NCT02489448):

• 55 patients with stage I-III primary TNBC pCR: n=25 (45%); No pCR: n=30 (55%)

• Treated with neoadjuvant immunotherapy + chemotherapy (durvalumab with weekly paclitaxel followed by dose-dense anthracycline/cyclophosphamide)

Results:

• DetermaIO-positive patients are 4x more likely to respond than DetermaIO-negative patients

• DetermaIO has 23.3% better predictive value than PD-L1

Odds Ratio 95% CI p-Value

4.125 1.36 – 13.47 < 0.015

PD-L1 Expression 2.63 0.82 – 9.21 0.11

Patients who had a lack of complete response had an average

DetermaIO score of -0.18

Patients who had a complete response had an average DetermaIO score of 0.24

Presented at ASCO 2020Currently in Press

TNBC

13

Today’s KOL Speakers

Priyanka Sharma, MDProfessor of Medicine

University of Kansas Medical Center

Giampaolo Bianchini, MDHead, Breast Cancer Group

San Raffaele Hospital, Milano, Italy

Unmet need for predicting immunotherapy response in

early stage TNBCPriyanka Sharma, MD

Professor of Medicine University of Kansas Medical Center

Immune Checkpoint Inhibitor (ICI) Therapy

James Allison, PhD Tasuku Honjo, MD, PhD

Nobel Prize in Physiology or Medicine, 2018

Immunotherapy in TNBC

Rationale for immunotherapy in TNBC

Early stage TNBCCurrent chemotherapy landscapeEmerging role of immune check point inhibitors

Future directionsSelection criterion BiomarkersPersonalized de-escalation and escalation

Rationale for Immunotherapy in TNBC• High TILs in TNBC: evidence of anti-tumor immune

response. • TIL-enrichment associated with better outcomes/pCR

Cold Hot

ER+ HER-2+ TNBCHigh TILsCD8+T cells/mRNAImmune signature

Luen et al, Breast 2016, Stanton et al, Jama Onc 2016, Nanda et al, JCO 2016, Adams et al Ann Oncol 2019, Emens et al, JAMA Onc 2019, Gatti-Mays et al, Nature Breast Cancer 2019, Loi et al, JCO 2019, Adams et al, JAMA Onc 2019, Denkert et al, Lancet Oncol 2018, Page et al, Nature Breast Cancer 2019, Galluzzi et al, Nat Rev Clin Oncol 2020, Chen Immunity 2013

Rationale for Immunotherapy in TNBC• High TILs in TNBC: evidence of anti-tumor immune

response. • TIL-enrichment associated with better outcomes/pCR

• PD-L1 expressed mainly in infiltrating immune cells in BC; blocking PD-1/PD-L1 can augment T-cell response

Cold Hot

ER+ HER-2+ TNBCHigh TILsCD8+T cells/mRNAImmune signature

Luen et al, Breast 2016, Stanton et al, Jama Onc 2016, Nanda et al, JCO 2016, Adams et al Ann Oncol 2019, Emens et al, JAMA Onc 2019, Gatti-Mays et al, Nature Breast Cancer 2019, Loi et al, JCO 2019, Adams et al, JAMA Onc 2019, Denkert et al, Lancet Oncol 2018, Page et al, Nature Breast Cancer 2019, Galluzzi et al, Nat Rev Clin Oncol 2020, Chen Immunity 2013

Rationale for Immunotherapy in TNBC• High TILs in TNBC: evidence of anti-tumor immune

response. • TIL-enrichment associated with better outcomes/pCR

• PD-L1 expressed mainly in infiltrating immune cells in BC; blocking PD-1/PD-L1 can augment T-cell response

• Chemotherapy SOC in TNBC and can have several immunogenic effects

Cold Hot

ER+ HER-2+ TNBCHigh TILsCD8+T cells/mRNAImmune signature

Luen et al, Breast 2016, Stanton et al, Jama Onc 2016, Nanda et al, JCO 2016, Adams et al Ann Oncol 2019, Emens et al, JAMA Onc 2019, Gatti-Mays et al, Nature Breast Cancer 2019, Loi et al, JCO 2019, Adams et al, JAMA Onc 2019, Denkert et al, Lancet Oncol 2018, Page et al, Nature Breast Cancer 2019, Galluzzi et al, Nat Rev Clin Oncol 2020, Chen Immunity 2013

Rationale for Immunotherapy in TNBC• High TILs in TNBC: evidence of anti-tumor immune

response. • TIL-enrichment associated with better outcomes/pCR

• PD-L1 expressed mainly in infiltrating immune cells in BC; blocking PD-1/PD-L1 can augment T-cell response

• Chemotherapy SOC in TNBC and can have several immunogenic effects

• Combination with chemotherapy synergistic by targeting different steps in the cancer immunity cycle

Cold Hot

ER+ HER-2+ TNBCHigh TILsCD8+T cells/mRNAImmune signature

Luen et al, Breast 2016, Stanton et al, Jama Onc 2016, Nanda et al, JCO 2016, Adams et al Ann Oncol 2019, Emens et al, JAMA Onc 2019, Gatti-Mays et al, Nature Breast Cancer 2019, Loi et al, JCO 2019, Adams et al, JAMA Onc 2019, Denkert et al, Lancet Oncol 2018, Page et al, Nature Breast Cancer 2019, Galluzzi et al, Nat Rev Clin Oncol 2020, Chen Immunity 2013

Neoadjuvant chemotherapy landscape for TNBC

EBCTCG meta-analysis: aggregate benefit for anthracycline and taxane-based regimens over CMF-based regimens

EBCTCG Lancet Oncology 2012

Addition of Taxane to Anthracycline 16% reduction in risk of recurrence

(absolute gain 4.6%) 14% reduction in risk of breast

cancer mortality (absolute gain 2.8%)

Anthracycline regimens compared to no chemotherapy 27% reduction in risk of recurrence

(absolute gain 9%) 21% reduction in risk of breast

cancer mortality (absolute gain 6.5%)

10-year risk of death from breast cancer can be reduced by about a third. Benefit independent of age, grade, ER status and stage

Priyanka Sharma, MD

Platinum agents

Neoadjuvant trials incorporating Platinum in TNBC

Study Design Chemotherapy Regimen N

pCR (%)

Control Platinum

pCR

deltaAnthracycline containing regimens

GeparSixto Randomized Phase IIWeekly Paclitaxel 80 mg/m2 + NPLD 20 mg/m2 weekly + bev 15 mg/kg q 3 wks ± carboplatin AUC 1.5-2 weekly x 18 wks

315 37% 53% 16%

Alliance/CALGB 40603

Randomized Phase II (2x2 factorial design)

Weekly paclitaxel 80 mg/m2 x 12 ± carboplatin AUC 6 q 3 wks x 4 → AC q 2 weeks x 4 ± bev 10 mg/kg q 2 wks x 9 cycles

433 41% 54% 13%

BrighTNessRandomized Phase III (3-arm)

Weekly paclitaxel ± carboplatin AUC 6 ± veliparib 50 mg x 12 wks, followed by AC q 2-3 wks x 4 cycles

634 31% 57% (carbo)

53% (carbo + vel)26%

ISPY-2 Randomized Phase IIWeekly paclitaxel 80 mg/m2 x 12 ± carboplatin AUC 6 q 3 wks x 4 and veliparib 50 mg BID PO → AC q 2 wks x 4 cycles

6026% (est)

51% (est) -

NeoSTOP Randomized phase II Weekly paclitaxel 80 mg/m2 x 12 + carboplatin AUC 6 q 3 wks x 4 → AC q 2 weeks x 4 (ARM A) vs Carboplatin AUC 6 + docetaxel 75 mg/m2 q 3 wks x 6 cycles (ARM B)

100 —54% (Arm A)

52% (Arm B)-

Anthracycline-sparing regimens

WSG-ADAPT Randomized Phase IIWeekly nab-paclitaxel 125mg/m2 + carboplatin AUC 2 or gemcitabine 1000 mg/m2 days 1 and 8 q 3 weeks x 4 cycles

336 29% 45%

Sharma et al Single ArmCarboplatin AUC 6 + docetaxel 75 mg/m2 q 3 wks x 6 cycles

190 — 55%

TBCRC 030 R d i d h II Paclitaxel 80 mg/m2 x 12 weeks or

140 12% 15%

Priyanka Sharma, MD

Neoadjuvant trials incorporating Platinum in TNBC

Study Design Chemotherapy Regimen N

pCR (%)

Control Platinum

pCR

deltaAnthracycline containing regimens

GeparSixto Randomized Phase IIWeekly Paclitaxel 80 mg/m2 + NPLD 20 mg/m2 weekly + bev 15 mg/kg q 3 wks ± carboplatin AUC 1.5-2 weekly x 18 wks

315 37% 53% 16%

Alliance/CALGB 40603

Randomized Phase II (2x2 factorial design)

Weekly paclitaxel 80 mg/m2 x 12 ± carboplatin AUC 6 q 3 wks x 4 → AC q 2 weeks x 4 ± bev 10 mg/kg q 2 wks x 9 cycles

433 41% 54% 13%

BrighTNessRandomized Phase III (3-arm)

Weekly paclitaxel ± carboplatin AUC 6 ± veliparib 50 mg x 12 wks, followed by AC q 2-3 wks x 4 cycles

634 31% 57% (carbo)

53% (carbo + vel)26%

ISPY-2 Randomized Phase IIWeekly paclitaxel 80 mg/m2 x 12 ± carboplatin AUC 6 q 3 wks x 4 and veliparib 50 mg BID PO → AC q 2 wks x 4 cycles

6026% (est)

51% (est) -

NeoSTOP Randomized phase II Weekly paclitaxel 80 mg/m2 x 12 + carboplatin AUC 6 q 3 wks x 4 → AC q 2 weeks x 4 (ARM A) vs Carboplatin AUC 6 + docetaxel 75 mg/m2 q 3 wks x 6 cycles (ARM B)

100 —54% (Arm A)

52% (Arm B)-

Anthracycline-sparing regimens

WSG-ADAPT Randomized Phase IIWeekly nab-paclitaxel 125mg/m2 + carboplatin AUC 2 or gemcitabine 1000 mg/m2 days 1 and 8 q 3 weeks x 4 cycles

336 29% 45%

Sharma et al Single ArmCarboplatin AUC 6 + docetaxel 75 mg/m2 q 3 wks x 6 cycles

190 — 55%

TBCRC 030 R d i d h II Paclitaxel 80 mg/m2 x 12 weeks or

140 12% 15%

Priyanka Sharma, MD

Increase in pCR but also increase in toxicities

Neoadjuvant trials incorporating Platinum in TNBC

Study Design Chemotherapy Regimen N

pCR (%)

Control Platinum

pCR

deltaAnthracycline containing regimens

GeparSixto Randomized Phase IIWeekly Paclitaxel 80 mg/m2 + NPLD 20 mg/m2 weekly + bev 15 mg/kg q 3 wks ± carboplatin AUC 1.5-2 weekly x 18 wks

315 37% 53% 16%

Alliance/CALGB 40603

Randomized Phase II (2x2 factorial design)

Weekly paclitaxel 80 mg/m2 x 12 ± carboplatin AUC 6 q 3 wks x 4 → AC q 2 weeks x 4 ± bev 10 mg/kg q 2 wks x 9 cycles

433 41% 54% 13%

BrighTNessRandomized Phase III (3-arm)

Weekly paclitaxel ± carboplatin AUC 6 ± veliparib 50 mg x 12 wks, followed by AC q 2-3 wks x 4 cycles

634 31% 57% (carbo)

53% (carbo + vel)26%

ISPY-2 Randomized Phase IIWeekly paclitaxel 80 mg/m2 x 12 ± carboplatin AUC 6 q 3 wks x 4 and veliparib 50 mg BID PO → AC q 2 wks x 4 cycles

6026% (est)

51% (est) -

NeoSTOP Randomized phase II Weekly paclitaxel 80 mg/m2 x 12 + carboplatin AUC 6 q 3 wks x 4 → AC q 2 weeks x 4 (ARM A) vs Carboplatin AUC 6 + docetaxel 75 mg/m2 q 3 wks x 6 cycles (ARM B)

100 —54% (Arm A)

52% (Arm B)-

Anthracycline-sparing regimens

WSG-ADAPT Randomized Phase IIWeekly nab-paclitaxel 125mg/m2 + carboplatin AUC 2 or gemcitabine 1000 mg/m2 days 1 and 8 q 3 weeks x 4 cycles

336 29% 45%

Sharma et al Single ArmCarboplatin AUC 6 + docetaxel 75 mg/m2 q 3 wks x 6 cycles

190 — 55%

TBCRC 030 R d i d h II Paclitaxel 80 mg/m2 x 12 weeks or

140 12% 15%Priyanka Sharma, MD

STUDY DESIGN

aEfficacy was assessed in all randomized patients and safety in all patients who received ≥1 doseAUC, area under the curve; BID, twice a day; ECOG PS, Eastern Cooperative Oncology Group performance status; EFS, event-free survival; OS, overall

survival; pCR, pathological complete response; Q2W, every 2 weeks; Q3W, every 3 weeks; R, randomization; TNBC, triple negative breast cancer.

Postsurgery assessment was performed every 3 months until 1 year after surgery, then every 6 months until 2 years after surgery, then yearly until 4 years after surgery, or until an EFS event

2–8 weeks afterthe last dose of chemotherapy

Doxorubicin, 60 mg/m2

Cyclophosphamide, 600 mg/m2, Q2W or

Q3W (4 cycles)

Paclitaxel, 80 mg/m2, weekly (12 doses in up to 16 weeks)

Paclitaxel + carboplatin placebo + veliparib placebo (N = 158)Carboplatin placebo, Veliparib placebo

Paclitaxel + carboplatin + veliparib (N = 316)Carboplatin, AUC 6 mg/mL/min, Q3W (4 cycles)

Veliparib, 50 mg, orally BID

Key inclusion criteria• Women aged ≥18 years• Histologically or cytologically confirmed invasive stage II/III TNBC• ECOG PS 0–1• Candidates for potentially curative surgery with documented gBRCA status

Segment 1 Segment 2 Surgery

Paclitaxel + carboplatin + veliparib placebo (N = 160)Carboplatin, AUC 6 mg/mL/min, Q3W (4 cycles)

Veliparib placebo

Randomization was stratified according to gBRCA status, nodal stage, and planned schedule of doxorubicin and cyclophosphamide administration

Endpointsa

Primary endpoint• pCRSecondary endpoints• EFS• OS• SafetyEFS according to pCR was also examined in a post hoc analysisRates of second primary malignancies were assessed per Standardized Medical Dictionary for Regulatory Activities (MedDRA) version 21.1

Key exclusion criteria• Previous anticancer treatment• Previous or concurrent cancer• On ovarian hormonal replacement therapy

Randomized patientsN = 634

R2:1:1

Loibl et al ESMO 2021

BrighTNess: EFS RESULTS

aStratified by BRCA status, lymph node status, and planned doxorubicin/cyclophosphamide dose intensity.C, carboplatin; CI, confidence interval; EFS, event-free survival; HR, hazard ratio; P, paclitaxel; V, veliparib.

censored

Prob

abilit

y of E

FS

Months since randomization

1.0

0.9

0.8

0.7

0.6

0.5

0.4

0.3

0.2

0.0

0.1

0 3 6 9 15 18 21 24 27 30 33 6012 4236 39 45 725448 51 57 63 66 69

No of patients at riskP + C + V

P + CP

316160158

311157147

301154147

290151142

273143132

266134125

257129120

248121115

241118112

228112102

21311095

0

1

283148139

281312

1999787

1889174

133 0

235115107

22211198

102

1305541

20610291

1959480

957

Paclitaxel + carboplatin + veliparib

Paclitaxel + carboplatin Paclitaxel

Events n/N 65/316 30/160 47/158

Hazard ratio (95% CI)a

Paclitaxel + carboplatin + veliparib vs paclitaxelPaclitaxel + carboplatin + veliparib vs paclitaxel + carboplatinPaclitaxel + carboplatin vs paclitaxel (post hoc analysis)

0.63 (0.43–0.92), P=0.021.12 (0.72–1.72), P=0.620.57 (0.36–0.91), P=0.02

4-year EFS, % (95% CI) 78.2 (73.5–83.2) 79.3 (72.9–86.2) 68.5 (61.3–76.6)

Loibl et al ESMO 2021

MEDIAN FOLLOW-UP OF 4.5 YEARS

BrighTNess: EFS RESULTS

aStratified by BRCA status, lymph node status, and planned doxorubicin/cyclophosphamide dose intensity.C, carboplatin; CI, confidence interval; EFS, event-free survival; HR, hazard ratio; P, paclitaxel; V, veliparib.

censored

Prob

abilit

y of E

FS

Months since randomization

1.0

0.9

0.8

0.7

0.6

0.5

0.4

0.3

0.2

0.0

0.1

0 3 6 9 15 18 21 24 27 30 33 6012 4236 39 45 725448 51 57 63 66 69

No of patients at riskP + C + V

P + CP

316160158

311157147

301154147

290151142

273143132

266134125

257129120

248121115

241118112

228112102

21311095

0

1

283148139

281312

1999787

1889174

133 0

235115107

22211198

102

1305541

20610291

1959480

957

Paclitaxel + carboplatin + veliparib

Paclitaxel + carboplatin Paclitaxel

Events n/N 65/316 30/160 47/158

Hazard ratio (95% CI)a

Paclitaxel + carboplatin + veliparib vs paclitaxelPaclitaxel + carboplatin + veliparib vs paclitaxel + carboplatinPaclitaxel + carboplatin vs paclitaxel (post hoc analysis)

0.63 (0.43–0.92), P=0.021.12 (0.72–1.72), P=0.620.57 (0.36–0.91), P=0.02

4-year EFS, % (95% CI) 78.2 (73.5–83.2) 79.3 (72.9–86.2) 68.5 (61.3–76.6)

Loibl et al ESMO 2021

MEDIAN FOLLOW-UP OF 4.5 YEARS

Carboplatin EFS 11%

BrighTNess: EFS RESULTS

aStratified by BRCA status, lymph node status, and planned doxorubicin/cyclophosphamide dose intensity.C, carboplatin; CI, confidence interval; EFS, event-free survival; HR, hazard ratio; P, paclitaxel; V, veliparib.

censored

Prob

abilit

y of E

FS

Months since randomization

1.0

0.9

0.8

0.7

0.6

0.5

0.4

0.3

0.2

0.0

0.1

0 3 6 9 15 18 21 24 27 30 33 6012 4236 39 45 725448 51 57 63 66 69

No of patients at riskP + C + V

P + CP

316160158

311157147

301154147

290151142

273143132

266134125

257129120

248121115

241118112

228112102

21311095

0

1

283148139

281312

1999787

1889174

133 0

235115107

22211198

102

1305541

20610291

1959480

957

Paclitaxel + carboplatin + veliparib

Paclitaxel + carboplatin Paclitaxel

Events n/N 65/316 30/160 47/158

Hazard ratio (95% CI)a

Paclitaxel + carboplatin + veliparib vs paclitaxelPaclitaxel + carboplatin + veliparib vs paclitaxel + carboplatinPaclitaxel + carboplatin vs paclitaxel (post hoc analysis)

0.63 (0.43–0.92), P=0.021.12 (0.72–1.72), P=0.620.57 (0.36–0.91), P=0.02

4-year EFS, % (95% CI) 78.2 (73.5–83.2) 79.3 (72.9–86.2) 68.5 (61.3–76.6)

Loibl et al ESMO 2021

MEDIAN FOLLOW-UP OF 4.5 YEARS

Carboplatin EFS 11%

No EFS benefit for addition of veliparib

BrighTNess: EFS RESULTS

aStratified by BRCA status, lymph node status, and planned doxorubicin/cyclophosphamide dose intensity.C, carboplatin; CI, confidence interval; EFS, event-free survival; HR, hazard ratio; P, paclitaxel; V, veliparib.

censored

Prob

abilit

y of E

FS

Months since randomization

1.0

0.9

0.8

0.7

0.6

0.5

0.4

0.3

0.2

0.0

0.1

0 3 6 9 15 18 21 24 27 30 33 6012 4236 39 45 725448 51 57 63 66 69

No of patients at riskP + C + V

P + CP

316160158

311157147

301154147

290151142

273143132

266134125

257129120

248121115

241118112

228112102

21311095

0

1

283148139

281312

1999787

1889174

133 0

235115107

22211198

102

1305541

20610291

1959480

957

Paclitaxel + carboplatin + veliparib

Paclitaxel + carboplatin Paclitaxel

Events n/N 65/316 30/160 47/158

Hazard ratio (95% CI)a

Paclitaxel + carboplatin + veliparib vs paclitaxelPaclitaxel + carboplatin + veliparib vs paclitaxel + carboplatinPaclitaxel + carboplatin vs paclitaxel (post hoc analysis)

0.63 (0.43–0.92), P=0.021.12 (0.72–1.72), P=0.620.57 (0.36–0.91), P=0.02

4-year EFS, % (95% CI) 78.2 (73.5–83.2) 79.3 (72.9–86.2) 68.5 (61.3–76.6)

Loibl et al ESMO 2021

MEDIAN FOLLOW-UP OF 4.5 YEARS

Carboplatin EFS 11%

? HRD/immune status on carboplatin EFS benefit

No EFS benefit for addition of veliparib

Immune Checkpoint Inhibition

Priyanka Sharma, MD

GeparNuevo: Addition of Durvalumab to a taxane-anthracycline containing chemotherapy in TNBC

Loibl Annals of Oncology 2019

N=88 N=86

pCR

Priyanka Sharma, MD

No adjuvnat ICB

GeparNuevo: Addition of Durvalumab to a taxane-anthracycline containing chemotherapy in TNBC

Loibl Annals of Oncology 2019

53.… 44…

0%20%40%60%80% P=0.28

N=88 N=86

pCR

Priyanka Sharma, MD

No adjuvnat ICB

PRESENTED BY: SIBYLLE LOIBL, MD PRESENTED AT:#ASCO21 │ Content of this presentation is property of the author, licensed by ASCO. Permission required for reuse

GeparNuevo: iDFS

3yr 77.2%

3yr 85.6%

Stratified HR* Durvalumab to Placebo = 0.48 (95%CI 0.24, 0.97), p=0.0398

Time (months)

Inva

sive

Dis

ease

-Fre

e Su

rviv

al R

ate

(%)

Patients at risk:* Stratified by sTILs

Median follow-up 43.7 (range 4.9-56.1) months

PRESENTED BY: SIBYLLE LOIBL, MD PRESENTED AT:#ASCO21 │ Content of this presentation is property of the author, licensed by ASCO. Permission required for reuse

Time (months)

Ove

rall

Surv

ival

Rat

e (%

)

3yr 83.5%

3yr 95.2%

Stratified HR* Durvalumab to Placebo = 0.24 (95%CI 0.08, 0.72), p=0.0108

GeparNuevo: DDFS and OSDDFS

Patients at risk:

OS

Time (months)

Dis

tant

Dis

ease

-Fre

e Su

rviv

al R

ate

(%)

Stratified HR* Durvalumab to Placebo = 0.31 (95%CI 0.13, 0.74), p=0.0078

Patients at risk:

3yr 78.4%

3yr 91.7%

* Stratified by sTILs

PRESENTED BY: SIBYLLE LOIBL, MD PRESENTED AT:#ASCO21 │ Content of this presentation is property of the author, licensed by ASCO. Permission required for reuse

iDFS in Subgroups (univariate Cox regression model)Subgroup Hazard RatioN p-Value Test for

(95% CI)patients Interaction

Overall 0.48 (0.24, 0.97)174 .0398

sTILs 0.705low (0-10%) .423 (.156, 1.15)66 0.090intermediate/high (11-100%) .553 (.205, 1.50)108 0.244

Window Arm 0.891w indow .524 (.220, 1.25)117 0.145no w indow .465 (.140, 1.55)57 0.211

Breast Cancer Stage 0.940Stage 0 or I .553 (.092, 3.31)61 0.517Stage IIA and higher .519 (.241, 1.12)113 0.093

Age 0.552<40 .344 (.089, 1.33)47 0.122>=40 .573 (.251, 1.31)127 0.187

PD-L1 0.463negative .795 (.133, 4.76)20 0.801positive .436 (.188, 1.01)138 0.053

pCR (ypT0 ypN0) 0.222no .674 (.295, 1.54)88 0.350yes .220 (.046, 1.06)85 0.059

10.1 0.2 0.5 2.0 3.0

Longer iDFS with Durvalumab Longer iDFS with Placebo

HR

*

* Stratified by sTILs

aMust consist of at least 2 separate tumor cores from the primary tumor. bCarboplatin dose was AUC 5 Q3W or AUC 1.5 Q1W.cPaclitaxel dose was 80 mg/m2 Q1W.

dDoxorubicin dose was 60 mg/m2 Q3W.eEpirubicin dose was 90 mg/m2 Q3W.fCyclophosphamide dose was 600 mg/m2 Q3W.

KEYNOTE-522 Study Design (NCT03036488)

Stratification Factors:• Nodal status (+ vs -)• Tumor size (T1/T2 vs T3/T4)• Carboplatin schedule (Q1W vs Q3W)

Key Eligibility Criteria• Age ≥18 years• Newly diagnosed TNBC of

either T1c N1-2 or T2-4 N0-2• ECOG PS 0-1• Tissue sample for PD-L1

assessmenta

Neoadjuvant Treatment 1(cycles 1-4; 12 weeks)

Neoadjuvant Treatment 2 (cycles 5-8; 12 weeks)

Adjuvant Treatment(cycles 1-9; 27 weeks)

Carboplatinb + Paclitaxelc

Doxod/Epirubicine+ Cyclophosphamidef

Pembrolizumab 200 mg Q3W

Pembrolizumab 200 mg Q3W

Placebo

Placebo

R 2:1

Neoadjuvant Phase Adjuvant Phase

Carboplatinb + Paclitaxelc

Doxod/Epirubicine + Cyclophosphamidef

SURGERY

Primary endpoints: pCR (ypT0/Tis ypN0) by local review, EFS by local review Secondary endpoints: pCR (ypT0 ypN0 and ypT0/Tis), OS, EFS, AE Exploratory endpoints: RCB, pCR by subgroups, EFS by pCR

KEYNOTE-522: Pathological complete response (IA1, N=602)

Schmidt et al NEJM 2020

KEYNOTE-522: EFS, IA4

EFS by pCREFS in subgroups

IMpassion031: Addition of Atezolizumab to Neoadjuvant Chemotherapy in Stage II-III TNBC

Harbeck. ESMO 2020. Abstr LBA11, Mittendorf et al Lancet 2020

pCR in ITT Population

Harbeck. ESMO 2020. Abstr LBA11, Mittendorf et al Lancet 2020

pCR (95% CI), ypT0/is ypN0

57.6%

41.1

95/165 69/168

Δ 16.5%

Atezo + CT0

20

40

60

80

100

pCR,

% (9

5% C

I)

Pbo + CT

P = .0044

n/N =

pCR by PD-L1 StatusPD-L1 Positive

68.8%

49.3%

53/77 37/75

Δ 19.5%

Atezo + CT0

20

40

60

80

100

pCR,

% (9

5% C

I)

Pbo + CT

n/N =

PD-L1 Negative

47.7%

34.4%

42/88 32/93

Δ 13.3%

Atezo + CT0

20

40

60

80

100

pCR,

% (9

5% C

I)

Pbo + CT

n/N =

IMpassion031: Pathologic Complete Response

P = .021a

asignificance boundary 0·0184

*HER-2 negative, ER and PgRnegativeearly high-risk (T1cN1; T2N1; T3N0) or locally advanced unilateralbreast cancer

Neoadjuvant Therapy in TRIPle Negative Breast Cancer With antiPDL1 (NeoTRIPaPDL1)

*Estrogen receptor, progesterone receptor, HER2 and PD-L1 were centrally assessed before randomization

FOLLOWUP

Carboplatin AUC 2 + nab-paclitaxel 125mg/m2weekly for 2 wks every 3for 8 cycles

Carboplatin AUC 2 + nab-paclitaxel 125mg/m2weekly for 2 wks every 3for 8 cycles+ Atezolizumab day 1 every 3 wks for 8 cycles

R

AC/EC/FECfor 4 cycles

AC/EC/FECfor 4 cycles

S

S

Gianni et al SABCS 2019

*HER-2 negative, ER and PgRnegativeearly high-risk (T1cN1; T2N1; T3N0) or locally advanced unilateralbreast cancer

Neoadjuvant Therapy in TRIPle Negative Breast Cancer With antiPDL1 (NeoTRIPaPDL1)

*Estrogen receptor, progesterone receptor, HER2 and PD-L1 were centrally assessed before randomization

FOLLOWUP

Carboplatin AUC 2 + nab-paclitaxel 125mg/m2weekly for 2 wks every 3for 8 cycles

Carboplatin AUC 2 + nab-paclitaxel 125mg/m2weekly for 2 wks every 3for 8 cycles+ Atezolizumab day 1 every 3 wks for 8 cycles

R

AC/EC/FECfor 4 cycles

AC/EC/FECfor 4 cycles

S

S

Gianni et al SABCS 2019

Primary end point: EFSSecondary end point: pCR

*HER-2 negative, ER and PgRnegativeearly high-risk (T1cN1; T2N1; T3N0) or locally advanced unilateralbreast cancer

Neoadjuvant Therapy in TRIPle Negative Breast Cancer With antiPDL1 (NeoTRIPaPDL1)

*Estrogen receptor, progesterone receptor, HER2 and PD-L1 were centrally assessed before randomization

FOLLOWUP

Carboplatin AUC 2 + nab-paclitaxel 125mg/m2weekly for 2 wks every 3for 8 cycles

Carboplatin AUC 2 + nab-paclitaxel 125mg/m2weekly for 2 wks every 3for 8 cycles+ Atezolizumab day 1 every 3 wks for 8 cycles

R

AC/EC/FECfor 4 cycles

AC/EC/FECfor 4 cycles

S

S

N=28087% Node positive45% T3-T456% PD-L1 positive

Gianni et al SABCS 2019

Primary end point: EFSSecondary end point: pCR

NeoTRIPaPDL1: pCR

Bianchini et al ESMO 2020

NeoTRIPaPDL1: pCR

Bianchini et al ESMO 2020

NeoTRIPaPDL1: pCR

Bianchini et al ESMO 2020

pCR and PD-L1 IC groups

Neoadjuvant chemo + ICI trials KEYNOTE-522 (NCT03036488)

GeparNeuvo IMpassion031(NCT03197935)

NeoTRIPaPDL1 (NCT02620280)

N=1174 N=174 N=333 N=280

End points Co-Primary: pCR and EFS Primary: pCRSecondary: iDFS, DDFS, OS

Primary: pCRSecondary: EFS

Primary: EFSSecondary: pCR

LN+ 51% 33%, stage I: 36% 36% 87%

Regimen Paclitaxel/carbo AC/EC + pembrolizumab/placebo CbP-AC

nab-paclitaxel EC +Durvalumab/placebonP-EC

nab-paclitaxel EC + durvalumab/placebo. nP-AC

Wkly carbo/nab-paclitaxel+Atezolizumab/Placebo X 8 cycles CbP

Adj treatment Pembro/placebo X 27 wks No ICI Atezo/placebo X 22 wks EC/AC/FEC

ICI Type Anti-PD-1 Anti PD-L1 Anti-PD-L1 Anti-PD-L1

Treatment duration

24 weeks 20 weeks 20 weeks 24 weeks

PD-L1+ 83% (CPS>1) 87%(SP263 antibody) 46% (IC >1%) 56% (IC>1%)PCR ITT: 65 vs 51% (63 vs 55.6%)

PD-L1+: 70 vs 55%PD-L1-ve: 45 vs 30%

53 vs 44%n.s ITT: 58 vs 41%PD-L1+: 69 vs 49%n.s

PD-L1-ve: 47 vs 34%

ITT: 52 vs 47%n.s.

PD-L1+: 56 vs 44%PD-L1-ve: 35 vs 41%

EFS/DFS/OS 3-year EFS 84.5% vs 76.8% HR=0.63, p=0.00033-year OS: 89.6% vs 86.9% HR=0.72, p=0.032n.s

3-year iDFS: 85.6% vs 77.2% HR=0.48, p=0.03983-year OS: 95% vs 83%HR=0.24, p=0.018

Pending Pending

Schmid et al, NEJM 2020, Mittendorf et al, Lancet 2020, Gianni et al SABCS 2019, Bianchini et al ESMO 2020, Schmidt et al ESMO virtual session, Loibl et al ASCO 2021

Safety of Immune check point inhibitors in metastatic TNBC

D’Abreo and Adams. Nat Rev Clin Oncol 2019, Brahmer et al, J Clin Oncol 2018

irAE incidence in eTNBC

• Any grade: 40-44%

• Grade 3-5: 14-15%

• Early recognition and prompt management

• Management guidelines ASCO/NCCN

KEYNOTE-522 : iAE

Most frequent iAEs: Infusion reactions (18%), hypothyroidism (15%), severe skin reactions (5.8%), Hyperthyroidism (5.2%), adrenal insufficiency (2.6%), pneumonitis (2,2%), thyroiditis (2%), Hypophysitis (1.9%)

IMpassion031: AEs of special interest in neoadjuvant phase

Neo/adjuvant IC inhibitors in TNBC

Neo/adjuvant IC inhibitors in TNBC Addition of ICI improves pCR and EFS/iDFSNeo (plus adjuvant) Pembrolizumab + chemotherapy FDA approved

Neo/adjuvant IC inhibitors in TNBC Addition of ICI improves pCR and EFS/iDFSNeo (plus adjuvant) Pembrolizumab + chemotherapy FDA approved

Improvement in outcomes but overtreatment of many 54-55% pCR with chemotherapy alone

4-year EFS 79% with CbT-AC (BrighTNess)iAEs in early vs. metastatic setting: Long term toxicity ? Cost

Neo/adjuvant IC inhibitors in TNBC Addition of ICI improves pCR and EFS/iDFSNeo (plus adjuvant) Pembrolizumab + chemotherapy FDA approved

Improvement in outcomes but overtreatment of many 54-55% pCR with chemotherapy alone

4-year EFS 79% with CbT-AC (BrighTNess)iAEs in early vs. metastatic setting: Long term toxicity ? Cost

Role of chemo backboneAthra+Platinum, Anthra, Platinum+taxane

Neo/adjuvant IC inhibitors in TNBC Addition of ICI improves pCR and EFS/iDFSNeo (plus adjuvant) Pembrolizumab + chemotherapy FDA approved

Improvement in outcomes but overtreatment of many 54-55% pCR with chemotherapy alone

4-year EFS 79% with CbT-AC (BrighTNess)iAEs in early vs. metastatic setting: Long term toxicity ? Cost

Role of chemo backboneAthra+Platinum, Anthra, Platinum+taxane

Future research Role of adjuvant ICI: after pCR? For RD after neoadjuvant ICI?Upfront vs guided by pathological response: S1418 de-escalating chemo back-bone: ISPY2, NeoPACTBiomarkers: PD-L1 not the best predictor of response in early stage TNBC

THANK YOU

Predictive value of gene-expression profiles (GEPs) and their dynamics during therapy in the NeoTRIPaPDL1 trial

Giampaolo Bianchini, Matteo Dugo, Chiun-Sheng Huang, Daniel Egle, Begoña Bermejo, Claudio Zamagni, Robert S Seitz, Tyler J Nielsen, Marc Thill, Antonio Anton, Stefania Russo, Eva Maria Ciruelos, Brock L Schweitzer, Balazs Gyorffy, Richard Greil, Vladimir Semiglazov, Pinuccia Valagussa, Giuseppe Viale, Maurizio Callari, Luca Gianni

Content of this presentation is copyright and responsibility of the author. Permission is required for re-use.

NeoTRIP trial: timing of successful RNA-sequencing (in PPP)

Giampaolo Bianchini (bianchini.giampaolo@hsr.it)

TN high-risk (T1cN1; T2N1; T3N0) or locally advanced Su

rger

y

R

Carboplatin (AUC2) + nab-paclitaxel (125 mg/m2) weekly for 2 wks every 3; 8 cy; Atezolizumab (1200 mg) day 1 every 3 wks for 8 cycles(§) Results in the Per-Protocol-Population (Bianchini G ESMO 2020 LBA13)

Carboplatin + nab-paclitaxel + Atezolizumab

Carboplatin+nab-paclitaxel

Gianni L SABCS 2019 (Abstract G3-02)PPP: Per-protocol-population (patients evaluable for pCR)

Content of this presentation is copyright and responsibility of the author. Permission is required for re-use.

NeoTRIP trial: timing of successful RNA-sequencing (in PPP)

Giampaolo Bianchini (bianchini.giampaolo@hsr.it)

TN high-risk (T1cN1; T2N1; T3N0) or locally advanced Su

rger

y

RCarboplatin + nab-paclitaxel + Atezolizumab

Carboplatin+nab-paclitaxel

Baseline(Pre-treatment)

Timing of tumor sample collection

Rate of successful RNA-seq 93.8 %

Gianni L SABCS 2019 (Abstract G3-02); Bianchini G ESMO 2020 (LBA13) PPP: Per-protocol-population (patients evaluable for pCR)

Rate oftissue collection 100 %

(242/258)

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Methods and Aim (I)

Giampaolo Bianchini (bianchini.giampaolo@hsr.it)

In this post-hoc study, we evaluated on pre-treatment samples the association with pCR of- IO score1 (research-based version of DetermaIOTM) which has been associated with immune checkpoint

inhibitor benefit independently of PD-L1 or TMB in NSCLC2 and metastatic urothelial cancer (IMvigor210)3, and also with pCR in TNBC treated with neoadjuvant durvalumab and chemotherapy (NCT02489448)4 (pre-specified analysis)

- TNBCtypes by 101-gene score algorithm (BL1, BL2, LAR, M and MSL)5(exploratory analysis)

1 Nielsen TJ Heliyon 2021; 2 Ranganath H SITC 2019; 3 Seitz RS AACR 2021; 4 Iwase T ASCO 2020; 5 Ring BZ BMC Cancer 2016

Chemotherapy +/- Atezolizumab

SurgeryPre-treatmentpCR

RDBaseline biopsy

IO scoreTNBCtypes

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Methods and Aim (II)

Giampaolo Bianchini (bianchini.giampaolo@hsr.it)

Analysis flow1) RNA-sequencing has been generated in OncoCyte’s lab (blinded to clinical outcome information)2) RNA-seq QC performed in my lab3) IO score (binary and continuous) and TNBC types generated in OncoCyte’s lab (blinded to clinical outcome

information)4) Results provided to my lab5) Association of IO score and TNBC types with PD-L1, sTILs and pCR (breast and nodes) according to a pre-

specified SOP- IO score binary (primary analysis)- IO score continuous and TNBC types (secondary exploratory analysis)

1 Nielsen TJ Heliyon 2021; 2 Ranganath H SITC 2019; 3 Seitz RS AACR 2021; 4 Iwase T ASCO 2020; 5 Ring BZ BMC Cancer 2016

IO score balanced among arms

IO score is associated with PD-L1 and sTILs

CT/Atezo OR 3.64 (1.68-7.90) p=0.001

Binary IO score (pos vs neg, primary analysis)

Test of interaction p=0.029(adjusted for PD-L1 ad sTILs)

CT OR 1.31 (0.64-2.67) p=0.46

Logistic regression analysis

IO score (continuous score, exploratory analysis)

CT/Atezo OR 3.65 (1.45-9.24) p=0.006CT OR 1.56 (0.69-3.54) p=0.283

Wilcoxon test

Logistic regression analysis

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How does IO score compare with immune signatures?

Giampaolo Bianchini (bianchini.giampaolo@hsr.it)

We also explored the association with pCR of 151 selected tumor intrinsic and extrinsic gene-signatures (HALLMARK1, Consensus clusters2, Nanostring3, and few selected from literature4,5,6,7,8) evaluated on pre-treatment samples. None of the immune-related signatures (over 60) outperformed IO score.

Pre-treatmentBaseline biopsy

151 tumor intrinsic and extrinsic gene-signatures

1 Liberzon A Cell Syst 2015; 2 Jimenez-Sanchez A Cancer Res 2019; 3 https://www.nanostring.com/; 4 Callari M CCR 2016; 5 Bianchini G Ann Oncol 2015; 6 Bianchini G Breast Cancer Res 2013; 7 Masiero M Cancer Cell 2013; 8 Mak MP CCR 2016

Only two immune related-signatures were associated with pCR in atezolizumab arm (with a p value between 0.01 and 0.05)

TNBC types balanced among arms

TNBC types association with PD-L1 and sTILs

• The LAR subtype had the lowest pCR rate (CT/A 22.2%, CT 18.8%), whereas BL1 had the highest [CT/A 70.3%, CT 54.3%) (p=0.001)

• All tests of interaction not significant

TNBC types association with pCR

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Conclusions (I)

• IO score, but not TNBCtype, is predictive of atezolizumab benefit over CT alone (significant test of interaction after adjustment for PD-L1 and sTILs)

Giampaolo Bianchini (bianchini.giampaolo@hsr.it)

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Acknowledgments

Giampaolo Bianchini (bianchini.giampaolo@hsr.it)

Patients, their families and all the investigators

HSRMatteo DugoBarbara GalbardiMarco Barreca

Fondazione MichelangeloMaurizio CallariGiuseppe VialePinuccia ValagussaLuca Gianni

Other collaboratorsH Raza AliBalazs Gyorffy Lucia Del MastroCatherine KellyMarco ColleoniGabriella Mariani

OncoCyteRobert S SeitzTyler J NielsenBrock L SchweitzerDouglas T Ross

@BianchiniGP @mauricallari @FondazioneBona1

Q&A Discussion