The significance of DNA mismatch repair in cancer biology cannot be overstated. Mismatch repair is a cellular process that corrects errors occurring during DNA replication, maintaining genomic stability. Deficiencies in this system can lead to an accumulation of mutations and, subsequently, tumorigenesis. In the context of UTUC, understanding how defective repair mechanisms contribute to cancer progression is crucial, as it holds potential implications for patient outcomes and treatment strategies.

Duan and colleagues’ research specifically investigates the link between DNA mismatch repair deficiencies and the overexpression of Nectin-4 in UTUC tissues. Nectin-4 is a cell adhesion molecule implicated in various cellular processes, including immune responses and cell proliferation. Its role as an oncofetal antigen has positioned it as a potential target for immunotherapy, but the interplay between Nectin-4 expression and DNA repair mechanisms has remained largely underexplored.

The study involved a comprehensive analysis of tumor samples from UTUC patients, enabling the researchers to identify correlations between the presence of mismatch repair defects and levels of Nectin-4 expression. The findings suggest that tumors exhibiting DNA mismatch repair deficiencies tend to show significantly elevated levels of Nectin-4 compared to proficient tumors. This raises intriguing questions about the biological processes driving these observations.

The implications of these findings extend well beyond academic interest. The data suggest that assessing Nectin-4 expression could serve as a valuable biomarker for identifying patients with a higher likelihood of having DNA mismatch repair deficiencies. Such stratification could not only enhance prognostic assessments but also inform therapeutic decisions, guiding oncologists toward more personalized treatment approaches.

Moreover, the therapeutic landscape for UTUC is evolving, with a growing interest in targeted therapies and immunotherapies. The identification of Nectin-4 as a relatable marker to DNA repair deficiency underscores the potential for developing innovative treatment strategies. By leveraging this information, clinical trials could pivot towards exploring combinations of immune checkpoint inhibitors with agents that target the underlying DNA repair defects.

As our understanding of the tumor microenvironment deepens, it becomes clear that the interaction between cancer cells and the immune system is complex and multifaceted. Nectin-4’s dual role as both a molecule involved in tumor progression and a potential target for immunotherapy adds another layer of intrigue. The study by Duan et al. encourages further investigation into how Nectin-4 influences immune evasion and whether modulating its expression can enhance the efficacy of immunotherapeutic agents.

In addition to these crucial insights, the study raises the question of whether Nectin-4 expression could be leveraged for early detection of UTUC. Given that early-stage cancers often yield better prognoses, the development of a screening strategy based on Nectin-4 levels could revolutionize how we approach diagnosis and treatment in upper tract urothelial carcinoma.

The findings presented in this research contribute to a growing body of literature that highlights the importance of integrating molecular diagnostics into clinical practice. The ability to classify tumors based on genetic and epigenetic markers is becoming increasingly vital in the era of precision medicine, where tailored treatment regimens can significantly impact outcomes for patients.

As researchers continue to unravel the complexities of UTUC, it is imperative that the scientific community collaborates to further explore these findings. Drawing connections between DNA mismatch repair deficiencies, Nectin-4 expression, and patient outcomes opens numerous research avenues. Initiating large-scale studies focusing on diverse populations may help validate these findings and determine the robustness of Nectin-4 as a clinical biomarker.

Importantly, the applicative potential of this research highlights the value of interdisciplinary collaboration in cancer research. The intersection of molecular biology, immunology, and clinical oncology is where groundbreaking discoveries often occur. It is essential for scientists, clinicians, and pharmaceutical companies to work together to translate these findings from bench to bedside, ensuring that they benefit patients in real-world settings.

In conclusion, the study by Duan and colleagues paves the way for a deeper understanding of upper tract urothelial carcinoma, particularly in relation to DNA mismatch repair mechanisms and Nectin-4 expression. As researchers continue to investigate the implications of these findings, the hope is that it will lead to improved diagnostic tools, more effective therapies, and ultimately, better outcomes for patients battling this challenging form of cancer.

Expanding the knowledge base surrounding UTUC through rigorous research and innovative clinical practices could potentially revolutionize the way this cancer is approached and treated. The journey towards understanding and effectively managing upper tract urothelial carcinoma is ongoing, and the contributions of studies like this one are invaluable in this effort.

The integration of molecular biomarkers like Nectin-4 within clinical protocols could soon become a standard practice, ushering in an era of personalized and precise oncology. It is through the dedication of researchers and clinicians alike that strides in cancer treatment will continue to evolve, enhancing patient quality of life and survival rates in the long term.

Subject of Research: Upper tract urothelial carcinoma, DNA mismatch repair, Nectin-4 expression
Article Title: Deficient DNA mismatch repair and Nectin-4 expression in upper tract urothelial carcinoma (UTUC)
Article References:

Duan, P., Yu, L., Hao, Y. et al. Deficient DNA mismatch repair and Nectin-4 expression in upper tract urothelial carcinoma (UTUC). J Cancer Res Clin Oncol 151, 280 (2025). https://doi.org/10.1007/s00432-025-06312-9

Image Credits: AI Generated
DOI: 10.1007/s00432-025-06312-9
Keywords: DNA mismatch repair, Nectin-4, upper tract urothelial carcinoma, cancer research, immunotherapy, biomarkers, precision medicine, tumor microenvironment.

Colorectal cancer remains a formidable global health issue, with recurrence after treatment posing substantial hurdles. Microsatellite instability—a condition resulting from defects in DNA mismatch repair mechanisms—is already established as a critical marker in CRC development. However, the prognostic contributions of genes associated with microsatellite stability, which defines the predominant subtype of CRC, have been less explored until now. This study fills that crucial knowledge gap by dissecting molecular signatures tied specifically to MSS tumors.

The investigation harnessed comprehensive datasets, including The Cancer Genome Atlas for Colorectal Cancer (TCGA-CRC) and multiple gene expression series (GSE17537, GSE39582, and GSE18088), ensuring robust and diverse sample representation. By comparing gene expression profiles not only between CRC patients and healthy controls but also among MSS and MSI-high (MSI-H) cases, the team isolated key gene candidates underpinning microsatellite stability’s role in tumor behavior.

Sophisticated bioinformatics methodologies, such as weighted gene co-expression network analysis (WGCNA), facilitated the identification of functionally interconnected genes relevant to CRC prognosis. This network-driven approach enabled the pinpointing of 11 pivotal prognostic genes: CHGB, FABP4, PLIN4, PLIN1, RPRM, C7, AQP8, C2CD4A, APLP1, ADH1B, and CD36. These genes emerged as molecular sentinels revealing pathways involved in tumor progression and immune microenvironment modulation.

Building upon this gene signature, the researchers constructed a prognostic risk model that demonstrated significant stratification of patient outcomes in both the primary TCGA cohort and the independent validation cohort from GSE17537. The model’s predictive accuracy was underscored by area under the curve (AUC) values exceeding 0.6 across 3, 5, and 7-year survival intervals. Such predictive reliability solidifies its potential clinical utility for risk assessment.

Further analysis revealed that this risk model, when integrated with conventional clinical indicators such as patient age, tumor stage, and pathological lymph node status (N stage), constitutes an independent prognostic factor. This insight led to the creation of a nomogram—a graphical tool illustrating individualized survival probabilities—that could revolutionize personalized patient management by tailoring therapeutic decisions according to predicted risk profiles.

Beyond mere prognostication, the study delved into the biological pathways encoded by the identified genes. Intriguingly, these genes appear to influence colorectal cancer progression through their impact on the tumor immune microenvironment (TIME), affecting immune cell infiltration and immune response modulation. This connection underscores the intricate interaction between tumor genetics and host immunity, a rapidly evolving frontier in oncology.

Additionally, the research spotlighted bleomycin, a chemotherapeutic agent, as a potentially effective treatment modality for CRC patients stratified by the newly defined risk model. This drug’s predicted efficacy opens pathways for repositioning existing therapeutics based on refined genetic profiling, aligning with precision medicine paradigms.

At the regulatory level, the genes CHGB and RPRM were found to be influenced by non-coding RNAs and transcription factors, suggesting complex layers of epigenetic and transcriptional control that may be pivotal in colorectal carcinogenesis. Decoding these regulatory networks offers fertile ground for future experimental validation and therapeutic targeting.

The implications of this study reach far beyond prognostication alone. By integrating microsatellite stability-associated molecular markers with clinical variables and immune landscape analyses, the research provides a comprehensive framework to understand CRC heterogeneity and improve patient stratification. This multi-dimensional model could ultimately guide the development of novel therapeutics aimed at specific molecular subtypes of CRC.

From a clinical perspective, the ability to predict patient outcomes with higher precision using gene expression signatures tied to MSS enables oncologists to fine-tune surveillance strategies, optimize adjuvant therapy selection, and potentially improve survival outcomes. The approach exemplifies the transformative power of integrating high-throughput genomics with bioinformatics to unravel cancer complexity.

Moreover, this research underscores the necessity of large-scale datasets and cross-cohort validation to ensure that prognostic models are generalizable and reliable across populations. The use of multiple CRC cohorts exemplifies rigorous scientific methodology, enhancing confidence in the model’s applicability.

Future research inspired by these findings could explore functional mechanisms driving the identified genes and their interactions within the tumor microenvironment. Experimental studies dissecting gene function, regulatory networks, and response to immunomodulatory therapies could pave the way for targeted interventions tailored to MSS-associated molecular profiles.

In the dynamic field of oncology, where tumor heterogeneity often thwarts uniform treatment responses, models like the one developed here represent a critical step forward. By interpreting the nuanced genetic and immunological milieu of colorectal tumors, clinicians and researchers can collectively advance toward truly personalized cancer care.

This study marks a pivotal moment in understanding the role of microsatellite stability-associated genes in colorectal cancer, bridging molecular biology with clinical outcomes through innovative modeling. The integration of prognostic genetics with immune contexture lays the foundation for improved prediction tools and unveils therapeutic opportunities that could reshape CRC management paradigms.

As the scientific community continues to uncover the layers of cancer biology, it is studies like these—melding bioinformatic rigor with clinical insight—that will catalyze breakthroughs in diagnosis, prognosis, and treatment, ultimately offering hope to millions affected by colorectal cancer worldwide.

Subject of Research: Development of a prognostic risk model for colorectal cancer based on microsatellite stability-associated genes.

Article Title: Development of a prognostic risk model for colorectal cancer based on microsatellite stability-associated genes.

Article References:
Zheng, X., He, Y., Tuo, Z. et al. Development of a prognostic risk model for colorectal cancer based on microsatellite stability-associated genes. BMC Cancer 25, 1490 (2025). https://doi.org/10.1186/s12885-025-14918-y

Image Credits: Scienmag.com

DOI: https://doi.org/10.1186/s12885-025-14918-y

In the ever-evolving landscape of cancer biology, one molecular pathway has captivated researchers due to its pivotal role in maintaining genomic fidelity: DNA mismatch repair (MMR). This intricate system is a molecular sentinel, intrinsically conserved across species, tasked with recognizing and correcting replication errors that inevitably arise during cell division. When this critical repair mechanism is compromised, the consequences reverberate at the genomic level, culminating in a condition known as mismatch repair deficiency (MMRd). The accumulation of mutations that ensues underpins the pathogenesis of various cancers, positioning MMRd as both a biomarker and a therapeutic target in oncology.

At the core of MMR’s biological function lies a sophisticated protein machinery that scans the genome to identify mismatches — single-base errors and small insertion-deletion loops introduced primarily during DNA replication. The MMR system recognizes these subtle aberrations, engages in excision of the erroneous DNA segment, and orchestrates accurate resynthesis to restore genetic fidelity. Perturbations in genes coding for key MMR proteins, including MLH1, MSH2, MSH6, and PMS2 among others, incapacitate this surveillance, allowing replication errors to persist, proliferate, and translate into mutational chaos.

The genomic hallmark of MMRd cancers is the pronounced mutational burden often manifesting as microsatellite instability (MSI). Microsatellites, short tandem repeat sequences scattered abundantly throughout the genome, become hotspots for insertions and deletions when MMR falters. This instability, detectable through molecular assays, serves as an unmistakable signature of MMR dysfunction. The MSI phenotype not only signals the presence of defective repair but also sheds light on the mutagenic landscape that drives tumorigenesis.

Clinically, MMRd exerts profound influence on cancer development, exemplified by hereditary cancer syndromes such as Lynch syndrome. Individuals with Lynch syndrome inherit germline mutations that cripple MMR activity, predisposing them to a spectrum of malignancies predominantly affecting the colorectal, endometrial, and other epithelial tissues. Beyond inherited cases, sporadic tumors arising from somatic MMR defects are increasingly recognized across diverse anatomical sites, underscoring the universal relevance of MMR inoncogenesis.

Remarkably, the intrinsic biology of MMRd tumors confers unique immunological characteristics. The high mutational load generates a wealth of neoantigens, rogue peptides unfamiliar to the immune system and capable of triggering robust immune surveillance. Consequently, MMRd and MSI-high cancers tend to exhibit heightened infiltration by immune effector cells, reflecting an ongoing immunologic engagement within the tumor microenvironment. This immunogenic phenotype is accompanied by an upregulation of immune checkpoint molecules, such as PD-1 and PD-L1, which tumors exploit to evade immune eradication.

This immunological interplay has galvanized the therapeutic paradigm surrounding MMRd malignancies, particularly in the context of immune checkpoint inhibitors (ICIs). These agents, exemplified by anti-PD-1 and anti-CTLA-4 antibodies, unleash pre-existing immune responses against tumor cells by negating inhibitory signals. Patients harboring MMRd tumors frequently achieve remarkable and durable clinical responses when treated with ICIs, transcending conventional distinctions of tumor origin. The unprecedented sensitivity of MMRd cancers to immunotherapy has reshaped treatment algorithms and generated a new frontier in personalized oncology.

Yet, the clinical reality is nuanced. Despite the overarching success of ICIs in MMRd contexts, a substantial fraction of patients fail to derive benefit, displaying intrinsic or acquired resistance. Deciphering the molecular and microenvironmental determinants of such resistance constitutes a major focus of contemporary research. Hypotheses under investigation include defects in antigen presentation pathways, alterations in interferon signaling, and the emergence of immunosuppressive cellular subsets within the tumor milieu that dampen therapeutic efficacy.

The implications of these findings are manifold, ranging from refining diagnostic paradigms to innovating combinatorial treatment strategies. Accurate identification of MMRd status is paramount, employing techniques such as immunohistochemistry for MMR proteins, PCR-based MSI testing, and next-generation sequencing approaches. Such diagnostics not only stratify patients for immunotherapy but also facilitate recognition of familial cancer syndromes, thereby informing surveillance and risk-reduction measures.

Therapeutically, the landscape is expanding beyond monotherapy ICI regimens. Investigators are exploring synergistic combinations incorporating epigenetic modulators, DNA-damaging agents, and vaccines aimed at enhancing neoantigen presentation or reversing immune suppression. The evolving understanding of MMRd tumor biology continues to inspire novel intervention avenues designed to overcome resistance and amplify immunogenicity.

At a fundamental level, the study of MMRd cancers exemplifies the convergence of genomic instability and immuno-oncology, highlighting how defects in DNA repair pathways can paradoxically render tumors more visible and vulnerable to the immune system. This interplay underscores the broader concept of synthetic lethality in cancer treatment, where exploiting specific molecular weaknesses yields therapeutic gain.

Beyond therapeutic impacts, MMR deficiency also serves as a window into cancer evolution and heterogeneity. The continuously accumulating mutations in MMRd tumors generate diverse subclones, fostering genetic and phenotypic variability within a single neoplasm. Such intratumoral heterogeneity complicates treatment responses and necessitates dynamic strategies that adapt to evolving tumor landscapes.

Moreover, the role of MMR extends beyond oncology into the realm of normal physiology and aging. The fidelity of DNA replication maintained by MMR contributes to genomic stability throughout an organism’s lifetime, with deficiencies implicated in mutational accumulation that may influence age-related diseases and developmental disorders. Thus, insights garnered from cancer-focused research may resonate across broader biomedical domains.

In conclusion, mismatch repair-deficient cancers occupy a unique niche at the intersection of genetic instability and immune responsiveness. The remarkable sensitivity of MMRd tumors to immune checkpoint blockade therapy heralds a triumph of precision medicine, yet calls attention to the complexities of resistance and the necessity for continued mechanistic elucidation. As multidisciplinary efforts converge, harnessing the full potential of MMR-targeted strategies may redefine cancer care, offering hope for improved outcomes and personalized interventions.

The ongoing research highlights not only the critical importance of understanding DNA repair pathways but also the translational potential of such knowledge in crafting next-generation therapies. By unraveling the molecular underpinnings of MMRd, scientists are charting a path toward more effective, tailored treatments that exploit the vulnerabilities unique to these genomically unstable tumors.

Subject of Research: Therapeutic targeting and biological characterization of mismatch repair-deficient cancers

Article Title: Therapeutic targeting of mismatch repair-deficient cancers

Article References:
Johannet, P., Rousseau, B., Aghajanian, C. et al. Therapeutic targeting of mismatch repair-deficient cancers. Nat Rev Clin Oncol (2025). https://doi.org/10.1038/s41571-025-01054-6

Image Credits: AI Generated

The prevalence of MSI-H/dMMR phenotypes is particularly pronounced in endometrial and colorectal malignancies, where they serve not just as molecular hallmarks but as markers intertwined with unique biological behaviors and clinical outcomes. These tumors, distinguished by their hypermutated genomic profiles, demonstrate a marked sensitivity to emerging anticancer therapies, notably immune-checkpoint inhibitors (ICIs). This therapeutic vulnerability arises from the tumors’ hypermutated state, a direct consequence of defective mismatch repair, which creates a permissive environment for increased neoantigen presentation. Such immunogenicity invites robust infiltration by immune cells, setting the stage for effective immunomodulatory interventions.

A nuanced dimension of MSI-H/dMMR cancers is introduced through the lens of hereditary cancer syndromes, predominantly Lynch syndrome. This autosomal dominant inherited condition results from germline pathogenic variants in mismatch repair genes, predisposing carriers to a spectrum of malignancies manifesting the MSI-H/dMMR phenotype. While the majority of MSI-H/dMMR cancers are sporadic, the subset arising from Lynch syndrome carries significant implications not only for personalized treatment strategies but also for familial genetic counseling and cancer risk assessment. Yet, the exact distinctions, if any, in molecular pathogenesis and clinical behavior between hereditary and sporadic MSI-H/dMMR tumors remain a subject of ongoing investigation, underscoring a critical knowledge gap.

The expanding interest in MSI-H/dMMR tumors has been propelled further by the remarkable clinical responses observed with ICIs in metastatic disease across diverse histologies. This histology-agnostic efficacy exemplifies precision oncology’s promise: targeting molecular vulnerabilities irrespective of the cancer’s tissue of origin. The mechanistic basis lies in the hypermutation driven by mismatch repair deficiency which produces a myriad of neoepitopes recognizable by the immune system. This intrinsic immunogenicity not only renders these cancers responsive to immune checkpoint blockade but also fuels optimism for expanding immunotherapies into adjuvant and neoadjuvant settings, potentially transforming management paradigms for early-stage MSI-H/dMMR malignancies.

Despite the shared molecular underpinning of MSI-H/dMMR status, tumors arising from different tissues exhibit distinct histopathological and biological features. These tissue-specific characteristics influence not only prognosis but also the degree of responsiveness to immune-based therapies. For example, MSI-H colorectal cancers often present with marked lymphocytic infiltration, whereas MSI-H endometrial cancers may display divergent tumor microenvironments influencing immunotherapy outcomes. Such variability underscores the necessity of integrating molecular profiling with histotype-specific contexts when devising treatment regimens, advocating for a precision medicine approach that respects both shared and unique tumor biology.

At a molecular level, mismatch repair involves a highly orchestrated proofreading system tasked with identifying and rectifying base-base mismatches and insertion-deletion loops during DNA replication. Key proteins such as MLH1, MSH2, MSH6, and PMS2 coordinate this repair cascade, preserving genomic integrity. Loss of function in any of these components through somatic mutations, epigenetic silencing—especially MLH1 promoter hypermethylation—or germline alterations impairs DNA repair fidelity. The resulting accumulation of mutations fosters microsatellite instability characterized by length alterations in repetitive DNA sequences scattered throughout the genome, a hallmark detected by specific diagnostic assays.

Clinically, MSI-H/dMMR status has become an indispensable biomarker for guiding therapeutic decision-making. Historically, its prognostic value varied by tumor type; for instance, MSI-H colorectal cancers often confer favorable prognosis compared to microsatellite stable counterparts. However, the advent of immunotherapy has shifted MSI-H/dMMR status to the forefront as a predictive biomarker for ICI responsiveness. Regulatory approvals now endorse MSI-H/dMMR testing as a standard component of diagnostic workflows for colorectal, endometrial, and other relevant cancers, reflecting a paradigm shift towards biomarker-driven oncology.

Diagnostic modalities include both molecular assays and immunohistochemical (IHC) staining to evaluate mismatch repair protein expression and assess microsatellite instability. Polymerase chain reaction (PCR)-based panels targeting mononucleotide and dinucleotide repeats remain gold standards for MSI detection, while IHC offers a practical approach to evaluate MLH1, MSH2, MSH6, and PMS2 protein presence within tumor samples. Concordance between these methods is generally high, yet discordances may arise, necessitating comprehensive evaluation especially in the context of clinical trial enrollment and treatment planning.

The therapeutic landscape for MSI-H/dMMR cancers is rapidly evolving. Immune-checkpoint blockade targeting programmed cell death protein 1 (PD-1) and its ligand (PD-L1), as well as cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), have demonstrated unprecedented efficacy. Clinical trials established durable responses and improved survival in metastatic MSI-H/dMMR colorectal and non-colorectal cancers, leading to histology-agnostic approvals by regulatory agencies. This success has spurred exploration of combinatorial regimens, immunotherapy in earlier disease stages, and the identification of biomarkers beyond MSI-H/dMMR to predict treatment response.

However, challenges remain. Not all MSI-H/dMMR tumors respond uniformly to immunotherapy, highlighting intrinsic resistance mechanisms and the influence of tumor microenvironmental factors. Variability in tumor-infiltrating lymphocyte density, expression of alternative immune checkpoints, and presence of immunosuppressive cells such as myeloid-derived suppressor cells may modulate therapeutic efficacy. Future research is prioritizing elucidation of these resistance pathways to optimize patient selection and develop next-generation immunotherapies.

Beyond immune checkpoint inhibitors, understanding the biology of MSI-H/dMMR tumors opens avenues for novel treatments targeting DNA repair deficiencies directly. Agents inducing synthetic lethality via interaction with other DNA damage response pathways, or epigenetic modulators reversing MLH1 promoter methylation, represent areas of active investigation. Integration of these strategies may potentiate immunotherapy effectiveness or provide alternatives for patients who are refractory to current standards.

Furthermore, the intersection of MSI-H/dMMR status with tumor genomics has unveiled complex pathogenetic landscapes. Co-occurring mutations in oncogenes and tumor suppressors, tumor mutational burden variability, and neoantigen heterogeneity contribute to clinical behavior and therapeutic responses. Advanced sequencing technologies and bioinformatics have become indispensable in dissecting these layers, enabling refined stratification and personalized treatment approaches.

The implications of MSI-H/dMMR extend beyond oncology clinics into public health domains. Identification of Lynch syndrome carriers through tumor testing facilitates cascade genetic screening in families, providing opportunities for cancer prevention and early detection. This necessitates coordinated multidisciplinary efforts encompassing molecular diagnostics, genetic counseling, and surveillance protocols, underscoring the societal impact of understanding MSI-H/dMMR biology.

In summary, the landscape of MSI-H/dMMR cancers reflects a remarkable convergence of molecular biology, clinical oncology, and immunotherapy innovation. From fundamental insights into DNA repair dysfunction to transformative immunotherapeutic successes, this tumor subtype exemplifies the potential of precision oncology approaches. Continued research to unravel tissue-specific nuances, resistance mechanisms, and novel therapeutic targets promises to refine patient management strategies further, heralding a new era where histology-agnostic molecular profiling guides individualized cancer care.

The burgeoning recognition of MSI-H/dMMR tumors’ complex biology and their role in shaping immune response underscores the necessity for comprehensive, multidisciplinary research and clinical integration. As the scientific community advances toward expanding therapeutic indications and refining diagnostic tools, patients with MSI-H/dMMR cancers stand at the forefront of benefit from personalized medicine breakthroughs. This evolving paradigm not only redefines treatment but also enriches understanding of carcinogenesis itself, providing hope for improved outcomes across cancer types.

Subject of Research: DNA mismatch repair deficiency (dMMR) and microsatellite instability-high (MSI-H) cancers including epidemiology, biology, pathogenesis, diagnosis, and treatment, with emphasis on immunotherapy and hereditary syndromes such as Lynch syndrome.

Article Title: Epidemiology, pathogenesis, biology and evolving management of MSI-H/dMMR cancers.

Article References:
Ambrosini, M., Manca, P., Nasca, V. et al. Epidemiology, pathogenesis, biology and evolving management of MSI-H/dMMR cancers.
Nat Rev Clin Oncol 22, 385–407 (2025). https://doi.org/10.1038/s41571-025-01015-z

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