On April 17, 2026 The Parker Institute for Cancer Immunotherapy (PICI), reported that research and expertise from across its network will be showcased at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, taking place April 17- 22 in San Diego, California. PICI leaders, investigators, and collaborators are contributing to nearly 100 posters, presentations, and discussions throughout the program – demonstrating the depth and breadth of the network’s contributions to the field of cancer immunotherapy.

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Notably, PICI’s newly appointed Chief of External Affairs Kristen Dahlgren is a co-chair of this year’s Annual Meeting Program Committee. She will also chair an educational session on communicating beyond academic audiences and a forum designed to help attendees gain actionable insights to improve trial efficiency, broaden representation, and enhance the relevance and impact of their research. PICI is also unveiling the latest results from the RADIOHEAD cohort, with the largest plasma proteomics study of its kind for checkpoint inhibitor therapy, alongside new methylation-based tools for monitoring tumor dynamics.

Additionally, Antoni Ribas, Director of the PICI Center at UCLA, will be honored with the 2026 AACR (Free AACR Whitepaper)-Margaret Foti Award for Leadership and Extraordinary Achievements in Cancer Research. This award is presented annually to an individual whose leadership and extraordinary achievements in cancer research have made a major impact in the field.

"Cancer doesn’t wait, and neither do the researchers of the PICI Network. The work our investigators are presenting at AACR (Free AACR Whitepaper) 2026 – across cell therapies, resistance mechanisms, precision platforms and beyond – represents years of collaboration designed to move faster than any single institution could alone," said Dr. Knudsen. "Through our investigators and portfolio companies, we are developing and accelerating access to breakthrough cancer therapies and curating innovation from discovery to commercialization, with the vision of converting all cancers to curable diseases."

Presentation Highlights from the Network

Select highlights from across the network include:

Kristen Dahlgren (PICI): Anatomy lesson: Finding the heart in your science (Saturday, April 18) and How survivor driven priorities can accelerate research innovation (Tuesday, April 21)

Karen Knudsen, MBA, PhD (PICI): Co-author of CBP/p300 and PARP inhibitor combination treatment synergistically enhances anti-tumor efficacy in models of advanced prostate cancer (Abstract 4047)
Oral Presentation, Monday, April 20 (O.I. Richter)
Translational Platforms & Liquid Biopsy

John Connolly, PhD (PICI): High-throughput protein profiling applied to the RADIOHEAD cohort—the largest plasma proteomics study of patients receiving checkpoint inhibitor therapy (Abstract 6332)

Samantha Liang (PICI): Methylation-based tumor fraction monitoring to identify patients who may benefit from comprehensive genomic profiling (Abstract 1122)

Christopher Cabanski (PICI): Hierarchical modeling of methylation-based tumor fraction dynamics for pan-cancer immunotherapy response assessment (Abstract 690)
CAR T & Engineered Cell Therapies

Crystal Mackall, MD (Stanford Medicine): Multiple presentations including IL-18 secreting CAR-T cells for antigen-heterogeneous solid tumors (Abstract 1351); targeting the oncofetal antigen GPC2 in medulloblastoma (Abstract 4009); and a longitudinal single-cell atlas of GD2-CAR T cell therapy in diffuse midline glioma (Abstract 6463)

Carl June, MD (UPenn): Spatial profiling of recurrent glioblastoma in a Phase I CAR T trial (Abstract 3444) and spatial remodeling of the tumor microenvironment by IL-18-armored CD19 CAR T cells (Abstract 6470)

Roddy O’Connor, PhD (UPenn): Metabolic fitness enhancement for CAR-T cells (Abstract 4272) and a novel nanoparticle platform for scalable adoptive immunotherapy manufacturing (Abstract 4291)

Michael Milone, MD, PhD (UPenn): Novel SynKIR-310 platform outperforming CD3-based CAR T in lymphoma models (Abstract 5193)
In Vivo Gene Editing & CRISPR

Alexander Marson, MD, PhD (Gladstone/UCSF): In vivo genome-wide CRISPR screens in human T cells for solid tumor therapy (Abstract 1532); virus-like particle-enabled gene engineering in primary human myeloid cells (Abstract 1580)
Tumor Microenvironment & Resistance

David Barbie, MD (DFCI): Multiple presentations including next-generation immune engagers derived from reprogrammed E. coli (Abstract 4904); co-targeting EZH2 and TEAD in Hippo pathway-mutated cancers (Abstract 1850); and B7-H3 targeting in the SCLC tumor-immune microenvironment (Abstract 5603)

Eli Van Allen, MD (DFCI): Six posters spanning bladder cancer resistance (Abstract 3458), myeloid-driven immunotherapy resistance in prostate cancer bone metastases (Abstract 4084), and tumor mass dormancy in melanoma (Abstract 3450)

Jedd Wolchok, MD, PhD (Weill Cornell Medicine): Tumor IDO1-driven resistance to adoptive cell transfer (Abstract 6537) and clinical strategies to enhance TIL therapy efficacy (Abstract 5624)
Neoantigens & TCR-Based Therapies

Hideho Okada, MD, PhD (UCSF): Splicing-landscape-derived shared neoantigens in IDH-mutant gliomas (Abstract 462) and viral vector vaccination driving brain-resident memory T cells (Abstract 4363)

Christopher Klebanoff, MD (MSK): Immunopeptidomic discovery of fetal WNT-associated antigen NKD1 for HLA-A2-restricted TCR-T therapy in microsatellite-stable metastatic colorectal cancer (Abstract 3714)
Pediatric & CNS Cancers

Robbie Majzner, MD (DFCI): Ganglioside targeting for neuroblastoma (Abstract 7814)

Kai Wucherpfennig, MD, PhD (DFCI): Pre-existing T cells driving durable anti-tumor immunity after oncolytic virus therapy in glioblastoma (Abstract 7743)
Breast Cancer & Solid Tumors

Elizabeth Mittendorf, MD, PhD (DFCI): Age-stratified therapeutic strategies targeting chemoresistance and immunosuppression in triple-negative breast cancer (Abstract 6825)

Lili Yang, PhD (UCLA): Three presentations advancing NKT cell therapy and nanoparticle-mediated disruption of tumor-nerve crosstalk in pancreatic cancer (Abstracts 4316, 153, 6384)

Padmanee Sharma, MD, PhD (MD Anderson): Peripheral immune profiling from the DIET trial in melanoma patients receiving immunotherapy (Abstract 6743)

(Press release, Parker Institute for Cancer Immunotherapy, APR 17, 2026, View Source [SID1234664491])

On April 17, 2026 Pyxis Oncology, Inc. (Nasdaq: PYXS), a clinical-stage company developing next-generation therapeutics for difficult-to-treat cancers, reported that it will present new preclinical data highlighting that a mouse analogue of MICVO (maMICVO) demonstrates anti-tumor activity in a preclinical head and neck squamous cell carcinoma (HNSCC) model as monotherapy, and synergistic anti-tumor activity in combination with anti-mouse PD-1. These data will be presented in a poster session at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 in San Diego, California, held April 17 – April 22, 2026.

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"These new preclinical data are particularly compelling as they further reinforce MICVO’s clinical development in HNSCC, both as a novel monotherapy treatment and in combination with anti-PD-1," said Tom Civik, Interim Chief Executive Officer and Director of Pyxis Oncology. "An important finding from the data is that combination treatment with maMICVO and anti-mouse PD-1 demonstrated synergistic anti-tumor activity and greater tumor control than either treatment alone in an immunotherapy-refractory preclinical HNSCC model, highlighting MICVO’s novel three-pronged mechanism of action and its potential to meaningfully enhance response to immunotherapy. Following our mid-year 2026 MICVO Phase 1 monotherapy update in 2L+ R/M HNSCC, we look forward to sharing updated data from the ongoing Phase 1/2 combination dose escalation study of MICVO in combination with pembrolizumab for 1L/2L+ R/M HNSCC patients in the second half of 2026."

Micvotabart pelidotin (MICVO), is a first-in-concept antibody drug conjugate (ADC) that targets extradomain-B of fibronectin (EDB+FN), a non-cellular structural component of the tumor extracellular matrix (ECM). MICVO is designed to treat solid tumors through a three-pronged mechanism of action: direct cancer cell killing, bystander effect and immunogenic cell death. MICVO is currently being evaluated as monotherapy in a Phase 1 clinical study in patients with recurrent and metastatic head and neck squamous cell carcinoma (R/M HNSCC) and in combination with Merck’s anti-PD-1 therapy, KEYTRUDA (pembrolizumab), in a Phase 1/2 clinical study in patients with R/M HNSCC and other solid tumors.

Poster Key Highlights:

Monotherapy with maMICVO inhibited tumor outgrowth in MOC2, a syngeneic preclinical model of HNSCC
maMICVO produced dose-dependent inhibition of EDB+FN-expressing MOC2 tumor outgrowth, with 6 mg/kg showing the strongest tumor growth inhibition
Treatment with maMICVO modulated the immune compartment of MOC2 tumors toward a more favorable immune-permissive environment for immunotherapy
Treatment with maMICVO reduced the overall abundance of immune-suppressive regulatory T cells (Tregs) in MOC2 tumors
maMICVO also increased the CD8 T cell-to-Treg ratio and enhanced the abundance of a progenitor exhausted T cell subset that is highly responsive to anti-PD-1 therapy

Combination treatment with maMICVO and anti-mouse PD-1 acted synergistically to produce greater tumor control than either treatment alone
The combination of maMICVO and anti-mouse PD-1 resulted in greater tumor control and tumor growth inhibition than monotherapy with either maMICVO or anti-mouse PD-1
Bliss independence analysis confirmed that maMICVO acted synergistically with anti-mouse PD-1 in a preclinical model unresponsive to anti-mouse PD-1 monotherapy
Poster Information:

Title: Mouse analog of micvotabart pelidotin, an antibody-drug conjugate targeting extradomain-B of fibronectin, demonstrates anti-tumor efficacy in an immunotherapy-refractory syngeneic head and neck squamous cell carcinoma model
Session Title: Antibody Technologies and Platforms 2
Date/Time: April 21, 2026 | 9:00 AM – 12:00 PM PT
Location: Poster Section 11
Poster Board Number: 14
Presentation Number: 4406

This poster presentation will also be available on the Pyxis Oncology website on the Scientific publications page following the event.

(Press release, Pyxis Oncology, APR 17, 2026, View Source [SID1234664507])

On April 17, 2026 Volastra Therapeutics, a clinical-stage oncology company pioneering therapies targeting chromosomal instability (CIN), reported multiple scientific disclosures coinciding with the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, taking place April 17–22 in San Diego, California. The data define an Rb pathway–driven pan-cancer development framework for KIF18A inhibitors and highlight a proprietary p16 IHC biomarker approach designed to translate that strategy clinically, reinforcing Volastra’s leadership in advancing CIN biology into therapeutic opportunity.

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Separate from its AACR (Free AACR Whitepaper) 2026 presentation, Volastra has posted "KIF18A Inhibition as a Therapeutic Strategy in Cancers with Rb Pathway Inactivation" (Andreu et al. DOI: View Source – preprint publication). Drawing on what is believed to be one of the largest datasets of its kind, the work identifies Rb pathway inactivation as the mechanistic basis of response to KIF18A inhibition and establishes a development path that extends well beyond high-grade serous ovarian cancer.

The study includes clinical data from a substantial cohort of 79 heavily pretreated patients with high-grade serous ovarian cancer treated with either of two distinct KIF18A inhibitors, sovilnesib and VLS-1488. The concordance of the biomarker-defined signal across both agents is particularly compelling and argues against a drug-specific observation. Biomarker-positive tumors were distinguished by marked enrichment for objective responses, durable disease control, and longer progression-free survival, yielding a sharp clinical separation from biomarker-negative disease and strongly supporting both the biomarker strategy and prospective clinical development.

These findings reposition KIF18A inhibition from a histology-defined opportunity into a pan-cancer synthetic lethal strategy centered on one of the most commonly disrupted tumor suppressor pathways in human cancer. This creates a credible path across what is estimated to represent approximately 15% of human cancers. Within that biology, Volastra has identified a proprietary p16 IHC biomarker strategy that enriches for response to its KIF18A inhibitors and provides a practical route to clinical translation.

"The data provide a strong scientific rationale for using p16 status to identify patients most likely to benefit from KIF18A inhibition," said David Southwell, Chief Executive Officer of Volastra Therapeutics. "Importantly, this work reframes KIF18A inhibition from a narrow single cancer-type opportunity into a broader pan-cancer strategy grounded in Rb pathway biology. This p16 biomarker approach provides a practical way to translate that insight into clinical development and patient selection."

AACR Poster Highlights Clear Synergy with Taxanes and Other Microtubule-Targeting Agents

Volastra will also present an official AACR (Free AACR Whitepaper) poster titled "Combination of VLS-1488 and taxanes induces anti-tumor synergistic effect in cancer cells" in the Experimental and Molecular Therapeutics, Novel Antitumor Agents 1 Session on April 19 from 2-5PM Pacific Time (PT) (Poster section 17, poster 18). The presentation will highlight preclinical combination data showing clear synergistic activity between KIF18A inhibition and taxanes and other microtubule-targeting agents. These findings support a development strategy that could extend KIF18A inhibitors into earlier lines of therapy, including combination approaches in frontline settings.

"The totality of these data help define both the monotherapy and combination development paths for KIF18A inhibitors," said Samuel F. Bakhoum, M.D., Ph.D., Co-Founder and Chief Scientific Officer of Volastra Therapeutics. "With this new mechanistic understanding of KIF18A inhibitor sensitivity, it is evident that the biomarker data will help us identify patients most likely to benefit from monotherapy, while the combination findings point to a precision-based approach to identify the most rational therapeutic partners for development in earlier line settings."

Separately, Dr. Bakhoum, also an adjunct faculty member at the Geisel School of Medicine at Dartmouth, will chair an AACR (Free AACR Whitepaper) educational session "Chromosomal Instability in Cancer: From Mechanism to Therapy and Clinical Translation" on Saturday, April 18, 2026, in his academic capacity. The session reflects the field’s growing appreciation of CIN as both a driver of aggressive disease and a source of therapeutic vulnerability.

"This momentum underscores the growing recognition of CIN biology and the increasing importance of CIN-directed therapeutic strategies across oncology," Dr. Bakhoum said.

(Press release, Volastra Therapeutics, APR 17, 2026, View Source [SID1234664476])

On April 17, 2026 Agenus Inc. (Nasdaq: AGEN), a leader in immuno-oncology innovation, reported data from an investigator-initiated Phase II trial at Memorial Sloan Kettering Cancer Center, investigating botensilimab (BOT) and balstilimab (BAL) in combination with agenT-797, MiNK’s allo-iNKT cell therapy, ramucirumab and paclitaxel in patients with advanced PD-1 refractory gastroesophageal adenocarcinoma. The data are being presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting, taking place April 17-22, 2026, in San Diego, CA.

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This Phase II trial, which is the first to combine BOT and BAL with agenT-797 in patients with gastroesophageal cancer who progressed after frontline therapy, was designed to explore the role of immune priming and treatment sequencing. Patients received induction with agenT-797 (alone or plus BOT/BAL) followed by the full combination regimen, or initiated the combination without induction, with longitudinal biomarker sampling throughout. In this study (n=17), the regimen delivered a 77% DCR with long-term survival beyond 20 months in a subset, and the induction arm showed meaningful gains in PFS (6.9 vs. 3.5 months; HR 0.19; p=0.015) and OS (9.5 vs. 5.2 months), with 43% of induction-treated patients alive at both 12 and 18 months—underscoring that durability and survival may be the most clinically relevant endpoints in this PD-1 refractory population.

"These findings illustrate the mechanistic synergy of agenT-797 with botensilimab and balstilimab in this PD-1 refractory setting," said Dhan Chand, Ph.D., Vice President of Research at Agenus. "The induction approach promoted significant intratumoral infiltration of T cells and dendritic cells, the formation of organized tertiary lymphoid structures in on-treatment biopsy tissue from a patient with durable benefit, and activation of peripheral CD4 and CD8 T-cell populations. These changes are consistent with immune priming and tumor immune reprogramming, providing a biological rationale for the improved progression-free survival observed with the induction strategy."

Efficacy findings from the Phase II (n=17) study included:

DCR was observed in 77% of all treated patients, and long-term survival beyond 20 months was seen in a subset
Patients who received induction cycle had longer progression-free survival (PFS) than those treated without induction, with median PFS of 6.9 months versus 3.5 months (HR 0.19; p=0.015), supporting the potential importance of immune priming and treatment sequencing.
Median overall survival (OS) was 9.5 months in the induction cohort versus 5.2 months without induction, with 43% of induction-treated patients alive at both 12 and 18 months, compared with 20% and 0%, respectively, in the non-induction cohort.
The study did not meet its primary endpoint of ORR; however, disease control and longer-term survival observed in a subset of patients support further study of this approach.
Correlative analyses showed that treatment with BOT, BAL, and agenT-797 was associated with significant intratumoral T cell and dendritic cell infiltration, the formation of organized tertiary lymphoid structures in on-treatment biopsies from a patient with prolonged benefit, and activation of peripheral CD4 and CD8 T cells.

The safety profile was consistent with the component agents. The most common treatment-emergent adverse events among all patients included fatigue, fever, diarrhea, anorexia, nausea and mucositis. Immune-related adverse events included dermatitis, colitis, gastritis, enteritis, hepatitis and hypothyroidism.

Additional analysis of the full biospecimen dataset is ongoing and is expected to provide further insight into immune mechanisms, optimal sequencing, and potential biomarkers that could help identify patients most likely to benefit.

Presentation Details:

Abstract Title: A phase II study of agenT-797, botensilimab (BOT) and balstilimab (BAL) in PD-1 refractory gastroesophageal cancer (GEC)
Presenter: Samuel L. Cytryn M.D.; Gastrointestinal Medical Oncologist, Memorial Sloan Kettering Cancer Center
Session Name: Phase II and Phase III Clinical Trials
Date/Time: April 20, 2026 | 2:00–5:00 PM PT; 5:00-8:00 PM EDT
Poster Section: 52
Abstract No.: CT166

(Press release, Agenus, APR 17, 2026, View Source [SID1234664492])

On April 17, 2026 Olema Pharmaceuticals, Inc. ("Olema" or "Olema Oncology", Nasdaq: OLMA), a clinical-stage biopharmaceutical company focused on the discovery, development, and commercialization of targeted therapies for breast cancer and beyond, reported new preclinical data for palazestrant, a complete estrogen receptor antagonist (CERAN) and selective estrogen receptor degrader (SERD), alone and in combination with OP-3136, a novel small molecule that potently and selectively inhibits acetyltransferase 6 (KAT6) inhibitor. The data will be presented in two poster presentations at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting taking place April 17-22 in San Diego, California.

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"We are very excited to share, for the first time ever, data that confirm the mechanism by which palazestrant completely blocks estrogen receptor transcription and signaling by recruiting the corepressor protein NCoR1," said David C. Myles, Ph.D., Chief Scientific Officer of Olema Oncology. "Further, the synergistic anti-tumor activity of OP-3136 combined with palazestrant in preclinical models highlights the role that both complete ER antagonism and KAT6 inhibition play in addressing acquired resistance associated with metastatic disease. We are pleased to continue to explore the potential of this combination in our ongoing Phase 1 study of OP-3136 and look forward to announcing top-line data from our Phase 3 OPERA-01 trial of palazestrant monotherapy, which is anticipated this fall."

Poster Presentation Details
Title: Palazestrant directly recruits the corepressor protein NCoR1 in vitro leading to complete antagonism of estrogen receptor alpha
Poster/Abstract: 2950
Session: Experimental and Molecular Therapeutics: Cellular Responses to Anticancer Drugs
Date/Time: April 20, 2026, from 2:00pm-5:00pm PT / 5:00pm-8:00pm ET

Key findings:

Palazestrant completely blocks estrogen-driven transcription and demonstrates robust anti-tumor activity in vitro.
In a split-luciferase assay, palazestrant was shown to fully recruit the corepressor, NCoR1, enabling complete estrogen receptor (ER) antagonism.
In both ESR1 wild-type and mutant models, palazestrant more potently suppressed ER-regulated and cell-cycle genes, including PGR and GREB1, than selective estrogen receptor modulators (SERMs), delivering complete inhibition of tumor cell proliferation without partial agonist effects.

These findings position palazestrant as a differentiated endocrine therapy designed to achieve deeper, more consistent ER pathway suppression in estrogen receptor-positive, human epidermal growth factor receptor 2-negative (ER+/HER2-) breast cancer.

Title: Palazestrant, a CERAN, in combination with OP-3136, a KAT6 inhibitor, synergistically downregulates cell proliferation and metastasis related gene signatures
Poster/Abstract: 2949
Session: Experimental and Molecular Therapeutics: Cellular Responses to Anticancer Drugs
Date/Time: April 20, 2026, from 2:00pm-5:00pm PT / 5:00pm-8:00pm ET

Key findings:

Combining OP-3136 with palazestrant drives synergistic anti-tumor activity in in vivo ER+/HER2- breast cancer models, which is mediated by suppression of cell-cycle and estrogen receptor-driven oncogenic signaling processes.
The combination of OP-3136 plus palazestrant downregulates genes associated with MYC, E2F, and G2M more effectively than either agent alone or OP-3136 in combination with fulvestrant.
Combining OP-3136 with palazestrant or fulvestrant suppresses expression of genes associated with MTORC1 signaling, indicating that targeting KAT6 and ER-alpha can suppress mechanisms of acquired resistance.

These findings provide a strong biological rationale for advancing palazestrant in combination with OP-3136 for the treatment of ER+ metastatic breast cancer.

Copies of these posters will be available on the Publications page of Olema’s website in alignment with the AACR (Free AACR Whitepaper) embargo. Additional information, including abstracts, is available on the AACR (Free AACR Whitepaper) Annual Meeting website.

(Press release, Olema Oncology, APR 17, 2026, View Source [SID1234664508])