The clinical stakes could hardly be higher. Locally advanced rectal cancer has traditionally been treated with neoadjuvant chemoradiotherapy followed by surgery, an approach that saves lives but often exacts a heavy toll, including permanent colostomies, radiation-related bowel dysfunction, urinary problems, and sexual health consequences. Total neoadjuvant therapy (TNT), which delivers chemotherapy and radiation before any operation, has improved outcomes and opened the door to organ preservation for patients whose tumors vanish completely. The TORCH trial took this concept further by adding immunotherapy to the neoadjuvant regimen, creating immunotherapy-based total neoadjuvant therapy, or iTNT, for MSS patients who would typically be excluded from immunotherapy-based strategies because their tumors lack the microsatellite instability that makes them immunotherapy-sensitive.

In the new study, the research team analyzed clinical and genetic data from 63 patients enrolled in the prospectively registered TORCH trial between May 1, 2021, and September 15, 2022. The investigators collected baseline tissue mutations, magnetic resonance tumor regression grade (mrTRG) scores from treatment-time MRI scans, and circulating tumor DNA (ctDNA) positivity measured at multiple points across the treatment course. Their goal was twofold: first, to determine which features measured before, during, or after iTNT best distinguished patients who achieved a complete response from those who did not, and second, to identify early markers of recurrence risk that could guide follow-up intensity and decisions about whether surgery could be safely avoided.

The genetic findings were striking. A baseline mutation in the SMAD4 gene, a well-known tumor suppressor involved in the TGF-beta signaling pathway that helps regulate cell growth and tissue architecture, was significantly associated with poor response to iTNT, with the association reaching statistical significance at P equals 0.007. Patients carrying SMAD4 mutations were markedly less likely to achieve a complete response, suggesting that this single genetic alteration encodes a fundamental resistance to the combined chemo-radiation-immunotherapy approach. The finding aligns with a growing body of evidence that SMAD4 loss reshapes the tumor microenvironment in ways that blunt immune attack and may drive more aggressive, metastasis-prone biology.

Beyond SMAD4, three additional features correlated with complete response rates: post-treatment mrTRG assessed on MRI (P less than 0.0001), tumor mutational burden, or TMB, which quantifies the number of mutations carried by the tumor (P equals 0.03), and the latest ctDNA status, a measure of whether fragments of tumor DNA were still detectable in the bloodstream after treatment (P equals 0.03). TMB is a classic immunotherapy biomarker, since tumors with more mutations tend to produce more neoantigens that the immune system can recognize, but its relevance in MSS rectal cancer treated with combination iTNT had been uncertain. The ctDNA measurement, meanwhile, represents the concept of a liquid biopsy: rather than sampling the tumor itself, clinicians can track fragments of tumor-derived DNA shed into circulation, gaining a real-time view of residual disease that imaging may miss.

The true advance, however, came when the researchers integrated these features into multivariable models. A model combining post-treatment mrTRG, SMAD4 mutation status, TMB, and latest ctDNA status achieved an area under the curve, or AUC, of 0.92 for discriminating complete responders from non-responders, compared with just 0.75 for a model based on mrTRG alone, a statistically significant improvement (P equals 0.0098). An AUC of 0.92 reflects excellent discriminative accuracy, while 0.75 represents only modest performance, so the jump is clinically meaningful. Importantly, the researchers also tested whether prediction could happen earlier in the treatment course. An early integrated model that used mid-iTNT mrTRG along with the genetic features achieved an AUC of 0.89 versus 0.76 for the mrTRG-only model (P equals 0.047), meaning clinicians might one day gauge a patient’s trajectory partway through therapy rather than waiting until the end.

The prognostic analysis added another layer of clinical utility. Using Cox proportional hazards regression and Kaplan-Meier survival analyses, the team found that baseline SMAD4 mutations and ctDNA positivity at later time points were both correlated with an increased risk of disease progression, including local recurrence and distant metastasis. In practical terms, a patient whose blood still shows molecular traces of tumor after treatment completion, or whose original tumor carried a SMAD4 mutation, faces a higher probability that the cancer will return, even if standard assessments look favorable. This kind of molecular residual disease detection is becoming one of the most actively pursued frontiers in oncology, because it can flag recurrence months or even years before radiographic evidence appears, when intervention may be most effective.

The implications for treatment strategy are substantial. For patients with locally advanced rectal cancer, the decision of whether to proceed to surgery or pursue nonoperative management, sometimes called watch and wait, hinges on the confidence with which a complete response can be established. Current assessments rely on a patchwork of digital rectal examination, endoscopy, MRI, and serum markers such as carcinoembryonic antigen, none of which is perfectly reliable. A molecular framework that adds SMAD4 status and serial ctDNA to the mix could give clinicians the confidence to safely spare surgery in true complete responders, while identifying poor responders early enough to intensify their therapy, enroll them in alternative trials, or avoid prolonging an ineffective course of immunotherapy. The study’s authors emphasize that these models are best understood as complementary risk stratification tools rather than standalone decision instruments, augmenting rather than replacing clinical judgment and imaging.

It is worth underscoring what makes the MSS population such an important target. Roughly the overwhelming majority of colorectal cancers are microsatellite stable, and for years, immune checkpoint inhibitors were considered largely futile in this group. The TORCH trial’s demonstration that adding immunotherapy to total neoadjuvant therapy can produce promising complete response rates in MSS patients was itself a paradigm-shifting result, and the current analysis addresses the critical next question: how do we know who is benefiting? Without reliable biomarkers, the field risks either overtreating patients who will never respond or undertreating those who would have responded with more time. The integrated models described here offer a data-driven way to navigate that uncertainty, converting a one-size-fits-all regimen into something closer to adaptive, biology-informed care.

Limitations remain, as they do in any single-trial biomarker analysis of 63 patients. The findings will need validation in larger, independent cohorts, and the logistics of serial ctDNA monitoring, including assay standardization, cost, and the optimal sampling schedule, remain active areas of investigation. The trial was registered as NCT04518280, and the analysis was funded by the National Natural Science Foundation of China and the Beijing Xisike Clinical Oncology Research Foundation. Still, the convergence of tissue genomics, liquid biopsy, and quantitative imaging in a prospectively registered trial represents a template for how biomarker-driven personalization should be developed in rectal cancer. If validated, the combination of SMAD4 mutation status, tumor mutational burden, serial ctDNA tracking, and mrTRG assessment could become a standard part of the decision-making toolkit for MSS locally advanced rectal cancer, helping more patients keep their organs, avoid futile toxicity, and face their disease with a clearer, molecularly grounded picture of what lies ahead.

Subject of Research: Predicting response and prognosis of immunotherapy-based total neoadjuvant therapy in microsatellite stable locally advanced rectal cancer using genetic features and serial circulating tumor DNA

Article Title: Application of genetic features and serial ctDNA in estimating response and prognosis of immunotherapy-based total neoadjuvant therapy (iTNT) for microsatellite stable locally advanced rectal cancer: data from TORCH trial

Article References: Wang, Y., Xu, Y., Lin, Y., Liu, Y., Jing, Q., Shen, L., Wan, J., Wang, Y., Zhang, H., Wu, R., Zhou, S., Chen, Y., Zhang, Z., Wang, J., Sun, Y., Bao, H., Ou, Q., Bao, H., Shao, Y., … Xia, F. (2026). Application of genetic features and serial ctDNA in estimating response and prognosis of immunotherapy-based total neoadjuvant therapy (iTNT) for microsatellite stable locally advanced rectal cancer: data from TORCH trial. Genome Medicine. https://doi.org/10.1186/s13073-026-01755-2

Image Credits: AI Generated

DOI: 10.1186/s13073-026-01755-2

Keywords: rectal cancer, immunotherapy, ctDNA, SMAD4 mutation, tumor mutational burden, total neoadjuvant therapy, microsatellite stable, TORCH trial, liquid biopsy, organ preservation, prognosis, complete response

Neoadjuvant chemoradiotherapy aims to shrink tumors before surgery, improving the likelihood of a successful resection and reducing the risk of metastasis. However, the variability in patient response has challenged oncologists worldwide. The investigative team analyzed genomic and transcriptomic data from 318 pre-treatment biopsies of microsatellite stable rectal cancers, pooling novel samples with available public datasets. This approach allowed for a comprehensive comparison of molecular signatures between tumors that completely responded to treatment and those that did not.

A striking discovery was that patients achieving a complete response (CR) not only showed no residual tumor post-treatment but also had a significantly reduced risk of both local recurrence and distant metastasis. This finding underscores the clinical importance of understanding the biology behind complete response, which could translate into more personalized treatment plans and surveillance strategies for rectal cancer patients.

The study revealed distinct differences in the DNA mutation profiles and gene expression patterns between complete responders and incomplete responders (ICR). Notably, certain mutations tended to co-occur or be mutually exclusive depending on the response group. This suggests that specific genetic interactions may underpin mechanisms of sensitivity or resistance to nCRT.

Moreover, the expression of genes involved in DNA repair pathways was markedly lower in complete responders. This counterintuitive observation points to defective or impaired DNA repair mechanisms potentially making cancer cells more vulnerable to chemoradiotherapy-induced damage, leading to better treatment outcomes. This contrasts with traditional assumptions that efficient DNA repair would enhance cell survival, highlighting the complexity of tumor biology in rectal cancer.

To quantify how these genetic alterations correlate with treatment response, the researchers developed a logistic regression model that accounted for clinical variables such as tumor size, stage, and patient age. The model identified that the presence of particular co-occurring mutations robustly predicted complete response, providing a potential tool for pre-treatment patient stratification.

When examining the tumors of incomplete responders, the team explored the molecular underpinnings of recurrence risk. They found abnormal cell-cell interaction signaling pathways were enriched in tumors that recurred after treatment, suggesting these disruptions may facilitate tumor survival and regrowth. Additionally, an increase in cancer-associated fibroblasts—cells known to support tumor growth and suppress immune responses—was associated with higher recurrence rates.

Beyond cellular interactions, immune profiling uncovered a subset of “immune-hot” tumors among incomplete responders. These tumors exhibited elevated expression of immune checkpoint proteins, markers that tumors exploit to evade immune system attack. Paradoxically, these immune-active tumors correlated with worse outcomes, implying that despite immune infiltration, effective antitumor immunity was compromised, potentially through immune checkpoint-mediated suppression.

Taken together, these findings represent a significant leap forward in understanding the complex molecular tapestry dictating treatment response and recurrence in rectal cancer. They highlight the multifaceted roles of DNA repair deficiencies, mutational landscapes, microenvironment components, and immune evasion strategies in shaping therapy outcomes.

This research paves the way for future clinical approaches that integrate molecular profiling into the management of rectal cancer. By identifying biomarkers predictive of treatment resistance, clinicians could tailor neoadjuvant therapy regimens, escalating or de-escalating treatment intensity as appropriate. Furthermore, strategies targeting cancer-associated fibroblasts or immune checkpoint pathways may improve outcomes in patients at high risk for recurrence.

The implications extend to the development of novel therapeutics aimed at exploiting defective DNA repair mechanisms or reversing immune suppression in rectal tumors. Such targeted interventions could convert non-responders into responders, ultimately enhancing survival rates and quality of life for patients.

In essence, the study reveals that rectal cancer’s response to nCRT is not a simple binary process but rather governed by a dynamic interplay of genetic mutations, transcriptional programs, stromal components, and immune landscapes. This complexity necessitates multifactorial analytical strategies and underscores the promise of precision oncology in this challenging disease.

Going forward, larger-scale validation studies and integration of these molecular predictors into clinical trials are imperative. Understanding how these biomarkers behave in diverse patient populations and across different therapeutic contexts will be critical for their successful translation into routine care.

The authors’ innovative combination of genomic, transcriptomic, and microenvironmental analyses represents a model for future cancer research. It highlights the power of combining big data with sophisticated statistical modeling to unravel the mysteries of treatment resistance and pave the way for personalized medicine.

Published in the 2025 volume of BMC Cancer, this study offers a beacon of hope for rectal cancer patients facing uncertain outcomes. It advances a new paradigm where the molecular constitution of each tumor guides therapeutic decisions, maximizing efficacy and minimizing unnecessary treatments.

In conclusion, these findings constitute a monumental step toward decoding the molecular determinants of neoadjuvant chemoradiotherapy response in rectal cancer. By unveiling the genetic and cellular processes linked to resistance and recurrence, the research opens new horizons for precision diagnostics and targeted therapeutics, promising to reshape the landscape of rectal cancer management.

Subject of Research: Molecular predictors of treatment resistance and recurrence in rectal cancer following neoadjuvant chemoradiotherapy.

Article Title: Molecular predictors of treatment resistance and recurrence following neoadjuvant therapy in rectal cancer.

Article References: Huang, F., McLeod, M.C., Irwin, R.K. et al. Molecular predictors of treatment resistance and recurrence following neoadjuvant therapy in rectal cancer. BMC Cancer 25, 1624 (2025). https://doi.org/10.1186/s12885-025-14958-4

Image Credits: Scienmag.com

DOI: https://doi.org/10.1186/s12885-025-14958-4

The study, encompassing 282 ESCC patients treated with NCRT followed by surgical intervention, focused on extracting nuanced lymph node characteristics that extend beyond traditional staging. Conventional pathology N (pN) staging primarily considers the presence and number of positive lymph nodes but often fails to capture deeper biological and anatomical complexities influencing patient prognosis. By evaluating factors such as the total number of lymph nodes removed, their size, anatomical location, intra-nodal tumor regression grade (LN-TRG), and extracapsular invasion, the researchers have constructed a model that surpasses standard staging in predictive accuracy.

One of the key findings highlighted is the relationship between the extent of lymph node clearance during surgery and overall survival (OS). Intriguingly, patients who had between 17 and 30 lymph nodes removed exhibited significantly better OS compared to those with fewer than 17 or more than 30 nodes cleared. This suggests an optimal surgical clearance threshold that balances maximal disease eradication without unnecessary tissue removal, potentially preserving immune function and reducing surgical morbidity.

Furthermore, the assessment of tumor regression within lymph nodes (LN-TRG) emerged as a potent prognostic factor. Lower LN-TRG, indicative of better tumor response to neoadjuvant therapy within lymph nodes, correlated strongly with improved OS and recurrence-free survival (RFS). This insight underscores the importance of not only the presence of metastatic disease but also the dynamic tumor response within the nodal microenvironment post-treatment.

Extracapsular invasion of lymph nodes, a pathological finding denoting tumor extension beyond the nodal capsule, was associated with poorer OS and RFS. This feature likely represents a more aggressive disease phenotype with enhanced potential for systemic dissemination, thus marking it as a vital element within the prognostic model.

Anatomical lymph node location also played a critical role in prognosis prediction. Abdominal lymph nodes, in particular, were identified as harboring the highest ratio of residual cancer cells after therapy. These nodes demonstrated the greatest hazard ratio for adverse outcomes and contained the largest number and proportion of positive cases, highlighting their significance in guiding post-surgical management and surveillance strategies.

To distill the complex array of lymph node variables into a clinically applicable tool, the research employed advanced statistical approaches including Lasso regression and Cox univariate analysis. These methods identified five paramount factors for prognosis: LN-TRG, total tumor diameter within lymph nodes, clearing 17–30 lymph nodes, proportion of positive lymph nodes, and presence of extracapsular invasion. Integrating these variables into a comprehensive predictive model produced impressive risk stratification capabilities for both OS and RFS, with area under the curve (AUC) values of 0.705 and 0.679 respectively, outperforming pN staging.

This multifaceted model promises to improve clinical decision-making by providing a more precise prognosis, enabling oncologists to identify high-risk patients who might benefit from intensified adjuvant therapies or closer surveillance. Moreover, it offers a personalized approach to lymph node evaluation post-neoadjuvant therapy, acknowledging the heterogeneity of treatment response and disease biology within the lymphatic system.

The study’s revelations carry profound implications for the surgical management of ESCC. Recognizing an optimal lymph node clearance range challenges the prevailing surgical dogma and may influence future guidelines to strike a balance between thorough disease removal and preservation of host defenses. Additionally, the prognostic weight of extracapsular invasion and tumor regression within nodes advocates for meticulous pathological examination and standardized reporting protocols.

From a research perspective, these findings pave the way for future explorations into the molecular underpinnings of nodal tumor regression and extracapsular spread. Understanding the biological mechanisms driving these phenomena could unlock novel therapeutic targets aimed at enhancing neoadjuvant therapy efficacy and curbing metastatic potential.

The predictive model also serves as a prototype for integrating multifactorial lymph node assessments in other cancers treated with neoadjuvant modalities. By illustrating the additive value of parameters like tumor regression grade and extracapsular invasion, the study sets a precedent for refining prognostication in complex oncologic landscapes where conventional staging falls short.

Clinicians and researchers alike stand to benefit from the enhanced prognostic accuracy of this model, translating into improved patient stratification and potentially better survival outcomes. As esophageal cancer continues to pose significant treatment challenges worldwide, advancements such as these offer a beacon of hope, bringing personalized medicine to the forefront of clinical oncology.

In sum, the development of a comprehensive lymph node evaluation system post-neoadjuvant therapy represents a paradigm shift in esophageal cancer prognosis, advocating for more sophisticated pathological assessments and data integration to inform clinical strategies. This approach underscores the evolving nature of cancer care, where precision and individualized treatment outlook are paramount.

The remarkable strides made in this study underscore the necessity of revisiting and refining existing cancer staging systems. Such innovation is critical in addressing the complexity of tumor biology and treatment response, ultimately aiming to enhance patient survival and quality of life.

As this enhanced prognosis prediction model gains traction, its incorporation into routine clinical workflows could become a standard of care, guiding therapeutic decisions and optimizing resource allocation in oncology settings worldwide.

This research not only enriches our understanding of lymph node dynamics in ESCC but also exemplifies the transformative potential of detailed pathological evaluation coupled with advanced statistical modeling in shaping the future of cancer prognosis.

The potential clinical utility of this model extends beyond survival prediction, potentially informing surgical approaches, postoperative surveillance, and the selection of candidates for adjuvant therapies, thereby personalizing patient management in a truly holistic manner.

Ongoing validation and prospective studies will be essential to confirm the model’s applicability across diverse populations and clinical scenarios, ensuring its robustness and generalizability in everyday oncology practice.

Overall, this innovative lymph node assessment framework signifies a vital advance in esophageal cancer research, carrying the promise of enhanced prognostic precision and improved patient outcomes through tailored therapeutic strategies.

Subject of Research: Prognosis prediction in esophageal squamous cell carcinoma (ESCC) through advanced lymph node evaluation after neoadjuvant chemoradiotherapy.

Article Title: Enhanced prognosis prediction model in esophageal cancer via lymph node assessment post-neoadjuvant.

Article References:
Zhou, Y., Xiao, M., Li, J. et al. Enhanced prognosis prediction model in esophageal cancer via lymph node assessment post-neoadjuvant. BMC Cancer 25, 1468 (2025). https://doi.org/10.1186/s12885-025-14785-7

Image Credits: Scienmag.com

DOI: https://doi.org/10.1186/s12885-025-14785-7

The research team embarked on a comprehensive retrospective analysis involving 151 patients diagnosed with LARC who received nCRT followed by surgical resection over a nine-year period from 2014 to 2023. Central to their investigation was the correlation between pre-treatment PET/CT metabolic data and tumor regression grade (TRG) post-surgery, categorized according to the Mandard classification system. Patients were dichotomized into complete responders (TRG1) and incomplete responders (TRG2–5), allowing for a focused assessment of clinical and pathological factors influencing outcomes.

Metabolic parameters derived from FDG PET/CT have long been hypothesized as potential biomarkers for tumor behavior and treatment sensitivity. SUVmax, referring to the peak uptake within the tumor, along with volumetric measures such as MTV and TLG, reflect both the metabolic activity and tumor burden. However, intriguingly, the study’s findings contradict expectations, as none of these PET/CT parameters demonstrated statistically significant predictive value for either pathological tumor regression or survival endpoints in the context of neoadjuvant therapy.

Instead, attention shifted to a host of clinico-pathological variables that emerged as robust predictors of therapeutic success and prognosis. Family history of cancer, baseline and post-treatment carcinoembryonic antigen (CEA) levels, radiotherapy-associated carbohydrate antigen 19-9 (CA19-9) dynamics, and the presence of concurrent chemotherapy (CC) stood out as critical factors determining complete response rates. These clinical indicators underscore the multifaceted nature of cancer progression and the limitations of relying solely on imaging data for comprehensive patient stratification.

The impact of histopathological features on treatment outcomes cannot be overstated. Perforation, lymphovascular invasion (LVI), and perineural invasion (PNI)—classic markers of aggressive tumor biology—invariably correlated with incomplete response and worse survival profiles. Their inclusion in multivariate analyses reinforced their independent prognostic significance, highlighting that microscopic tumor behavior ultimately governs response to nCRT beyond what can be visualized metabolically.

From a survival perspective, TRG1 patients enjoyed markedly improved overall survival (OS) and disease-free survival (DFS), reflecting the clinical importance of achieving a complete pathological response. Kaplan–Meier survival curves neatly illustrated these disparities, reinforcing TRG1 as a pivotal biomarker for patient prognosis. Moreover, multivariate Cox regression models revealed that TRG1 status, administration of concurrent chemotherapy, and absence of tumor perforation independently predicted improved survival outcomes.

The lack of correlation between pre-treatment FDG PET/CT parameters and treatment response represents a significant paradigm shift. This revelation urges oncologists and radiologists to reconsider the predictive weight traditionally assigned to metabolic imaging in the neoadjuvant setting for rectal cancer. It further emphasizes the necessity of integrating a more holistic clinical and pathological approach when designing personalized treatment strategies.

Neoadjuvant chemoradiotherapy is a cornerstone in managing LARC, frequently enabling tumor downstaging and sphincter-sparing surgeries. However, individualized responses vary greatly, posing challenges to optimizing treatment. The study’s integrative methodology, combining imaging, biochemical markers, and histological data, provides a robust framework that could streamline prognostication and allow for more nuanced clinical decision-making.

CEA and CA19-9, both serum tumor markers, have long been employed in gastrointestinal oncology for monitoring disease progression and recurrence. Their demonstrated associations with TRG and survival in this study reaffirm their clinical utility in tandem with conventional diagnostic tools. Importantly, post-treatment CEA levels emerged as a particularly powerful indicator, reflecting residual tumor burden and potential microscopic disease persistence.

Concurrent chemotherapy, when administered alongside radiotherapy, was associated with better pathological response and improved survival metrics. This finding aligns with existing literature advocating for combination regimens to enhance radiosensitization and maximize tumor eradication. It validates current therapeutic protocols and paves the way for further investigations into optimizing concurrent treatment modalities.

The study also explored the role of family history, traditionally a surrogate for genetic predisposition and shared environmental risk factors, in modulating treatment response. The strong association observed suggests that genetic and epigenetic influences may play a more significant role in therapeutic sensitivity than previously recognized, warranting further molecular profiling studies to elucidate underlying mechanisms.

Importantly, the presence of perforation—an indicator of tumor invasion into surrounding tissues—was strongly predictive of poorer outcomes. This emphasizes the aggressive nature of certain rectal cancers and the need for early detection and intervention. Histopathological assessment after surgery remains indispensable for accurate staging and prognosis.

Perineural invasion and lymphovascular invasion, both indicative of tumor dissemination pathways, independently impacted treatment response and survival, reaffirming their value as critical prognostic factors. Their detection necessitates thorough pathological evaluation to guide adjuvant therapy considerations.

While FDG PET/CT remains invaluable for cancer staging and detecting distant metastases, this study cautions against overreliance on baseline metabolic parameters as solitary prognostic tools in the context of nCRT for LARC. A multimodal diagnostic strategy incorporating serum markers, histopathological examination, and clinical context remains paramount.

The findings presented in this study have profound implications for clinical practice. They suggest that clinicians should place greater emphasis on molecular and histopathological markers when predicting response to nCRT in rectal cancer. Additionally, the study advocates for continued research into novel biomarkers and imaging techniques that might better capture the complexity of tumor biology and treatment effects.

This comprehensive investigation lays the foundation for refining patient selection criteria and tailoring neoadjuvant treatment protocols. By recognizing the limited prognostic role of baseline FDG PET/CT metabolic parameters and amplifying the significance of clinical-pathological features, oncologists can enhance therapeutic precision, improve survival rates, and ultimately advance patient care in rectal cancer management.

Subject of Research: Predictive value of baseline F-18 FDG PET/CT metabolic parameters and clinico-pathological variables in tumor regression and survival outcomes in locally advanced rectal cancer patients undergoing neoadjuvant chemoradiotherapy.

Article Title: Evaluation of pre-treatment F-18 FDG PET/CT according to Mandard classification in locally advanced rectal cancer patients undergoing neoadjuvant chemoradiotherapy.

Article References:
Aras, F., Parvizi, M., Nalbant, O.A. et al. Evaluation of pre-treatment F-18 FDG PET/CT according to Mandard classification in locally advanced rectal cancer patients undergoing neoadjuvant chemoradiotherapy. BMC Cancer 25, 1262 (2025). https://doi.org/10.1186/s12885-025-14659-y

Image Credits: Scienmag.com

DOI: https://doi.org/10.1186/s12885-025-14659-y