On April 10, 2026 Allogene Therapeutics, Inc. (Nasdaq: ALLO), a clinical-stage biotechnology company pioneering the development of allogeneic CAR T (AlloCAR T) products for cancer and autoimmune disease, reported the Company will host a conference call and webcast to review the interim futility analysis from its pivotal, randomized Phase 2 ALPHA3 trial with cemacabtagene ansegedleucel (cema-cel) in first-line (1L) consolidation large B-cell lymphoma (LBCL) on Monday, April 13, 2026.

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The live conference call and webcast will take place at 5:30 a.m. PT / 8:30 a.m. ET. Please use this link to register. The webcast will be made available on the Company’s website at www.allogene.com under the Investors tab in the News and Events section.

(Press release, Allogene, APR 10, 2026, View Source [SID1234664297])

On April 10, 2026 Corcept Therapeutics Incorporated (NASDAQ: CORT), a commercial-stage company engaged in the discovery and development of medications to treat severe endocrinologic, oncologic, metabolic and neurologic disorders by modulating the effects of the hormone cortisol, reported final overall survival data from its pivotal Phase 3 ROSELLA trial of Lifyorli (relacorilant) combined with the chemotherapeutic agent nab-paclitaxel in patients with platinum-resistant ovarian cancer in a late-breaking oral presentation at the Society of Gynecologic Oncology (SGO) 2026 Annual Meeting on Women’s Cancer. The SGO presentation slides can be found here.

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These data were simultaneously published in The Lancet: "Overall survival with relacorilant and nab-paclitaxel in patients with platinum-resistant ovarian cancer (ROSELLA): a phase 3 randomised controlled trial."

Lifyorli plus nab-paclitaxel has now been added to the National Comprehensive Cancer Network Clinical Practice Guidelines in Oncology (NCCN Guidelines) as a preferred regimen for patients with platinum-resistant ovarian cancer. Lifyorli, in combination with nab-paclitaxel, was approved by the U.S. Food and Drug Administration (FDA) in March 2026 for the treatment of adults with platinum-resistant epithelial ovarian, fallopian tube, or primary peritoneal cancer who have received one to three prior systemic treatment regimens, at least one of which included bevacizumab. Lifyorli is the first FDA-approved selective glucocorticoid receptor antagonist (SGRA).

The ROSELLA trial met its dual primary endpoints of overall and progression-free survival, regardless of biomarker status and without an increased safety burden. Patients treated with Lifyorli in addition to nab-paclitaxel chemotherapy experienced a 35 percent reduction in the risk of death compared to patients treated with nab-paclitaxel alone (hazard ratio: 0.65; p-value: 0.0004). Median overall survival was 4.1 months longer for patients who received Lifyorli, compared to patients receiving nab-paclitaxel alone (16.0 v. 11.9 months). Patients who received Lifyorli in addition to nab-paclitaxel also experienced a 30 percent reduction in the risk of disease progression (hazard ratio: 0.70; p-value: 0.0076), as assessed by blinded independent central review compared to patients treated with nab-paclitaxel alone.

The combination of Lifyorli with nab-paclitaxel was well-tolerated. Adverse events in the combination arm were comparable to those in the nab-paclitaxel monotherapy arm. The prescribing information for Lifyorli includes warnings and precautions for neutropenia and severe infections, adrenal insufficiency, exacerbation of conditions treated with glucocorticoids and embryo-fetal toxicity. The most common adverse reactions experienced by more than 20 percent of patients (including laboratory abnormalities) were decreased hemoglobin, decreased neutrophils, fatigue, nausea, diarrhea, decreased platelets, rash, and decreased appetite.

"The safety and efficacy findings from ROSELLA are remarkable," said Alexander B. Olawaiye, M.D., Professor and Vice Chair of Diversity and Inclusion at Magee-Women’s Hospital of the University of Pittsburgh, Principal Investigator in the ROSELLA trial, SGO presenter and Lancet publication author. "They give hope to patients and oncologists now that we have a new preferred regimen in this devastating and difficult-to-treat cancer."

"Patients with platinum-resistant ovarian cancer need more good treatment options. Relacorilant provides one. It significantly extends overall survival, with very little added toxicity," said Domenica Lorusso, M.D., Ph.D., Director of the Gynaecological Oncology Unit at Humanitas Hospital San Pio X in Milan, and Full Professor of Obstetrics and Gynaecology at Humanitas University, Pieve Emanuele, Lancet publication senior author and European Network of Gynaecological Oncological Trial groups (ENGOT) investigator in the ROSELLA trial. "This regimen is firmly positioned as a new standard-of-care treatment for patients in the United States. We anticipate regulatory approval in Europe soon."

"ROSELLA’s positive findings affirm our confidence that selective glucocorticoid receptor (GR) antagonists, such as relacorilant, may help treat any patient whose tumor type expresses the GR," said Bill Guyer, PharmD, Corcept’s Chief Development Officer. "With our recent FDA approval, we are now focused on delivering this therapy to patients and continuing cortisol modulation research in solid tumors that express GR across many different treatment settings. We are grateful for the patients and investigators who make our trials possible."

ROSELLA enrolled 381 patients with platinum-resistant ovarian cancer at sites in the United States, Europe, South Korea, Brazil, Argentina, Canada and Australia. Patients were randomized 1:1 to receive either relacorilant plus nab-paclitaxel or nab-paclitaxel alone. The ROSELLA trial was conducted in collaboration with The GOG Foundation, Inc. (GOG-F) (GOG-3073), the European Network of Gynaecological Oncological Trial groups (ENGOT) (ENGOT-ov72), the Asia-Pacific Gynecologic Oncology Trials Group (APGOT) (APGOT-Ov10), the Latin American Cooperative Oncology Group (LACOG) (LACOG-0223) and the Australia New Zealand Gynaecological Oncology Group (ANZGOG) (ANZGOG-221/2023).

About Ovarian Cancer

Ovarian cancer is the fifth most common cause of cancer death in women. Patients whose disease returns less than six months after receiving platinum-containing therapy have "platinum-resistant" disease. There are few treatment options for these women. Approximately 20,000 women with platinum-resistant disease are candidates to start a new therapy each year in the United States, with at least an equal number in Europe.

About Cortisol’s Role in Oncology

Cortisol plays a role in tumor growth through several mechanisms. It helps solid tumors resist chemotherapy by inhibiting cellular apoptosis — the tumor-killing effect chemotherapy is meant to stimulate. In some cancers, cortisol promotes tumor growth by activating oncogenic signaling in the cells to which it binds. Cortisol also suppresses the body’s immune response, which weakens its ability to fight all diseases, including cancer.

Corcept is developing relacorilant in ovarian, endometrial, cervical, pancreatic and prostate cancers. Relacorilant is proprietary to Corcept and is protected by composition of matter, method of use and other patents. It has been designated an orphan drug by the European Commission (EC) for the treatment of ovarian cancer. Corcept has submitted a Marketing Authorisation Application (MAA) to the European Medicines Agency (EMA) for relacorilant to treat patients with platinum-resistant ovarian cancer.

About Lifyorli

Lifyorli (relacorilant), approved in combination with nab-paclitaxel, is the first U.S. Food and Drug Administration (FDA)-approved selective glucocorticoid receptor antagonist for adults with platinum-resistant ovarian cancer. Lifyorli is an oral medication taken the day before, the day of and the day after treatment with nab-paclitaxel. There is no biomarker requirement for Lifyorli. Lifyorli competitively binds to the glucocorticoid receptor (GR), where it enhances chemotherapy sensitivity by inhibiting cortisol’s suppression of apoptosis – the programmed cell death that chemotherapies such as nab-paclitaxel are meant to cause. Lifyorli does not have any effect at the body’s other steroid receptors.

Corcept is committed to timely patient access for Lifyorli. For questions regarding product availability, please contact Lifyorli Support at 1-85-LIFYORLI (1-855-439-6754).

LIFYORLI Indication & Usage

LIFYORLI is indicated in combination with nab-paclitaxel for the treatment of adults with platinum-resistant epithelial ovarian, fallopian tube, or primary peritoneal cancer who have received 1-3 prior systemic treatment regimens, at least one of which included bevacizumab.

IMPORTANT SAFETY INFORMATION

Contraindications:

LIFYORLI is contraindicated in patients receiving systemic glucocorticoids for lifesaving purposes (e.g., immunosuppression after organ transplantation) because LIFYORLI antagonizes the effect of glucocorticoids.

Warnings and Precautions:

Neutropenia and Severe Infections

LIFYORLI in combination with nab-paclitaxel can cause neutropenia, including febrile neutropenia and severe infections. There was one fatal event of septic shock with febrile neutropenia. Thirty-eight percent of patients initiated granulocyte colony-stimulating factor (G-CSF) during the first or second cycle of therapy.

Monitor complete blood counts prior to each weekly treatment with LIFYORLI in combination with nab-paclitaxel and as clinically indicated. Based on the severity of neutropenia, delay dose, reduce dose or permanently discontinue LIFYORLI in combination with nab-paclitaxel. Consider short-acting G-CSF administration as applicable. Consider the possibility of concurrent adrenal insufficiency, particularly in the setting of serious infection.

Adrenal Insufficiency

LIFYORLI is a reversible glucocorticoid receptor antagonist and can cause adrenal insufficiency. Adrenal insufficiency can occur at any time during treatment with LIFYORLI. The risk of adrenal insufficiency is increased in situations of stress, such as acute illness, infection, or surgery. Consider whether supplemental glucocorticoids are required in the perioperative period in patients who have received LIFYORLI within 30 days of surgery. Monitor patients receiving LIFYORLI for signs and symptoms of adrenal insufficiency. Withhold LIFYORLI and administer glucocorticoid therapy if adrenal insufficiency is suspected. High doses of supplemental glucocorticoids may be needed to overcome the glucocorticoid receptor antagonism produced by LIFYORLI. After resolution of adrenal insufficiency, resume previous dose, reduce dose or permanently discontinue LIFYORLI based on severity.

Exacerbation of Conditions Treated with Glucocorticoids

Use of LIFYORLI in patients taking systemic glucocorticoids for other conditions (e.g., autoimmune disorders) may exacerbate these conditions. LIFYORLI is a glucocorticoid receptor antagonist that may make systemic glucocorticoids less effective. Similarly, coadministration of systemic glucocorticoids may make LIFYORLI less effective. Monitor patients for reduced effectiveness of LIFYORLI and glucocorticoids in patients receiving both.

Embryo-Fetal Toxicity

LIFYORLI can cause fetal harm when administered to a pregnant woman. Advise pregnant women of the potential risk to a fetus. Verify pregnancy status of females of reproductive potential prior to initiating LIFYORLI treatment. Advise females of reproductive potential, including male patients with female partners of reproductive potential, to use effective contraception during treatment with LIFYORLI and for 1 week after the last dose.

Adverse Reactions:

Serious adverse reactions occurred in 35% of patients who received LIFYORLI in combination with nab-paclitaxel. Serious adverse reactions (≥2%) in patients were neutropenia (4%), pneumonia (3.2%), pleural effusion (3.2%), febrile neutropenia (2.1%), and fatigue (2.1%). Fatal adverse reactions (2.1%) in patients were septic shock (0.5%), cardiac arrest (0.5%), ischemic stroke (0.5%), and intestinal perforation (0.5%).

Permanent discontinuation of LIFYORLI in combination with nab-paclitaxel due to adverse reactions occurred in 9% of patients. The adverse reaction (>2%) that resulted in permanent discontinuation of LIFYORLI in patients was intestinal obstruction (2.6%). Dosage interruptions of LIFYORLI due to an adverse reaction occurred in 72% of patients. Adverse reactions (≥5%) that required dosage interruptions of LIFYORLI in combination with nab-paclitaxel in patients included neutropenia (44%), anemia (12%), and fatigue (7%). Adverse reactions requiring dose reductions of LIFYORLI included fatigue (1.6%), decreased appetite (1.2%), abdominal pain (0.5%), neutropenia (0.5%), edema (0.5%), and sciatica (0.5%). LIFYORLI should be interrupted or discontinued when nab-paclitaxel is interrupted or discontinued.

The most common adverse reactions (>20%) of patients treated with LIFYORLI plus nab-paclitaxel, including laboratory abnormalities, were decreased hemoglobin, decreased neutrophils, fatigue, nausea, diarrhea, decreased platelets, rash, and decreased appetite.

Drug Interactions:

Strong CYP3A Inducers: Avoid coadministration of LIFYORLI plus nab-paclitaxel with strong CYP3A inducers. Both relacorilant and paclitaxel are CYP3A substrates. Coadministration of strong CYP3A inducers can decrease concentrations of relacorilant and paclitaxel, which may reduce their effectiveness.
CYP2C8 and Moderate CYP3A Inducers: Monitor for reduced effectiveness of LIFYORLI plus nab-paclitaxel with CYP2C8 inducers and moderate CYP3A inducers. Paclitaxel is a substrate of CYP2C8 and CYP3A, and relacorilant is a CYP3A substrate. Coadministration of CYP2C8 and moderate CYP3A inducers can decrease concentrations of paclitaxel and relacorilant, which may reduce their effectiveness.
CYP2C8 Inhibitors: Monitor for increased adverse reactions and modify the dosage for adverse reactions as recommended. Paclitaxel is a substrate of CYP2C8. Coadministration of CYP2C8 inhibitors may increase concentrations of paclitaxel, which may increase the risk of adverse reactions.
CYP3A Substrates: Avoid concomitant use unless otherwise recommended in the Prescribing Information for CYP3A substrates. Relacorilant is a strong CYP3A inhibitor. Relacorilant increases exposure of CYP3A substrates which may increase the risk for adverse reactions related to these substrates.
Certain CYP2C8 Substrates: Avoid concomitant use unless otherwise recommended in the Prescribing Information for CYP2C8 substrates where minimal concentration changes may lead to reduced effectiveness. Relacorilant is a weak CYP2C8 inducer. Relacorilant decreases exposure of CYP2C8 substrates which may decrease the effectiveness related to these substrates.
Use in Specific Populations:

Lactation: Advise women not to breastfeed during treatment with LIFYORLI and for 1 week after the last dose.
Geriatric Use: A higher incidence of grade 3-4 adverse events and dosage modification occurred in patients aged ≥65 years compared to younger adult patients.
Hepatic Impairment: Avoid LIFYORLI in combination with nab-paclitaxel in patients with moderate or severe hepatic impairment (total bilirubin >1.5 to 10x ULN and any AST).
Please see the full Prescribing Information for additional Important Safety Information.

(Press release, Corcept Therapeutics, APR 10, 2026, https://ir.corcept.com/news-releases/news-release-details/corcept-presents-complete-data-pivotal-rosella-trial-sgo-late [SID1234664298])

On April 9, 2026 HUTCHMED (China) Limited ("HUTCHMED") (Nasdaq/AIM:HCM; HKEX:13) reported that new and updated data from several studies of compounds discovered by HUTCHMED will be presented at the upcoming American Association of Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, taking place on April 17-22, 2026 in San Diego, California.

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Preclinical data for HMPL-A580, a first-in-class PI3K/PIKK-EGFR Antibody-Targeted Therapy Conjugate ("ATTC") will be presented. The payload of HMPL-A580 potently inhibited PI3K and PIKK family kinases, with IC50 ranging around 1 to 10 nM. Eurofins profiling across 418 kinases revealed the payload has excellent selectivity. By conjugating this potent payload with an anti-EGFR antibody via a cleavable linker, the ATTC compound HMPL-A580 demonstrated robust anti-tumor effect. Upon binding to EGFR-expression cancer cell line, HMPL-A580 underwent rapid internalization, lysosomal trafficking, payload release, and PAM and PIKK signaling inhibition to induce tumor cell apoptosis. In a 38-human solid tumor cell line panel, HMPL-A580 potently inhibited EGFR-expression tumor cell proliferation. The tumor cells harboring EGFR high expression, EGFR mut or PAM alterations were more sensitive to HMPL-A580. HMPL-A580 showed a strong bystander effect when EGFR-negative cells co-cultured with EGFR-expression cells. In human tumor xenograft models in mice, HMPL-A580, administered intravenously at 1~10 mg/kg once weekly for two weeks, demonstrated a dose / exposure-dependent anti-tumor activity in multiple EGFR-expression models, which is associated with much stronger target inhibition and suppression of downstream functions than antibody and payload alone treatment. The preliminary results demonstrated that HMPL-A580 was stable in human, monkey, rat and mouse plasma, and showed favorable PK property in cynomolgus monkeys.

Updated results from a multicenter, single-arm Phase Ib/II trial of surufatinib plus sintilimab and capecitabine in previously treated metastatic small bowel adenocarcinoma and appendiceal carcinoma, as well as results from a exploratory Phase II study of surufatinib combined with gemcitabine and nab-paclitaxel ("AG") for the treatment of locally advanced or metastatic pancreatic ductal adenocarcinoma patients following AG induction therapy will also be presented.

Details of the presentations are as follows:

Abstract title

Presenter / Lead author

Presentation details

SPONSORED STUDIES

Discovery of HMPL-A580, a first-in-class antibody-targeted therapy conjugate (ATTC) of a novel PI3K/PIKK inhibitor payload linked to an anti-EGFR antibody

Yu Cai, HUTCHMED, Shanghai, China

4549

Poster Session (PO.ET01.03)

Tuesday, April 21, 2026

INVESTIGATOR-INITIATED STUDIES

Updated multicenter phase Ib/II analysis of surufatinib plus sintilimab and capecitabine in previously treated metastatic small bowel adenocarcinoma and appendiceal carcinoma

Xiaoyu Xie, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China

CT160

Poster Session (PO.CT01.05)

Monday, April 20, 2026

Sequential treatment with surufatinib combined with gemcitabine and nab-paclitaxel (AG) or AG alone as first-line therapy for locally advanced or metastatic pancreatic ductal adenocarcinoma (mPDAC) after 6 weeks of AG induction therapy: A two-cohort, exploratory phase II study

Jin Xu, Fudan University Shanghai Cancer Center, Shanghai, China

CT146

Poster Session (PO.CT01.05)

Monday, April 20, 2026

About the ATTC Platform and HMPL-A580

HUTCHMED’s ATTC platform represents a next-generation approach to precision oncology, combining monoclonal antibodies with proprietary small-molecule inhibitor payloads to deliver dual mechanisms of action. Unlike traditional cytotoxin-based Antibody Drug Conjugates, ATTCs combine targeted therapies to achieve synergistic anti-tumor activity and durable responses in preclinical models, outperforming standalone antibody or small-molecule inhibitor components in efficacy and safety.

The first family of ATTCs are based on a novel payload that targets the PI3K/AKT/mTOR ("PAM") pathway, a critical intracellular network involved in cell growth, survival, and division. Alterations in the PAM pathway are frequently associated with poor prognosis and resistance to treatment across various cancers. However, existing PAM-targeted drugs face significant challenges, including on-target toxicities that restrict dosing, feedback loops that enable pathway reactivation, and insufficient tumor-specific delivery. Preclinical data from the first ATTC candidate based on this potent novel PI3K/PIKK inhibitor payload, HMPL-A251, was presented at AACR (Free AACR Whitepaper)-NCI-EORTC in October 2025.

HMPL-A580 is the second ATTC candidate based on this novel payload. It is a first-in-class ATTC comprising a highly selective and potent PI3K/PIKK small-molecule inhibitor payload linked to an anti-EGFR antibody via a cleavable linker. EGFR is highly expressed in multiple types of solid tumors and is well recognized as a driving force in tumorigenesis and disease progression. By conjugating this highly novel PI3K/PIKK payload to an anti-EGFR antibody, HMPL-A580 is designed to deliver targeted pathway inhibition directly into EGFR-expressing tumor cells, thereby potentially overcoming the systemic toxicity and narrow therapeutic index historically associated with PI3K/PIKK inhibitors. This approach aims to achieve deeper and more durable target inhibition while improving the overall tolerability profile.

HUTCHMED has demonstrated how its partnerships leverage the expertise of multinational pharmaceutical companies to accelerate bringing novel medicines to address large unmet needs around the world, and plans to apply this strategy to its ATTC technology this year.

About Surufatinib

Surufatinib is a novel, oral angio-immuno kinase inhibitor that selectively inhibits the tyrosine kinase activity associated with VEGFRs and fibroblast growth factor receptor (FGFR), which both inhibit angiogenesis, and colony stimulating factor-1 receptor (CSF-1R), which regulates tumor-associated macrophages, promoting the body’s immune response against tumor cells. Surufatinib is marketed in China by HUTCHMED under the brand name SULANDA. HUTCHMED currently retains all rights to surufatinib worldwide.

(Press release, Hutchison China MediTech, APR 9, 2026, View Source [SID1234664267])

On April 9, 2026 BostonGene, a developer of the leading AI foundation model for tumor and immune biology, reported that 13 abstracts have been selected for presentation at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, held from April 17 – 22, at the San Diego Convention Center in San Diego, CA. BostonGene will be exhibiting at booth #4613.

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BostonGene will demonstrate how its leading AI foundation model for tumor and immune biology is redefining the drug development lifecycle by providing biopharma partners with a biologically grounded roadmap from early discovery through late-stage clinical trials. Integrating genomic, transcriptomic, and spatial insights, BostonGene’s presentations highlight a sophisticated suite of AI-driven capabilities designed to accelerate and de-risk the pharmaceutical pipeline. Key research includes the use of ReadyScore and Lymphly for precision patient stratification and target identification, RNA-aware diffusion models to predict drug-induced tissue dynamics, and AI-based image batch correction to ensure trial data integrity by focusing on true biologic signals. Furthermore, in collaboration with leading institutions, BostonGene will showcase how longitudinal multiomic profiling identifies actionable biomarkers and resistance pathways often missed by traditional methods.

Details of BostonGene’s presentations at AACR (Free AACR Whitepaper) are below:

Oral presentation
Session: CT012
Title: A phase 2 single-arm open-label trial evaluating zanidatamab in patients with early-stage HER2-positive breast cancer: The NeoZanHER study
Date & time: April 18 | 12:50 PM – 1:00 PM
Presenter: Funda Meric-Bernstam, MD, UT MD Anderson

BostonGene’s integrated whole exome sequencing (WES) and RNA-seq platform was applied to uncover markers of response to HER2-targeting zanidatamab in a small cohort of patients with early-stage HER2-positive breast cancer. Early findings revealed high efficacy and manageable safety profile in select patients, underscoring the feasibility of de-escalating to HER2-targeted therapy alone for this cancer.

Research done in collaboration with UT MD Anderson

Poster presentations
Poster: 114
Title: Unraveling tumor- and tissue-specific gene expression patterns from plasma-derived cfRNA
Date & time: Sunday, April 19 | 2:00 PM – 5:00 PM
Presenter: Desiree Schenk, BostonGene

BostonGene explored the utility of minimally invasive plasma-derived cell-free RNA (cfRNA) profiling for deconvolving tumor- and tissue-specific signals from a single blood draw. We uncovered tumor- and tissue-specific expression patterns in cfRNA that correlated with donor health or cancer status. Our findings support cfRNA signatures as a clinically relevant resource for optimizing patient stratification, trial design, discovery of novel drug targets and plasma-based biomarkers, and disease and treatment response monitoring.

Poster: 0452
Title: Therapeutic potential of AURKA inhibition in ER+ inflammatory breast cancer
Date & time: April 19 | 2:00 PM – 5:00 PM
Presenter: Surbhi Shivhare, PhD, UT MD Anderson

Applying BostonGene’s Tumor PortraitTM to analyze samples from ER+ inflammatory breast cancer (IBC) tumors, researchers at MD Anderson discovered amplified AURKA expression and an inverse relationship between AURKA and SMARCA4 expression. These findings suggest SMARCA4 as a putative synthetic lethality partner of AURKA, where therapeutic targeting of both could lead to cell death. BostonGene’s Tumor PortraitTM integrated genomic and transcriptomic data with clinical data to generate biologically grounded, actionable insights.

Research done in collaboration with UT MD Anderson

Poster: 2437
Title: A comparative scoring framework for BCMA-, GPRC5D- and CD38-targeted therapies in multiple myeloma
Date & time: Monday, April 20 | 9:00 AM – 12:00 PM
Presenter: Konstantin Chernyshov, PhD, BostonGene

BostonGene leveraged ReadyScore, a proprietary, next-generation sequencing-based scoring framework for BCMA-, GPRC5D-, and CD38-targeted therapies in multiple myeloma. This molecular stratification tool integrates tumor and microenvironment features to provide a comprehensive readiness profile to predict CAR-T response, T-cell engagers and monoclonal antibodies. By highlighting target readiness and treatment resistance pathways, the framework enables more precise biomarker-driven patient selection, informs therapeutic prioritization, and offers potential utility for optimizing trial design and translational decision-making.

Poster: 1451
Title: Visualizing the genotype–phenotype link: Predicting drug-induced tissue dynamics with RNA-based diffusion models
Date & time: Monday, April 20 | 9:00 AM – 12:00 PM
Presenter: Alexander Bagaev, PhD, BostonGene

BostonGene presents an RNA-aware diffusion model that predicts tissue morphology from gene expression to better understand genotype–phenotype relationships in cancer. The model integrates RNA embeddings from over 20,000 genes with histological image generation, trained on extensive paired RNA and H&E datasets. It produced realistic tissue images and successfully simulated drug-induced gene expression changes, capturing biologically meaningful tissue dynamics such as tertiary lymphoid structures and B-cell signatures. The approach helps predict how drugs affect tissue architecture, improving drug candidate selection, guiding early trial design, and reducing risks in drug development.

Poster: 3877
Title: Integrative application of Lymphly reveals shared molecular landscape across B-cell lymphomas
Date & time: Monday, April 20 | 2:00 PM – 5:00 PM
Presenter: Konstantin Chernyshov, PhD, BostonGene

BostonGene applied Lymphly, a unique, stable genetic classification framework for diffuse large B-cell lymphoma (DLBCL). When applied to ~3,500 samples, it uncovered previously unrecognized molecular relationships between DLBCL subtypes and other B-cell lymphomas. The analysis identified distinct subtype–disease links and shared genetic patterns, improving understanding of how lymphomas may transform into DLBCL and highlighting potential therapeutic targets across the B-cell lymphoma landscape.

Poster: 1468
Title: Germline whole exome sequencing implicates homologous recombination repair pathway genes as risk factors in SMARCB1 deficient renal medullary phenotypes without sickle hemoglobinopathies
Date & time: April 20 | 9:00 AM – 12:00 PM
Presenter: Pankaj Kumar Chauhan, PhD, UT MD Anderson

BostonGene’s genomic analysis explored two rare and aggressive kidney cancers: renal medullary carcinoma (RMC) and renal cell carcinoma with medullary phenotype (RCCU-MP). The study found that while both cancers showed similar immune-rich tumor environments, distinct genomic alterations were present in RCCU-MP that were absent in RMC. These results point to new genetic risk factors in RCCU-MP and support broader germline testing for patients with RCCU-MP.

Research done in collaboration with UT MD Anderson

Poster: 3763
Title: CCR7 expression and spatial distribution in inflammatory breast cancer: A baseline characterization for therapeutic targeting
Date & time: April 20 | 2:00 PM – 5:00 PM
Presenter: Surbhi Shivhare, PhD, UT MD Anderson

In collaboration with The University of Texas MD Anderson Cancer Center, BostonGene applied its multimodal molecular profiling platform to advance target discovery in inflammatory breast cancer. By integrating genomic, transcriptomic, and spatial data, BostonGene uncovered key biological features of CCR7 that support its therapeutic relevance. This work highlights BostonGene’s ability to generate clinically actionable insights to prioritize targets, refine patient selection strategies, and accelerate oncology drug development.

Research done in collaboration with UT MD Anderson

Poster: 5251
Title: Precise description of metabolomic states using NGS uncover new potential biomarkers of response to TKIs in ccRCC
Date & time: Tuesday, April 21 | 9:00 AM – 12:00 PM
Presenter: Nikita Kotlov, PhD, BostonGene

BostonGene developed specific metabolic gene signatures to inform prediction of tyrosine kinase inhibitor (TKI) response in patients with clear cell renal cell carcinoma (ccRCC). Our refined metabolic signatures uniquely integrate transcriptomic and metabolic data to reveal strong associations with TKI response, overall survival and tumor microenvironment subtypes, representing potent candidate biomarkers for early-phase clinical trial design and patient stratification aimed at overcoming TKI resistance.

Poster: 4164
Title: Implementation of a diffusion-based color checker for histological image batch correction
Date & time: Tuesday, April 21 | 9:00 AM – 12:00 PM
Presenter: Alexander Bagaev, PhD, BostonGene

BostonGene will present a novel AI-powered tool to enhance histological image analysis through batch correction. Leveraging stable diffusion models, the tool standardizes whole slide images collected on different scanners by mitigating technical variations and artifacts. The diffusion-based framework optimizes AI-driven image analysis workflows, offering a scalable solution for harmonizing large multi-site histological datasets.

Poster: 5421
Title: Determining the benefit of comprehensive molecular testing in advanced cancers: BostonGene and Exigent Genomic INsight (BEGIN) study
Date & time: Tuesday, April 21 | 9:00 AM – 12:00 PM
Presenter: Sibel Blau, MD, Northwest Medical Specialties

The BEGIN study, a collaboration between BostonGene and the Exigent Research Network, evaluated integrated DNA/RNA genomic profiling in community oncology practices. Among patients with advanced cancers, 93% had actionable findings, with many identified through RNA sequencing only. Comprehensive results influenced treatment decisions, including matching patients to standard of care and ongoing trial options, highlighting the patient-level impact of combined DNA/RNA testing in expanding precision oncology options in community settings.

Research done in collaboration with Exigent Research Network Investigators

Poster: CT277
Title: IvoLoC trial: A phase II trial evaluating the efficacy of ivonescimab in metastatic endocrine refractory HR-positive HER2-negative or triple negative invasive lobular carcinoma (ILC)
Date & time: Tuesday, April 21 | 2:00 PM – 5:00 PM
Presenter: Jason Mouabbi, MD, UT MD Anderson

In an ongoing clinical trial with MD Anderson Cancer Center, BostonGene performed multimodal longitudinal blood and tissue analysis of metastatic invasive lobular carcinoma patients receiving the bispecific antibody targeting PD-1 and VEGF, ivonescimab. Beyond efficacy and durability, this study evaluated the molecular correlates linking clinical outcomes with tumor microenvironment subtypes while assessing circulating tumor DNA dynamics, biomarkers of response and resistance, and predictive responder scores.

Research done in collaboration with UT MD Anderson

Poster: 7935
Title: Multimodal immunotherapy remodels the tumor microenvironment in hepatocellular carcinoma: Integrative spatial and transcriptomic profiling from a Phase II trial
Date & time: April 22 | 9:00 AM – 12:00 PM
Presenter: Lionel Aurelien Kankeu Fonkoua, MD, Mayo Clinic Cancer Center

BostonGene’s spatial and transcriptomic analysis was used in a Phase II trial to show that combining radiotherapy, dendritic cell vaccination, PD-L1 blockade, and VEGF inhibition could reshape the tumor environment in hepatocellular carcinoma (HCC). This multimodal approach helped turn immune-resistant "cold" tumors into immune-active states, improving T-cell responses and vascular health. The findings highlight promising strategies to overcome treatment resistance in HCC and reinforce BostonGene’s role in advancing precision immunotherapy.

Research done in collaboration with Mayo Clinic

The abstracts will be published in an online-only Proceedings supplement to the AACR (Free AACR Whitepaper) journal Cancer Research.

(Press release, BostonGene, APR 9, 2026, View Source [SID1234664283])

On April 9, 2026 Tempus AI, Inc. (NASDAQ: TEM), a technology company leading the adoption of AI to advance precision medicine, reported an expanded, multi-year collaboration with Gilead Sciences, Inc. (Nasdaq: GILD) aimed at building and advancing Gilead’s oncology pipeline.

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To date, Gilead has leveraged Tempus’ extensive repository of de-identified multimodal data to inform a range of oncology R&D initiatives, including trial design, indication selection, biomarker strategy, health outcomes analysis and clinical real world evidence. The expanded agreement provides Gilead with enterprise-wide access to Tempus’ AI-driven Lens platform, unlocking access to broader datasets across multiple indications and integrating dedicated Tempus analytical services.

"We are excited to announce this expanded partnership with Tempus that reflects our shared priority of putting patients at the heart of innovation," said Patrick Loerch, SVP of Clinical Data Science at Gilead Sciences. "By combining Gilead’s scientific expertise with Tempus’ real world data insights in oncology, we aim to maximize generation of key insights to help inform clinical decision making and ultimately improve care for cancer patients."

"By providing access to the Tempus multimodal data library, we are empowering the Gilead team to further fuel its R&D engine with AI-driven insights," said Ryan Fukushima, CEO of Tempus Data & Apps. "We are thrilled to expand this collaboration, offering the multimodal depth necessary to uncover critical biological insights. This approach helps navigate billions of data points to find the ‘signal in the noise,’ ultimately increasing the probability of success for life-altering medicines."

(Press release, Tempus, APR 9, 2026, View Source [SID1234664284])