The decision to centre emerging investigators rather than established luminaries is itself a statement about how science should evolve. The authors argue that researchers early in their careers are uniquely positioned to challenge prevailing assumptions, adopt interdisciplinary approaches and redirect priorities that may have calcified over decades. The resulting collection of perspectives spans an unusually wide technical range, from neoadjuvant immunotherapy in colorectal cancer to somatic mosaicism in healthy tissues, from the nervous system’s role in tumour progression to artificial intelligence models that predict cellular responses to genetic perturbation. Together, the six contributions sketch a research agenda that is more integrated, more prevention-focused and more computationally ambitious than anything the field has attempted before.

One thread running through the article is the remarkable maturation of cancer immunotherapy, particularly when treatment is moved earlier in the disease course. Myriam Chalabi, a medical oncologist and physician scientist at the Netherlands Cancer Institute in Amsterdam, has built her research programme around immunotherapy delivered in the neoadjuvant setting, using novel treatment combinations within innovative trial designs. The clinical evidence underpinning this shift is striking: recent work has demonstrated neoadjuvant immunotherapy in mismatch-repair-proficient colon cancers, while separate research has shown that non-operative management of mismatch repair deficient tumours can produce durable responses, in some cases allowing patients with rectal cancer to avoid surgery entirely. These results suggest that the immune system, when engaged before a tumour has been removed, can eliminate disease that conventional staging would consider established, and they raise the prospect of organ-preserving treatment as a realistic goal rather than an aspirational one.

Yet immunotherapy has also exposed the limits of tumour-centric thinking, and several of the authors argue that the next 25 years must focus on the host as much as the tumour. James L. Reading, an associate professor of cancer immunology at UCL who leads the Pre-cancer Immunology Laboratory, studies T cell-driven cancer interception — the idea of detecting and eliminating tumours before they become clinically invasive. His work builds on the discovery that reservoirs of stem-like CD8-positive T cells in tumour-draining lymph nodes sustain ongoing antitumor immune responses, and that conventional type I dendritic cells maintain pools of proliferative, tumour-antigen-specific TCF1-positive CD8-positive T cells in those same nodes. Understanding how these immune reservoirs are established and maintained during pre-invasive disease, he argues, could transform early detection from passive imaging into active, immune-guided interception, catching malignancy at a stage when cure rates approach certainty.

The genomic dimension of this preventive agenda is developed most fully by Tim H. H. Coorens, a group leader at the European Bioinformatics Institute who studies how somatic mutations accumulate in normal cells. Twenty-five years ago, cancer genomes were largely studied in isolation from the tissues that produced them. Today, it is clear that essentially every cell in the body accrues mutations over a lifetime, and that clones of mutant cells — some harmless, some pre-malignant — expand and compete in otherwise healthy tissue. Coorens contributed to the Somatic Mosaicism Across Human Tissues network, an effort to catalogue this variation systematically, and recent analyses have shown that age itself can distinguish selective clonal expansion from simple mutational causation in cancer genomes. Meanwhile, the real-world clinical utility of tumour whole-genome sequencing in solid cancers has now been demonstrated at scale, suggesting that comprehensive genomic profiling is moving from research luxury to standard of care. The conceptual shift is profound: cancer becomes not a foreign invader but one possible endpoint of a lifelong evolutionary process, and the levers for prevention may lie in the dynamics of normal tissue.

Perhaps the most visually striking frontier is cancer neuroscience. Leanne Li, a group leader at the Francis Crick Institute in London, combines cancer genetics with neurotechnologies to decipher the logic of interactions between tumours and the nervous system in mouse models. The field’s roots reach back more than a century to observations of nerves within tumours made using methylene blue vital staining, but modern cancer neuroscience has exploded in the past decade. Recent single-neuron sequencing has revealed how individual neurons are reprogrammed by pancreatic cancer, and comprehensive reviews have mapped the past, present and future of the discipline. Li also leads InteroCANCEption, a multidisciplinary team funded by Cancer Grand Challenges to tackle the broader question of how interoception — the body’s sensing and regulation of its own internal signals, a concept elaborated in modern neuroscience — shapes tumour initiation, growth and response to therapy. If tumours co-opt neural circuitry the way they co-opt blood vessels, then neuromodulatory drugs already approved for other conditions could become unexpected additions to the oncology arsenal.

Resistance to therapy, the stubborn core of cancer mortality, is the focus of Shensi Shen, associate professor at West China Hospital, Sichuan University. His work centres on drug-tolerant persister cells — a subpopulation of cancer cells that survives initial treatment not through genetic mutation but through reversible shifts in cell state. Reviews have traced the journey of persister cell biology from basic questions to clinical opportunities, and single-cell analyses have shown that genetically homogeneous cancer cells can diverge into multiple distinct clonal fates when exposed to the same drug. Shen’s particular interest is in layered translational control: the regulation of how messenger RNA is decoded into protein, which allows cancer cells to deploy hidden protein functions and switch states under therapeutic pressure. Because these transitions are non-genetic, they are also potentially reversible, which makes the persister state an attractive target for combination strategies designed to block the escape routes that tumours use to survive targeted therapy and immunotherapy alike.

Underpinning all of these biological questions is a computational revolution, examined by Ewa Szczurek, associate professor at the University of Warsaw and director of the Institute of AI for Health at Helmholtz Munich. Szczurek develops artificial intelligence models for molecular biology and medicine, and her perspective is notably sober about the current state of the field. While foundation models promise to predict how cells respond to genetic and pharmacological perturbations — an ambition exemplified by recent preprint work on state-based prediction of cellular responses — independent evaluations have shown that deep-learning-based gene perturbation effect prediction does not yet outperform simple linear baselines in many settings. Her message is that the next 25 years of AI in cancer research will be defined not by model size but by data quality, experimental validation and careful benchmarking. If the field heeds that warning, machine learning could genuinely accelerate target discovery and personalised treatment; if it does not, hype risks outrunning biology.

Woven together, the six perspectives describe a field in mid-revolution. The tumour-as-isolated-entity model is giving way to a systems view in which cancer is embedded in the evolutionary dynamics of normal tissues, the immune landscape of pre-invasive disease, the neural circuitry of the host body and the non-genetic plasticity of individual cells. Clinical paradigms are shifting in parallel: treatment is moving earlier, surgery is sometimes becoming optional, and molecular residual disease monitoring — exemplified by analyses of adjuvant osimertinib in resected EGFR-mutated lung cancer — is becoming a guide for post-operative decisions. The anniversary article also translates premalignant biology into strategies for intercepting non-small-cell lung cancer, illustrating how laboratory insight can be converted directly into prevention trials.

What emerges most clearly is a demand for interdisciplinarity as a structural principle rather than a slogan. The authors themselves embody it: a clinician designing immunotherapy trials, a bioinformatician decoding mutation accumulation, a neuroscientist engineering tools to interrogate tumour-nerve crosstalk, an immunologist chasing T cells before invasion, a molecular biologist tracking protein-level resistance and a computer scientist stress-testing the field’s newest models. Their collective wager is that the major killers of the next quarter-century will not be defeated by any single breakthrough but by the deliberate integration of genomics, immunology, neuroscience, developmental biology and computation — and by the willingness of a new generation to ask questions their predecessors did not think to ask.

Subject of Research: Emerging investigators' perspectives on the future priorities of cancer research over the next 25 years

Article Title: The next 25 years of cancer research: emerging perspectives and priorities

Article References: Chalabi, M., Coorens, T. H. H., Li, L., Reading, J. L., Shen, S., & Szczurek, E. (2026). The next 25 years of cancer research: emerging perspectives and priorities. Nature Reviews Cancer. https://doi.org/10.1038/s41568-026-00975-3

Image Credits: AI Generated

DOI: 10.1038/s41568-026-00975-3

Keywords: cancer research, Nature Reviews Cancer, immunotherapy, neoadjuvant therapy, somatic mosaicism, cancer neuroscience, cancer interception, drug-tolerant persister cells, tumour heterogeneity, whole-genome sequencing, artificial intelligence, early detection

Thetis cells, a rare subset of immune cells identified by MSK researchers in 2022, play a pivotal role in early life immune education. These cells are essential in teaching the developing immune system to tolerate benign environmental elements such as beneficial gut microbes and common dietary proteins. Timing is of the essence: Thetis cells emerge prominently during the weaning period before their numbers precipitously decline. Despite their critical function, their cellular origin and the molecular cues orchestrating their temporal abundance remained elusive until now.

In a recent study led by Dr. Chrysothemis Brown’s laboratory within the Immuno-Oncology Program at MSK, the lineage of Thetis cells has been meticulously mapped. Researchers identified a precursor cell in the fetal liver dubbed the Thetis-Lymphoid Tissue inducer progenitor (TLP), which bifurcates to produce both Thetis cells and lymphoid tissue inducer (LTi) cells, the latter instrumental in lymph node formation. Notably, these progenitors diminish with age while their differentiation into Thetis cells is contingent upon a critical developmental signal—the molecule RANKL—secreted by specialized stromal cells whose presence coincides with the Thetis cell surge. This intricate temporal coordination defines a “window of opportunity” wherein the immune system is most receptive to programming tolerance. These findings not only elucidate fundamental immune development but also pave the way for targeted interventions to manipulate Thetis cells in preventing autoimmune disorders and food allergies.

Parallel advances by MSK researchers explore the nuanced inflammatory signaling that determines the fate of key immune effectors, natural killer (NK) cells, and CD8+ T lymphocytes. These cells must negotiate the balance between serving as transient frontline combatants and longer-lasting memory guardians essential for protective immunity. The decisive factor lies in the sequence and intensity of signals they receive during immune activation.

In experimental murine models, the team, including Dr. Simon Grassmann under the guidance of senior author Dr. Joseph Sun from the Sloan Kettering Institute, demonstrated that recognition of antigenic fragments before cytokine-mediated inflammatory stimuli engenders epigenetic remodeling conducive to memory formation. Conversely, an early inflammatory cytokine signal biases cells towards terminal effector states, characterized by rapid but short-lived responses. Further refinement occurs depending on antigen recognition strength, where robust engagement favors memory differentiation. This “stepwise model” dissects the paradoxical roles played by inflammatory cytokines and offers a blueprint for optimizing vaccine formulations and immunotherapies by fine-tuning the temporal orchestration of antigen and cytokine exposure.

The third major advance leverages single-nucleus DNA sequencing of pancreatic cancer samples from 24 patients, encompassing 137,000 individual cells—including both primary tumors and metastatic lesions—to reconstruct the clonal evolution of this lethal malignancy. Under the leadership of Dr. Christine Iacobuzio-Donahue and co-first authors Dr. Haochen Zhang and Dr. Palash Sashittal, this study decodes the genomic trajectories that define cancer progression and therapeutic resistance.

One particularly revelatory insight concerns the heterogeneity in reliance on mutant KRAS, a driver gene ubiquitously implicated in pancreatic tumorigenesis. Contrary to prior assumptions of uniformity, some cancer cell subpopulations lose mutant KRAS or activate alternative proliferative pathways. This complexity potentially explains variable clinical responses to KRAS inhibitors and underscores the necessity for precision stratification of patients likely to benefit from these agents.

Another critical observation relates to hereditary BRCA2 mutations. While these defects predispose patients to pancreatic cancer, tumors circumvent genomic instability by sequentially inactivating both gene copies—albeit at variable times. Understanding this timing bears direct clinical significance since it may predict responsiveness to PARP inhibitors and other DNA repair-targeting drugs, guiding treatment decisions in BRCA2-mutant cases.

Additionally, the investigation exposes the multifaceted mechanisms tumors employ to disable TGF-beta signaling, a pathway conventionally acting to restrain malignancy invasiveness and metastasis. Tumors engage diverse molecular routes to abrogate TGF-beta’s tumor-suppressive effects, elucidating why therapies targeting this pathway have yielded disappointing results in clinical trials. This revelation urges a reconsideration of therapeutic strategies and advocates for combination approaches to circumvent adaptive resistance mechanisms.

Collectively, these studies from MSK illuminate critical facets of immunology and cancer biology with profound translational potential. They demonstrate how detailed interrogation of immune cell ontogeny, signaling dynamics, and tumor genomics can unlock strategies to prevent disease or tailor more efficacious therapies. The precision immune modulation approaches inspired by these findings may transform management paradigms not only for autoimmune conditions and allergies but also for immuno-oncology. Simultaneously, insights into pancreatic cancer evolution offer a roadmap to surmount therapeutic resistance and enhance patient outcomes in one of the most recalcitrant cancers.

The synergy of advanced molecular biology techniques, including single-cell and single-nucleus sequencing, and sophisticated computational modeling heralds a new era in biomedical research driven by granular data integration at the cellular level. Continued multidisciplinary exploration promises to refine our understanding of intricate biological systems and translate these discoveries into clinical innovation. These revelations underscore the importance of temporal and spatial context in immune system function and cancer progression, setting the stage for transformative breakthroughs in biomedical science.

Subject of Research: Immune cell differentiation, inflammatory signaling pathways, and pancreatic cancer genomics
Article Title: Emerging Insights into Thetis Cells, Immune Cell Fate Decisions, and Pancreatic Cancer Evolution from Memorial Sloan Kettering Cancer Center
News Publication Date: Not specified
Web References:
– https://www.nature.com/articles/s41586-026-10198-z (Thetis cells)
– https://www.cell.com/immunity/fulltext/S1074-7613(26)00004-X (Immune cell fate)
– https://www.nature.com/articles/s41588-025-02468-9 (Pancreatic cancer evolution)
References: Incorporated within web references
Image Credits: Memorial Sloan Kettering Cancer Center
Keywords: Cancer research, Pancreatic cancer, Immunology, Immune system

Gynecological cancers, particularly those that have recurred or metastasized, remain a major clinical challenge worldwide. Traditional chemotherapy approaches often provide limited benefit and are associated with substantial toxicity. Immunotherapy, by contrast, harnesses the body’s own immune system to combat tumor cells, opening new pathways for durable responses. Cadonilimab, developed as a bispecific antibody targeting both PD-1 and CTLA-4 checkpoints, represents a sophisticated approach to reinvigorate immune surveillance. Its unique dual blockade mechanism potentially overcomes resistance mechanisms observed with single-agent checkpoint inhibitors.

The study retrospectively examined data from 60 patients diagnosed with recurrent or metastatic gynecological malignancies between July 2022 and December 2024. These patients had pathology or cytology-confirmed tumors and received at least two cycles of Cadonilimab, either as monotherapy or combined with chemotherapy or bevacizumab. Notably, the study design reflects real-world clinical practice rather than controlled clinical trial conditions, enabling assessment of Cadonilimab’s performance in a more heterogeneous patient population.

Among patients evaluated for treatment efficacy—56 in total—the findings were striking, especially in those receiving first-line therapy for advanced cervical cancer. This subgroup demonstrated an objective response rate (ORR) of 81.3%, with nearly 94% achieving disease control, including stable disease or better. These figures significantly surpass response rates typically observed with standard therapies, pointing to Cadonilimab’s robust antitumor activity. Meanwhile, second-line patients, often more challenging to treat due to prior therapies and disease progression, achieved an ORR of 36.7% and a disease control rate of 90%, which remains clinically meaningful given the refractory nature of their disease.

Importantly, because this analysis was conducted outside of randomized controlled trial parameters, the lack of a comparator arm does introduce limitations when interpreting efficacy results. Nevertheless, the consistent response rates among different treatment lines and tumor types underscore Cadonilimab’s potential as a versatile therapeutic agent. The real-world setting reflects everyday clinical scenarios, including varying performance status, comorbidities, and prior treatments, all of which may influence outcomes.

Safety is paramount when considering immunotherapeutic agents, which can cause immune-related adverse events (irAEs) due to nonspecific immune activation. In this cohort, 73.2% of patients experienced at least one treatment-related adverse event (TRAE). The most common toxicities included anemia, nausea, and myelosuppression. While a considerable proportion of patients encountered side effects, the majority were manageable. Grade 3-4 TRAEs occurred in 16.1% of patients, a figure aligned with or lower than those reported for other immune checkpoint inhibitors in oncology. Furthermore, no treatment-related deaths were recorded, suggesting that Cadonilimab’s safety profile is acceptable in this patient population.

Immune-related adverse events, specifically those graded 1 to 2, were observed in 19.6% of patients. These events, although generally mild to moderate, require vigilant monitoring and timely management to prevent escalation. The safety outcomes reaffirm that, while Cadonilimab reactivates antitumor immunity effectively, it does so with a toxicity spectrum that oncologists can reasonably control, reducing the risk-benefit concerns associated with aggressive immunomodulation.

The combination strategies involving chemotherapy or bevacizumab are of particular interest. Chemotherapy can modulate the tumor microenvironment and enhance antigen presentation, potentially synergizing with immunotherapy to improve outcomes. Bevacizumab, a monoclonal antibody targeting VEGF, may normalize tumor vasculature and optimize immune cell infiltration. The study’s inclusive regimen approach allowed exploration of Cadonilimab’s compatibility with these agents, revealing promising clinical results without compromising tolerability.

Cervical cancer remains a global health burden, particularly affecting women in low- and middle-income countries. The rapid development and approval of Cadonilimab in China highlight regional advancements in drug innovation responding to this unmet need. This study’s data offer reassurance that Cadonilimab can be safely and effectively integrated into clinical protocols for recurrent or metastatic disease, potentially transforming the therapeutic landscape.

Moreover, the real-world evidence emphasis provides valuable insights that complement findings from controlled clinical trials. Translationally, such data support expanding access and inform guidelines, especially in diverse healthcare settings where patients often differ from those enrolled in trials. The study advocates for Cadonilimab’s role as an important addition to the gynecological oncology armamentarium, bridging gaps between clinical research and practice.

Looking forward, ongoing investigations will need to address long-term outcomes such as overall survival and quality of life, parameters not fully captured in this retrospective review. Similarly, identification of biomarkers predicting response or resistance to Cadonilimab could further personalize therapy, maximizing benefit while minimizing unnecessary toxicity. Continued pharmacovigilance and post-marketing surveillance will also be critical in understanding rare or late-onset adverse events associated with this novel immunotherapy.

In conclusion, this pivotal real-world study demonstrates that Cadonilimab, alone or in combination with chemotherapy or bevacizumab, exhibits compelling antitumor activity and an acceptable safety profile in patients with advanced gynecological malignancies. The high objective response and disease control rates observed, even in heavily pretreated populations, underscore the promise of dual checkpoint inhibition in this challenging disease subset.

As immunotherapy continues to revolutionize cancer treatment paradigms, Cadonilimab’s swift development and demonstrated efficacy offer substantial hope for improving survival and quality of life among affected women globally. This study paves the way for larger, prospective trials that could ultimately solidify Cadonilimab’s status as a new standard of care in recurrent and metastatic gynecological cancers.

Subject of Research: Clinical evaluation of Cadonilimab’s efficacy and safety in treating advanced recurrent/metastatic gynecological malignancies.

Article Title: Clinical efficacy and safety of Cadonilimab in the treatment of advanced gynecological malignancies: a retrospective, real-world study

Article References: Huang, Y., Zeng, Y., Zhang, C. et al. Clinical efficacy and safety of Cadonilimab in the treatment of advanced gynecological malignancies: a retrospective, real-world study. BMC Cancer 25, 1338 (2025). https://doi.org/10.1186/s12885-025-14603-0

Image Credits: Scienmag.com

DOI: https://doi.org/10.1186/s12885-025-14603-0

CAR-T cell therapy—short for Chimeric Antigen Receptor T-cell therapy—revolutionized cancer treatment by genetically engineering patients’ own T cells to recognize and eliminate cancer cells. While these engineered cells have demonstrated unprecedented success in treating blood cancers like leukemia and lymphoma, solid tumors have remained recalcitrant due to their complex microenvironments and limited accessibility. Overcoming these barriers calls for refined and specialized CAR designs tailored to the unique biology of solid tumors.

The Nagoya team singled out Eva1, a less explored but compelling antigen, given its unusually high expression on lung, pancreatic, and liver tumor cells, alongside relatively sparse distribution on normal tissues. This antigen’s small molecular footprint augurs well for enhanced immune cell engagement. Eva1’s diminutive size enables CAR-T cells to form stronger and more effective immunological synapses—critical junctions where immune cells and their targets physically connect, facilitating superior signaling that boosts T-cell activation and antitumor functions.

Central to their breakthrough was the intricate engineering of the CAR construct itself, focusing on two pivotal aspects: the spacer region and the intracellular domains. The spacer dictates the spatial configuration between the CAR-T cell and the tumor cell during contact, influencing the strength and duration of cell-to-cell interactions. Meanwhile, intracellular signaling domains modulate the activation state, persistence, and cytotoxic potency of the CAR-T cells. By creating sixteen variant CARs featuring combinations of humanized Eva1-binding antibodies, tailored spacer lengths, and distinct intracellular co-stimulatory motifs, the researchers identified ideal configurations that maximized therapeutic impact.

Humanization of the antibody fragment was crucial for clinical translation. Originally derived from mouse antibodies against Eva1, the binding domains were restructured to closely mimic human antibodies, minimizing the risk of adverse immune rejection when administered to patients. This refined design specifically increased affinity and selectivity for Eva1, reducing off-target effects and ensuring that the CAR-T cells preferentially recognize malignant, high-Eva1-expressing tumor cells.

Among the configurations tested, those employing a short spacer combined with co-stimulatory intracellular domains 4-1BB or a dual CD79A/CD40 module stood out. These constructs conferred superior expansion, cytokine secretion, and cytotoxic capabilities upon CAR-T cells, culminating in highly effective elimination of tumors in murine models that mimic human lung and pancreatic cancers. Such preclinical success underscores a potential leap forward in tackling solid tumors, which have been notoriously refractory to existing immunotherapies.

Safety, a paramount concern in CAR-T therapy, was rigorously evaluated given that Eva1 is not completely tumor-specific and is also present in low amounts on normal monocytes, a subset of white blood cells. Encouragingly, the engineered CAR-T cells demonstrated exquisite sensitivity to antigen density, activating robustly only upon encountering cells with high Eva1 expression typical of cancer cells, while largely sparing normal monocytes. This on-target, off-tumor discrimination signifies a promising safety profile, essential to minimize collateral damage and treatment-related toxicities in future clinical applications.

The sophisticated immune synapse formation observed with Eva1CAR-T cells may hold the key to their enhanced efficacy. Due to Eva1’s molecular structure and size, the engineered T cells can establish more intimate and stable physical contacts with cancer cells, reinforcing sustained T-cell receptor signaling, cytokine production, and proliferative responses. These features collectively drive more potent and durable antitumor immunity, overcoming the limitations seen in earlier CAR-T designs targeting bulkier or less accessible antigens.

Dr. Seitaro Terakura, lead investigator from Nagoya University’s Graduate School of Medicine, emphasized the clinical significance of these findings. He noted that the strategy offers a tangible pathway for treating solid tumors that have thus far evaded effective immune-based therapies. Tumors of priority include lung, pancreatic, and liver cancers—malignancies responsible for significant global mortality, often diagnosed at advanced stages with poor prognosis under current therapeutic regimes.

The team is now poised to translate this promising preclinical research into human trials. Before this can occur, thorough safety assessments are underway using mouse models engineered to express mouse Eva1. Developing a murine Eva1-specific CAR-T allows detailed toxicity profiling, verifying that the therapy does not induce deleterious damage to normal tissue expressing basal levels of Eva1. Successful demonstration of safety will pave the way for pivotal clinical trials in patients, moving closer to the ultimate goal of offering a lifesaving intervention.

Looking forward, the researchers plan to collaborate with biotech and pharmaceutical partners to advance clinical development. The optimization framework established here—combining antigen selection, CAR spacer engineering, and intracellular co-stimulatory domain tuning—may also provide a blueprint for developing therapies against other challenging tumor antigens. This modular and rational design paradigm promises to expand the arsenal of effective, safe, and targeted CAR-T cell therapies for solid malignancies.

As this approach transitions from bench to bedside, it promises enormous implications not only for patient outcomes but also for the broader field of cancer immunotherapy. Harnessing the immune system’s power with precision-engineered cellular therapies signals a new dawn where even the most intractable cancers might be conquered with minimal toxicity and maximal clinical benefit.

The success of Eva1-targeting CAR-T cells embodies the fusion of cutting-edge molecular engineering, immunological insight, and translational ambition. It underscores how targeted molecular design can overcome biological hurdles previously thought insurmountable, offering hope for more effective treatments against the world’s deadliest cancers in the near future.

Subject of Research: Animals
Article Title: Development and optimization of Eva1 (MPZL2) targeting chimeric antigen receptor T cells
News Publication Date: 7-May-2025
Web References: Journal for ImmunoTherapy of Cancer, DOI: 10.1136/jitc-2024-009825
Image Credits: Keiko Itano, Nagoya University
Keywords: Cancer immunotherapy, Immune cells, Antibodies, Antigens, Immune response, Cancer cells, Cancer research, Liver cancer, Lung cancer, Pancreatic cancer, Adoptive T cell therapy