Pancreatic cancer remains one of the most lethal malignancies worldwide, with dismal five-year survival rates that have stubbornly resisted improvement despite decades of research. Gemcitabine, a nucleoside analog, has long been employed in treating PDAC, yet its clinical benefit is limited by intrinsic or acquired resistance mechanisms inherent to tumor cells. The molecular underpinnings of this chemoresistance have been a key focus in oncological research, aiming to uncover co-targets that could be modulated to potentiate gemcitabine’s efficacy.

The team led by Ye, W. and colleagues embarked on an in-depth investigation into the intracellular signaling milieu of PDAC cells treated with Derazantinib in combination with gemcitabine. Importantly, Derazantinib functions as an inhibitor of the fibroblast growth factor receptor (FGFR), a family of tyrosine kinase receptors implicated in the pathogenesis and progression of several cancers. In PDAC, aberrant FGFR signaling has been documented to promote oncogenic processes such as cellular proliferation, invasion, and survival, thereby representing a promising therapeutic target.

Through meticulous molecular analyses, the researchers uncovered that treatment with Derazantinib attenuated the activation levels of the NF-κB and MAPK pathways. NF-κB is a pivotal transcription factor orchestrating a broad array of cellular responses, including inflammation, apoptosis avoidance, and proliferation. Its hyperactivation is frequently associated with tumor aggressiveness and poor prognosis in pancreatic cancer. Similarly, the MAPK signaling cascade, which transduces extracellular growth signals into diverse cellular responses, is frequently deregulated in malignancies, facilitating oncogenic transformation and chemoresistance.

By dampening these pro-survival and pro-proliferative pathways, Derazantinib undermines the cellular defenses that PDAC cells typically mount against chemotherapeutic insult. One of the most striking findings from the study is the consequential suppression of MUC5AC expression. MUC5AC is a gel-forming mucin that constitutes a major component of the extracellular mucus barrier, and its overexpression in pancreatic tumors contributes to an environment conducive to tumor growth and metastasis, while simultaneously impairing drug delivery and efficacy.

Notably, the downregulation of MUC5AC serves a dual purpose: it dismantles the physical and biochemical shield that cancer cells exploit, and it simultaneously disrupts the signaling loops that sustain their malignant phenotype. This dual impact is hypothesized to underlie the observed enhancement of gemcitabine’s cytotoxic effects when co-administered with Derazantinib.

The implications of these insights are profound. First, they offer a mechanistic rationale for combining FGFR inhibitors with conventional chemotherapy to overcome resistance barriers in PDAC. Second, they provide a compelling example of the potential to modulate tumor microenvironment factors, such as mucins, to improve drug delivery and response. Finally, they underscore the intricate crosstalk between oncogenic signaling pathways and extracellular matrix components, shedding light on novel angles for therapeutic intervention.

The methodology employed in this study was comprehensive, encompassing both in vitro and in vivo models. PDAC cell lines exposed to the combinatory regimen exhibited significant reductions in cell viability relative to gemcitabine alone, validating the synergistic effect. Moreover, xenograft experiments in murine models confirmed the enhanced tumor growth suppression with Derazantinib and gemcitabine co-treatment. These findings provide strong translational potential for clinical application, highlighting a pathway to increase survival outcomes for PDAC patients.

One of the technical highlights involves the quantification of NF-κB and MAPK pathway activity via Western blot analysis and immunofluorescence staining. The study revealed that phosphorylation events critical to signal transduction were markedly diminished upon Derazantinib treatment. This biochemical attenuation translated into decreased nuclear localization and transcriptional activity of NF-κB, thereby weakening the expression of downstream anti-apoptotic genes.

Furthermore, transcriptomic analyses demonstrated a consistent downregulation of MUC5AC mRNA levels, corroborating the protein expression data and reinforcing the conclusion that Derazantinib exerts a suppressive effect at the transcriptional level. The data also suggest that MUC5AC downregulation may itself feed back to further inhibit the MAPK pathway, indicating a complex interdependence between these molecular players.

The study also addressed potential concerns regarding toxicity and off-target effects. The combined treatment was well-tolerated in preclinical models, with no significant weight loss or organ damage observed, indicating a favorable therapeutic index. This safety profile is crucial when considering the translation into clinical trials, as PDAC patients often suffer from treatment-associated morbidity that limits chemotherapy dosing.

Importantly, this research aligns with the growing paradigm shift towards combination therapies tailored to disrupt multiple facets of tumor biology simultaneously. By specifically targeting both cell-intrinsic signaling mechanisms and extracellular protective factors such as mucins, therapeutic regimens can potentially surmount the multifactorial barriers that have historically curtailed progress in pancreatic cancer treatment.

While the study primarily centers on the interplay between Derazantinib and gemcitabine, it also raises intriguing questions about the broader application of FGFR inhibitors in other mucin-overexpressing tumors, such as certain subtypes of lung and colorectal cancers. The molecular mechanisms delineated here may serve as a blueprint for exploring analogous combinatorial strategies in diverse oncologic contexts.

Looking forward, the translational momentum generated by these findings could catalyze early-phase clinical trials assessing the efficacy of Derazantinib plus gemcitabine in PDAC patients. Biomarker-driven patient stratification, for example based on FGFR expression or MUC5AC levels, may optimize response rates and facilitate precision medicine approaches. Additionally, further exploration into resistance mechanisms against FGFR inhibitors themselves remains warranted.

This seminal contribution by Ye, W. et al. represents a pivotal moment in the endeavor to subvert pancreatic cancer’s formidable defense mechanisms. By illuminating the molecular choreography by which Derazantinib dismantles pro-survival signaling and mucin-mediated protection, their work opens unprecedented avenues to amplify the impact of existing chemotherapy and improve the bleak prognosis associated with this disease.

In sum, this research charts a compelling course towards more effective treatment paradigms in PDAC, marshalling the power of molecular targeted therapies to reshape the future of pancreatic cancer care. With continued scientific momentum, the hope is that these insights will not only extend survival but also enhance the quality of life for countless patients battling this devastating malignancy.

Subject of Research: Enhancement of gemcitabine efficacy in pancreatic ductal adenocarcinoma (PDAC) through modulation of NF-κB and MAPK pathways to reduce MUC5AC expression.

Article Title: Derazantinib enhances gemcitabine efficacy in PDAC by attenuating the NF-κB and MAPK pathways to suppress MUC5AC expression.

Article References:
Ye, W., Huang, Y., Hong, L. et al. Derazantinib enhances gemcitabine efficacy in PDAC by attenuating the NF-κB and MAPK pathways to suppress MUC5AC expression. Med Oncol 43, 107 (2026). https://doi.org/10.1007/s12032-025-03222-1

Image Credits: AI Generated

DOI: https://doi.org/10.1007/s12032-025-03222-1

At the University of Illinois Chicago, a multidisciplinary team consisting of surgeons, anesthesiologists, and engineers is making strides toward improving treatment outcomes for pancreatic cancer patients. Their groundbreaking research focuses on the impact of lidocaine, a widely used local anesthetic, on cancer cells shed into the bloodstream during surgical tumor removal. A recently published study in the journal Lab on a Chip describes novel advances in isolating these circulating tumor cells (CTCs) using innovative microfluidic technologies. This approach offers promising potential in mitigating metastatic spread during the vulnerable perioperative period.

Dr. Gina Votta-Velis, professor of anesthesiology at UIC College of Medicine and a principal investigator on the project, emphasizes the transformative potential of this research. Lidocaine, a mainstay in anesthesia for over six decades primarily for pain relief, may possess unrecognized anti-metastatic properties. Preliminary findings suggest that administering lidocaine intraoperatively could hinder the ability of CTCs to invade new tissues, thereby reducing the risk of cancer metastasis and ultimately enhancing patient prognoses.

In 2018, Dr. Votta-Velis secured funding from the American Society of Regional Anesthesia and Pain Medicine to explore this hypothesis. CTCs are cancer cells that detach from the primary tumor mass during surgery and enter systemic circulation. Their presence is strongly correlated with worse clinical outcomes and higher rates of tumor recurrence. Because these cells are exceedingly rare in blood compared to normal cells, capturing and studying them has remained a significant challenge in oncology.

Typically, patients must recover from surgery before commencing chemotherapy, creating a critical temporal window where CTCs can disseminate and seed secondary tumors. However, early in vitro experiments demonstrate that lidocaine may disrupt the ability of these cells to survive and exit the bloodstream. Instead, the anesthetic appears to facilitate their entrapment and subsequent clearance by immune cells. This innovative concept reframes lidocaine as not only an analgesic but also a potential agent to impede metastatic progression.

“Circulating tumor cells are essentially the seeds from which metastases grow,” explained Dr. Votta-Velis. “Identifying these cells and diminishing their virulence during critical treatment intervals offers an unprecedented approach to curtailing the metastatic cascade, which accounts for the majority of cancer-related deaths.” The implications for extending patient survival and quality of life could be profound.

The rarity and heterogeneity of CTCs present formidable obstacles to accurate isolation and analysis. To overcome the proverbial “needle in a haystack” problem, the UIC team collaborated with Dr. Ian Papautsky, a biomedical engineering professor specializing in microfluidics—the manipulation of tiny fluid volumes through microscale channels. The team developed a novel microfluidic device composed of glass and plastic, measuring just a few inches and containing narrow channels only slightly wider than a human hair. This platform exploits size differences to separate larger, softer cancer cells from smaller blood components, facilitating a gentle, label-free liquid biopsy.

In 2019, Dr. Papautsky’s group demonstrated the device’s remarkable efficacy, achieving 93 percent accuracy in identifying CTCs without damaging them. In the latest work, they compared their microfluidic technique to the widely used EasySep system, which relies on magnetic bead-based cell separation. Unlike magnetic methods that can be harsh and compromise cell integrity, the microfluidic device retrieves significantly more viable cancer cells at greater speed—processing patient blood samples in as little as 20 minutes with an eightfold increase in recovery rate.

“Early and accurate detection of CTCs is indispensable for silent cancers like pancreatic cancer, where routine imaging often fails to identify disease progression,” said Dr. Papautsky. “Our device enables minimally invasive diagnostics, opening the door for personalized treatment strategies that target metastatic mechanisms at their earliest stages.” This technological innovation complements clinical efforts to intercept cancer dissemination before it culminates in full-blown metastasis.

Dr. Pier Giulianotti, co-investigator and chief of general, minimally invasive, and robotic surgery at UIC College of Medicine, echoed the significance of these findings. A globally recognized expert in pancreatic cancer surgeries, he highlighted that most malignant tumors metastasize via the bloodstream. “Understanding how cancer cells enter circulation and developing methods to control this phenomenon is not just important—it is essential to transforming how we manage aggressive cancers,” he stated.

The research team also comprises UIC scholars Celine Macaraniag, Ifra Khan, Alexandra Barabanova, Valentina Valle, and Alain Borgeat, as well as Jian Zhou from Rush University Medical Center. Together, they are forging a multidisciplinary path at the intersection of engineering, anesthesiology, and oncology, paving the way for therapies that could revolutionize pancreatic cancer treatment.

This pioneering effort exemplifies how integration of advanced microfluidic technologies with clinical research can yield transformative insights and novel interventions. While pancreatic cancer remains a formidable adversary, such innovative approaches to intercepting circulating tumor cells offer a glimmer of hope for improving survival rates and patient outcomes in what is often considered a high-mortality disease.

Subject of Research: The interaction of lidocaine with circulating pancreatic cancer cells and advancements in microfluidic isolation techniques.

Article Title: Lidocaine’s Potential to Inhibit Metastasis: Microfluidic Innovations in Pancreatic Cancer Treatment

News Publication Date: Not specified in source content.

Web References:
– U.S. Cancer Statistics: https://seer.cancer.gov/statfacts/html/common.html
– Pancreatic Cancer Survival Rates: https://seer.cancer.gov/statfacts/html/pancreas.html
– American Society of Regional Anesthesia and Pain Medicine: https://asra.com/news-publications/asra-updates/blog-landing/legacy-b-blog-posts/2021/01/29/past-carl-koller-memorial-research-grant-recipients
– Lab on a Chip Article DOI: http://dx.doi.org/10.1039/D5LC00512D
– Microfluidic Cell Separation Accuracy: https://www.nature.com/articles/s41378-019-0045-6

References:
Lab on a Chip, DOI: 10.1039/D5LC00512D

Image Credits: Photo by Sana Sheybanikashani, University of Illinois Chicago

Keywords: Pancreatic cancer, Microfluidics, Circulating tumor cells, Lidocaine, Metastasis, Liquid biopsy, Biomedical engineering, Cancer diagnostics

Pancreatic cancer remains among the deadliest malignancies, with a dismal five-year survival rate hovering around 13%. One reason for this poor prognosis is the cancer’s ability to survive in hostile environments and evade the cytotoxic effects of traditional chemotherapy and radiation. To combat this resilience, Indiana University researchers examined the molecular underpinnings that enable tumor cells to flourish despite aggressive treatments. They zeroed in on Ref-1, a multifunctional protein involved in DNA repair, redox signaling, and cellular response to oxidative stress, hypothesizing that its inhibition could sensitize tumors to therapy.

Intriguingly, the study revealed that another protein, peroxiredoxin-1, operates in tandem with Ref-1 to bolster pancreatic cancer cells’ survival. PRDX1 is an antioxidant enzyme that reduces peroxides, thus protecting cells from oxidative damage. This partnership appears to be a key driver of the cancer’s robust defense system. When researchers selectively knocked down PRDX1 alongside pharmacologically inhibiting Ref-1 with a novel agent called APX2014, the dual attack provoked substantial tumor shrinkage and increased cancer cell death in preclinical models.

The specificity of PRDX1’s role was a surprising finding. Of all the related peroxiredoxins tested, only loss of this protein sensitized tumors significantly to Ref-1 blockade. This suggests a unique and exploitable vulnerability within the pancreatic tumor microenvironment. Mark Kelley, PhD, the lead author of the study and a distinguished pediatric oncology researcher at Indiana University, noted that the combined inhibition of both Ref-1 and PRDX1 outperformed treatments targeting either protein alone. Animal experiments supported this conclusion, showing smaller tumors and enhanced survival outcomes.

The ramifications extend beyond pancreatic cancer. The dual protein inhibition strategy also impacts the tumor microenvironment — the surrounding tissue, immune cells, and extracellular matrix that collectively support tumor growth and spread. By disrupting these interactions, the therapy undermines the cancer’s capacity to adapt and resist treatment, potentially translating into improved clinical responses. This broad efficacy suggests applicability to other aggressive cancers with similar survival pathways.

The innovative drug APX2014, developed by the team, is a potent inhibitor of Ref-1’s redox functions. Ref-1 regulates transcription factors such as NF-κB and HIF-1α, which are essential to cancer cell proliferation and survival under oxidative stress. By blocking Ref-1, APX2014 impairs the tumor’s ability to respond to DNA damage and oxidative insults. Coupling this with PRDX1 suppression amplifies oxidative stress within the cancer cells, pushing them toward apoptosis.

Future work will build on these promising results by identifying additional agents capable of targeting PRDX1 effectively. Researchers are also planning to test the combined therapeutic approach in other cancer types to assess its wider impact. Beyond laboratory models, there is an active interest in designing clinical trials that can evaluate the safety and efficacy of these drug combinations in patients, seeking to translate the molecular insights into tangible medical benefits.

This discovery underscores the evolving understanding of redox biology in cancer pathophysiology. Tumor cells exploit redox-modulating proteins to survive the hostile conditions generated by both their own metabolism and therapeutic interventions. Targeting these proteins simultaneously disrupts essential survival pathways. Such insights could revolutionize how researchers approach drug resistance, enabling development of more durable and precise anticancer regimens.

Furthermore, the study highlights the importance of tumor microenvironmental factors in dictating therapy outcomes. By not only attacking the cancer cells but also their ecological niche, researchers hope to prevent relapse and metastasis, which remain major challenges in pancreatic cancer management. This comprehensive strategy may be the key to finally improving prognoses for patients afflicted by this formidable disease.

Funding for this research was provided by the National Institutes of Health and the Riley Children’s Foundation, reflecting the collaborative effort required to tackle complex cancers. Collaboration among the Indiana University School of Medicine’s Herman B Wells Center for Pediatric Research and the IU Melvin and Bren Simon Comprehensive Cancer Center was instrumental in achieving these breakthroughs.

The research team encourages continued exploration of combination therapies that dismantle multiple layers of tumor defense, aiming to outsmart pancreatic cancer’s notorious resistance mechanisms. By thoroughly understanding and targeting cancer’s cellular and microenvironmental survival strategies, the scientific community moves closer to devising treatments that could transform outcomes for one of the most challenging cancers to manage.

In summary, Indiana University researchers have identified a novel double-target strategy against pancreatic cancer by inhibiting Ref-1 and PRDX1 concurrently. This approach causes significant tumor regression and prolongs survival in preclinical models, heralding a new frontier in cancer therapeutics. The balance of redox signaling within tumors is crucial, and its disruption offers a promising weapon in the fight against cancer’s deadliest forms.

Subject of Research: Pancreatic cancer; redox biology; tumor microenvironment; combination cancer therapy targeting Ref-1 and PRDX1 proteins.

Article Title: Combination Inhibition of Ref-1 and PRDX1 Reveals Novel Vulnerabilities in Pancreatic Cancer

News Publication Date: Not explicitly stated in content

Web References:

• Redox Biology journal article: https://www.sciencedirect.com/science/article/pii/S2213231725003611?via%3Dihub
• IU School of Medicine: https://medicine.iu.edu/
• Herman B Wells Center for Pediatric Research: https://medicine.iu.edu/research-centers/pediatrics
• IU Melvin and Bren Simon Comprehensive Cancer Center: https://cancer.iu.edu/index.html

Image Credits: Tim Yates, IU School of Medicine

Keywords: Pancreatic cancer, Ref-1, PRDX1, redox biology, cancer therapy, drug resistance, tumor microenvironment, APX2014, combination therapy, oxidative stress, cancer research, Indiana University

A fundamental obstacle in advancing PDAC treatment is the paucity of actionable molecular targets. Unlike other malignancies that have benefitted immensely from targeted therapies, PDAC’s genomic landscape has long been dominated by mutations in the KRAS oncogene, which until recently was deemed ‘undruggable’. The relentless predominance of mutant KRAS drives oncogenic signaling cascades that promote tumorigenesis, tumor growth, and metastasis, yet attempts to directly inhibit KRAS have been largely unsuccessful due to its high affinity for GTP/GDP and lack of suitable binding pockets. However, recent innovations in drug development, including covalent inhibitors targeting specific KRAS mutations such as G12C, have ushered in a new era of optimism. These advances are rekindling interest in precision medicine approaches tailored to specific KRAS genotypes, providing a glimmer of hope in a field previously stymied by the gene’s elusive nature.

However, the complexity of PDAC extends far beyond its genetic mutations. The tumor microenvironment (TME) of PDAC is notoriously immunosuppressive, creating a fortress-like niche that actively thwarts anti-tumor immune responses. Dense desmoplastic stroma composed of cancer-associated fibroblasts (CAFs), extracellular matrix components, and immunosuppressive cells such as regulatory T cells and myeloid-derived suppressor cells (MDSCs) collectively form a physical and biochemical barrier. This environment not only impedes drug delivery but also subverts immune system activation, rendering conventional immunotherapies largely ineffective. Overcoming this immunosuppressive milieu is critical, and emerging strategies aim to reprogram the stromal and immune components to reinvigorate tumor-specific immunity, an approach that could revolutionize PDAC therapeutics.

Recent research is focusing heavily on harnessing the anti-tumor immune response through novel immunotherapeutic avenues. Unlike the remarkable successes seen with immune checkpoint inhibitors (ICIs) in melanoma and lung cancer, PDAC’s response to ICIs has been disappointing, largely due to the dense stromal barrier and low neoantigen burden. Innovative approaches are exploring combination therapies that prime the immune system, such as vaccination strategies, oncolytic viruses, and adoptive cell therapies—including engineered T cells or natural killer cells designed to penetrate the TME. Researchers are also investigating agents that can modulate the stroma or deplete immunosuppressive cell populations, thereby creating a more permissive environment for immune effectors to exert their functions.

While therapeutic innovation is critical, early detection of PDAC remains a cornerstone that could dramatically improve clinical outcomes. Unfortunately, PDAC is often diagnosed at an advanced and inoperable stage because it develops silently with nonspecific symptoms. Current screening methods lack sensitivity and specificity, hampering efforts for timely intervention. Cutting-edge research is exploring novel biomarkers, liquid biopsy technologies, and advanced imaging modalities to identify PDAC at a stage amenable to curative surgery. The integration of multi-omics data—encompassing genomics, proteomics, and metabolomics—into diagnostic algorithms promises to enhance the accuracy of early detection, offering a pathway to intercept the disease before it becomes fatal.

Clinical trial design in PDAC faces unique hurdles, from patient recruitment and retention to endpoint selection and heterogeneity of the disease. Traditional trial designs often fail to capture the nuances of tumor biology or the variable patient responses to treatment. Adaptive trial structures and biomarker-driven enrollment criteria are gaining traction, allowing for more flexible and efficient evaluation of novel therapeutics. Moreover, real-world data and patient-reported outcomes are increasingly recognized as valuable tools to complement traditional metrics, ensuring that clinical trials better reflect the complexities of PDAC management and patient experience.

Community and institutional barriers also impede progress in PDAC research and care. Limited awareness of the disease’s rapid progression among both patients and providers can delay diagnosis and treatment initiation. Additionally, disparities in healthcare access and variations in supportive care quality contribute to uneven outcomes across different populations. Addressing these systemic challenges requires coordinated efforts encompassing education, healthcare policy reform, and the establishment of multidisciplinary care teams equipped with the resources and expertise to manage the disease’s multifaceted nature.

Given the aggressive biology of PDAC, therapeutic windows are narrow. The rapid clinical deterioration associated with PDAC means that many patients are not eligible for clinical trials or aggressive treatments by the time of diagnosis. This reality underscores the importance of integrating supportive care early and tailoring interventions to individual health status and disease characteristics. Palliative care must be considered an integral component of treatment strategies, aiming not only to alleviate symptoms but also to maintain quality of life during therapeutic escalation.

Recent breakthroughs in the molecular understanding of PDAC have also led to the identification of subtypes based on genetic, transcriptomic, and metabolic profiles. These classifications could inform personalized treatment approaches, moving away from one-size-fits-all regimens toward precision oncology models. For example, subsets of patients harboring defects in DNA damage repair pathways may respond better to platinum-based chemotherapies or poly (ADP-ribose) polymerase (PARP) inhibitors, representing a tailored strategy that capitalizes on tumor vulnerabilities.

Metabolic adaptation is another hallmark of PDAC cells, which have evolved to thrive in nutrient-poor, hypoxic environments. Tumor cells reprogram their energy metabolism to support survival and growth despite these harsh conditions. Therapeutic efforts targeting metabolic pathways—such as glutamine metabolism, autophagy, and oxidative phosphorylation—are currently under investigation, representing a promising avenue to disrupt tumor fitness and sensitize PDAC to other treatments.

The role of KRAS extends beyond oncogenic signaling—mutant KRAS influences the tumor immune microenvironment and modulates stromal interactions. Understanding these multifaceted roles opens up the possibility of combination therapies that simultaneously target KRAS, stromal elements, and immune checkpoints. Such integrated strategies could overcome the redundancy and compensatory mechanisms that have limited single-agent efficacy in the past.

Advancements in drug delivery technologies also hold promise for PDAC management. Nanoparticle formulations, stromal depletion agents, and localized drug-release systems aim to circumvent the physical barriers posed by the dense stroma and improve intratumoral drug concentrations. These innovations could enhance the effectiveness of existing chemotherapies and new targeted agents, potentially translating into improved patient outcomes.

In the realm of clinical trials, there is growing recognition of the need to incorporate biomarker-driven stratification and early surrogates of response, which can accelerate the identification of efficacious treatments. Collaborative consortia and international networks are being leveraged to pool resources and patient cohorts, increasing the statistical power and generalizability of trial results. Such collaborations are essential in a disease characterized by rapid progression and limited therapeutic options.

In summary, the battle against pancreatic ductal adenocarcinoma is entering a pivotal phase, marked by both daunting challenges and unprecedented scientific momentum. The convergence of molecular biology, immunology, diagnostics, and clinical innovation forms the foundation for a new era in PDAC research and treatment. While obstacles remain formidable, the recent breakthroughs in targeting mutant KRAS, reengineering the immune microenvironment, enhancing early detection, and refining clinical trial methodologies collectively inspire cautious optimism. The coming years may indeed herald transformative progress that improves survival and quality of life for patients afflicted with this devastating disease.

Subject of Research: Improving outcomes of patients with pancreatic ductal adenocarcinoma through molecular targeting, immunotherapy, early detection, and clinical trial innovation.

Article Title: Improving outcomes of patients with pancreatic cancer.

Article References:

Dreyer, S.B., Beer, P., Hingorani, S.R. et al. Improving outcomes of patients with pancreatic cancer.
Nat Rev Clin Oncol 22, 439–456 (2025). https://doi.org/10.1038/s41571-025-01019-9

Image Credits: AI Generated