This mini-review synthesizes key evidence on breast cancer in Morocco from major studies published over the past two decades. Moroccan breast cancer is characterized by a distinct profile: A younger median age at diagnosis (45-50 years), a high frequency of advanced-stage disease (stage III or higher in > 60% of hospital-based series), and prolonged diagnostic intervals driven by low symptom awareness and systemic barriers. Pathologically, invasive ductal carcinoma predominates, with hormone receptor-positive/human epidermal growth factor receptor 2-negative being the most common molecular subtype. The evolution towards guideline-concordant, multimodal care in specialized centers, including improved access to targeted therapies, is strongly associated with improved survival, with 5-year disease-free survival rates reaching 80% for appropriately managed patients. However, significant challenges persist, including severe financial toxicity, care access disparities, and gaps in supportive care. Future national strategies must prioritize organized early detection, strengthened patient navigation, universal financial protection, and integrated supportive care to translate research gains into equitable improvements in survival and quality of life.
BACKGROUND Soft tissue sarcomas (STSs) of the lower extremities are rare malignancies increasingly treated with limb-sparing surgery combined with radiotherapy (RT). While this approach provides excellent oncologic control and preserves function, it is associated with late skeletal complications. Postoperative pathologic fractures (PPFs) represent a serious and potentially disabling outcome, often requiring additional surgical intervention and impairing quality of life. Reported fracture rates and associated risk factors vary widely, and contemporary data incorporating modern surgical and radiotherapeutic techniques remain limited. AIM To identify independent predictors of PPFs following limb-sparing surgery for lower extremity STS. METHODS This retrospective cohort study included 266 patients with intermediate- or high-grade lower extremity STS treated with limb-sparing surgery between 2010 and 2020. Clinical, tumor-related, surgical, and treatment variables were collected. PPF was defined as a low-energy fracture occurring within the surgical field. Cumulative fracture incidence was estimated using Kaplan-Meier analysis. Risk factors were assessed using univariable analyses and multivariable Cox regression with Firth’s penalized likelihood. RESULTS During a median follow-up of 48.9 months, 23 postoperative pathological fractures occurred. The cumulative fracture incidence was 1.8% at 1 year, 13.0% at 5 years, and 20.6% at 10 years. Fractures most frequently involved the femur. In univariable analyses, older age, arterial hypertension, larger tumor size, RT, and bone-involving surgical procedures were associated with increased fracture risk. In multivariable analysis, bone resection and osteoporosis remained independently associated with PPF, whereas RT, age, and arterial hypertension were not statistically significant. Tumor size was not included in the multivariable model due to lack of significance in univariable analysis but remains clinically relevant. CONCLUSION PPFs are a relevant late complication following limb-sparing surgery for STS. Fracture risk is primarily associated with bone-involving surgical procedures and osteoporosis, whereas RT shows an elevated but not statistically significant association.
BACKGROUND Extramedullary hematopoiesis (EMH) in lymph nodes, particularly following neoadjuvant chemotherapy for breast cancer, is a rare phenomenon. Its occurrence in the context of combined immunochemotherapy remains underreported. Here, we present the first case of trilineage EMH in axillary lymph nodes following neoadjuvant immunochemotherapy for triple-negative breast cancer (TNBC). CASE SUMMARY A patient in her 50 years with newly diagnosed TNBC (cT1N1M0, stage IIA) underwent neoadjuvant therapy with epirubicin/cyclophosphamide and nab-paclitaxel, in combination with the PD-1 inhibitor toripalimab. Post-surgical pathological evaluation revealed a pathological complete response (ypT0N0) in both the breast and axillary lymph nodes, with undetectable circulating tumor DNA. However, histological examination of five axillary lymph nodes identified foci of trilineage EMH, comprising myeloid precursors, erythroblasts, and megakaryocytes, confirmed by immunohistochemistry for MPO, CD71, and CD61. No residual carcinoma or lymphoma was detected. CONCLUSION This case highlights EMH as a rare benign finding after effective neoadjuvant chemoimmunotherapy. The development of EMH likely involves multiple factors: Chemotherapy-induced bone marrow suppression, granulocyte colony-stimulating factor-mediated mobilization, and speculatively PD-1 blockade-related microenvironment remodeling. Recognition prevents misdiagnosis. Direct mechanistic evidence is lacking.
Glioblastoma (GBM) remains a devastating diagnosis, and since 2021, the field has witnessed both incremental advances and renewed paradigms in diagnosis, therapeutic development, and trial design. The 2021 WHO Central Nervous System 5 classification redefined GBM as isocitrate dehydrogenase (IDH)-wildtype, sharpening the molecular underpinnings of clinical trial cohorts. Targeted approaches in selected molecular subsets (e.g., IDH inhibitors) have matured, while tumor-treating fields remains a debated but utilised adjunct. Immunotherapy via checkpoint inhibitors has been disappointing in unselected populations, but newer vaccines, oncolytic viral, and combination strategies are under active development. The most hopeful advances in the 2023-2025 window come from engineered cell therapies, especially chimeric antigen receptor T-cell delivered locoregionally or with multivalent antigen specificity. Advances in liquid biopsy, spatial transcriptomics, imaging biomarkers, and adaptive trial platforms are converging to accelerate translation. This narrative review synthesises developments since 2021, integrating translational insight and practical guidance, and outlines a roadmap for the next decade of GBM research.
Breast cancer is the leading cause of cancer-related deaths among women worldwide. Early screening is crucial for reducing the mortality rate of this disease. The study by Improta et al , published in the recent issue of the World Journal of Clinical Oncology , compared and analyzed the differences between palpable and non-palpable breast cancers. The results revealed that palpable tumors exhibited larger volume, higher histological grade, elevated Ki-67 proliferation index, a higher proportion of aggressive molecular subtypes, and greater invasiveness. Based on the above research results, this article further explores the influence of tumor subtypes, patient age, and other factors on prognosis, elaborates on the current application status, advantages and disadvantages of existing screening techniques, as well as the limitations of innovative technologies. At the same time, it summarizes the application value of combined screening, risk stratification, and the integration of traditional Chinese and Western medicine in the prevention and diagnosis of breast cancer. This article clarifies that early screening for breast cancer can effectively improve the prognosis of patients, and proposes that multiple-modal screening techniques should be integrated, precise risk stratification screening should be carried out, and the traditional Chinese medicine prevention concept of “prevention before disease onset, and prevention of disease progression after onset” should be incorporated. The aim is to enhance the overall prevention and control efficiency of breast cancer and provide scientific references and practical basis for clinical diagnosis and treatment practices.
This editorial highlights a study which examines immune checkpoint markers and inflammation indices in lymphoproliferative neoplasms in Egypt. A study by Sherief et al , published in World Journal of Clinical Oncology , present a novel combination of prognostic markers, showing that co-expression levels of programmed death-ligand 1/C-X-C motif chemokine receptor 3 (CXCR3) and programmed death-1 (PD-1)/CXCR3 were significantly elevated, particularly PD-1/CXCR3 in stage IV lymphoma (area under the curve = 0.959). The systemic inflammatory response index (SIRI) increased in late-stage patients (area under the curve = 0.846) but decreased after treatment (P < 0.001). The study challenges previous beliefs regarding SIRI and PD-1/CXCR3’s impact on survival rates. Importantly, SIRI relies only on routine blood test data, making it feasible for use in resource-limited settings. This research establishes an immune-inflammatory biomarker system for lymphoma in areas with high hepatitis C virus prevalence in Egypt and offers a low-cost, effective prognostic model for better patient stratification and improved cancer healthcare equity.
The management of small rectal neuroendocrine tumors (NETs) with positive vertical margins after endoscopic resection remains controversial. In light of the recent study by Qiao et al published in World Journal of Clinical Oncology , which reported excellent oncologic outcomes following both endoscopic submucosal dissection (ESD) and hybrid ESD for stage 1 rectal NETs, we provide a pathology-centered reinterpretation of margin positivity. Despite multiple non-R0 resections, predominantly due to positive vertical margins, no patients developed local recurrence or metastasis. From a histopathological perspective, apparent margin involvement is frequently attributable to technical artifacts such as thermal injury, tissue distortion, tangential sectioning, or specimen fragmentation rather than true residual viable tumor. Moreover, the intrinsic biological indolence of small, well-differentiated (G1) rectal NETs further explains the low risk of recurrence. Together, these observations support a risk-stratified, surveillance-oriented management strategy and underscore the importance of nuanced pathological interpretation to avoid unnecessary salvage surgery while maintaining oncologic safety.
Although immunotherapy for colorectal cancer (CRC) has recently gained widespread attention, many patients continue to exhibit inherent or acquired resistance due to a lack of tumor-infiltrating lymphocytes and the poor immunogenicity of cancer cells within an immunosuppressive tumor microenvironment. Advances in high-throughput sequencing and bioinformatics have increasingly highlighted the role of the gut microbiome (GM) in modulating the quantity and phenotypes of innate and/or adaptive immune cells, thereby influencing CRC pathogenesis and the clinical response to immunotherapy. The GM maintains a symbiotic relationship with the host, contributes to protection against opportunistic pathogens, and supports intestinal homeostasis. Dysbiosis in GM composition and metabolite profiles drive uncontrolled inflammatory cascades, induces oxidative DNA damage, and promotes neoplastic progression. Furthermore, targeting GM populations, such as next-generation probiotics or dietary interventions, can enhance the prevalence of effector T cells in a “hot” immunogenic microenvironment, thereby ameliorating the efficacy of CRC immunotherapy, improving survival and potentially reducing toxicities in patients. This review briefly summarizes current findings and molecular mechanisms underlying host-GM mutualism under physiological and cancerous conditions, which may inform the development of novel strategies for CRC diagnosis, treatment, and prevention.
In the challenging landscape of esophageal squamous cell carcinoma (ESCC), where late diagnosis often brings progressive dysphagia, feeding difficulties, and chronic caloric-protein deficits that accelerate muscle wasting even before treatment begins, Xiao et al offer a compelling insight in the World Journal of Clinical Oncology . Their retrospective analysis of 360 patients undergoing definitive chemoradiotherapy reveals that baseline body mass index (BMI) is a powerful, readily available predictor of low muscle mass (LMM). Each additional BMI unit is linked to roughly a 39% lower odds of LMM (odds ratio: 0.613; 95%CI: 0.531-0.707), with a clear inflection point around 21.5 kg/m2 marking heightened risk below this threshold. What truly stands out is the synergistic prognostic impact: Patients burdened by both low BMI and LMM face the bleakest outlook, with a median overall survival of only 17 months. This underscores that LMM is far more than a nutritional byproduct — it acts as an independent driver of poorer treatment tolerance, heightened toxicities, and reduced survival in locally advanced ESCC. These observations open a practical window for action in everyday oncology practice. A simple BMI measurement at diagnosis can serve as an immediate, zero-cost alert to prompt detailed body composition evaluation (ideally via pretreatment computed tomography) and swift multidisciplinary intervention. Early nutritional reinforcement — through hypercaloric, high-protein oral nutritional supplements (ONS) delivering ≥ 1.5-2.0 g protein/kg ideal body weight daily — has been shown in dedicated trials to preserve weight, BMI, albumin, and prealbumin levels while attenuating radiation esophagitis, myelosuppression, and other toxicities during radiotherapy or chemoradiotherapy in ESCC patients. Meta-analyses further support that high-protein ONS reduces complications and aids lean mass maintenance in high-sarcopenia-risk cancers such as esophageal cancer. When oral intake falters due to tumor-related dysphagia, enteral routes become essential, complemented by individualized dietitian guidance and frequent reassessments. Adding supervised resistance training (2-3 sessions/week) where performance status allows provides a vital non-nutritional countermeasure against sarcopenia progression. By viewing BMI and LMM not merely as prognostic signals but as modifiable targets, we can shift toward more proactive, personalized supportive care — potentially transforming outcomes in one of oncology’s most demanding diseases.
The 2025 European Society for Medical Oncology Annual Meeting unveiled pivotal advances across the therapeutic spectrum of renal cell carcinoma, marking a decisive shift towards precision medicine. In localized disease, adjuvant therapy is being refined through risk stratification, as demonstrated by the RAMPART trial, which showed significant benefit for dual immune-checkpoint inhibition specifically in high-risk patients. The Neoadjuvant Study With Combination Immuno-oncology for Primary Clear Cell Renal Cell Cancer study further demonstrated that even a short course of neoadjuvant dual immunotherapy could induce meaningful pathological responses in locally advanced clear-cell renal cell carcinoma. For advanced stages, the treatment paradigm is rapidly evolving beyond standard immuno-tyrosine kinase inhibitor combinations. Investigational triple therapies, such as adding a hypoxia-inducible factor 2-alpha inhibitor to first-line regimens, show promise for deeper and more durable responses. A central theme of the conference was the parallel development of predictive biomarkers—including molecular classifiers, dynamic plasma markers, tumor microenvironment signatures, and AI-based histology analysis—to guide individualized treatment selection and avoid ineffective therapy. Following disease progression on first-line treatment, the management landscape is expanding with new evidence from direct comparative trials (e.g. , LenCabo), novel drug combinations, and emerging modalities like stereotactic radiotherapy.
Cancer cells frequently rewire serine/glycine one-carbon metabolism to sustain nucleotide synthesis, redox balance, and epigenetic regulation, pathways that also shape antitumor immunity within the tumor microenvironment. Here, we review two natural agents, shilajit (a fulvic-acid-rich exudate) and glycine, with convergent immunomodulatory and antitumor activities relevant to breast and liver cancers. Shilajit exhibits antioxidant and anti-inflammatory effects and has shown selective cytotoxicity and anti-migratory activity in preclinical cancer models, including when incorporated into nanoformulations. Glycine supports glutathione-dependent redox defense, attenuates inflammatory signaling, and intersects with amino-acid metabolic programs that influence tumor cell fitness and immune cell function. We synthesize mechanistic and preclinical evidence to position shilajit and glycine as complementary, low-cost candidates for modulating tumor immunity and stress responses. Finally, we outline translational priorities, including standardized formulations, pharmacokinetics, safety, biomarker-guided patient stratification, and rational combinations with established systemic therapies.
Lactylation, a recently discovered post-translational modification, is crucial in cancer biology, linking cellular metabolism to the regulation of gene expression. This modification involves the attachment of a lactyl group to lysine residues, which affects protein function and plays a key role in cancer progression by influencing major hallmarks of the disease. These hallmarks include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, promoting invasion and metastasis, reprogramming metabolism, avoiding immune destruction, enhancing genomic instability, and fueling tumor-promoting inflammation. Lactylation modifies key signaling pathways, including phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin and nuclear factor kappa-light-chain-enhancer of activated B cells, which are vital for tumor cell survival, growth, and metabolic adaptation. Furthermore, lactylation affects immune evasion and genomic instability, increasing the adaptability and metastatic potential of cancer cells. This review highlights the growing importance of lactylation in regulating cancer hallmarks and its potential as a biomarker for early cancer diagnosis and prognosis. Additionally, enzymes involved in lactylation, such as lactate dehydrogenase and acyltransferases, present promising therapeutic targets. Inhibiting these enzymes may decrease lactylation, inhibit tumor growth, and improve the effectiveness of immunotherapy. A deeper understanding of lactylation’s molecular mechanisms opens new avenues for developing more personalized and effective treatments, underscoring its role as a crucial factor in precision oncology.
BACKGROUND Gastrointestinal stromal tumor (GIST) represent the most common mesenchymal neoplasms of the gastrointestinal tract, with evolving management driven by advances in molecular profiling, targeted therapy, and minimally invasive surgical techniques. However, longitudinal regional data describing real-world outcomes remain limited. AIM To evaluate trends in presentation, surgical management, risk stratification, and outcomes of GIST over three decades in a Middle Eastern tertiary referral center. METHODS A retrospective cohort study included patients with GIST who were managed between 1995 and 2024. We analyzed demographic, clinicopathological, radiological, and treatment-related variables. We compared clinicopathological characteristics across risk stratification groups (low-, intermediate-, and high-risk) and by surgical approach (open vs minimally invasive). Survival outcomes were evaluated using Kaplan-Meier analysis. RESULTS A total of 282 patients were included. The mean age was 53.4 +/- 13.5 years, and 64.9% were male. Gastric tumors predominated (67.7%), followed by small-bowel GIST (21.3%). Most tumors were localized at presentation (64.5%), while 12.8% had distant metastases. The median tumor size was 5.5 cm (range 0.3-29.0). Mitotic count was <= 5 per 50 high-power field in 66.2%, 6-10 in 19.7%, and > 10 in 14.1%. Risk categories included low (57.1%), intermediate (14.2%), and high (28.7%). Resection was performed in 94.3% of cases (open 46.6%, laparoscopic 42.9%, robotic 10.5%), and R0 margins were achieved in 85.5% of cases. Minimally invasive surgery (MIS) made up 53.4% of resections. It was associated with smaller tumors, more localized disease, fewer positive margins, and shorter hospital stay compared with open surgery. Adjuvant or systemic therapy was given in 51.4% of patients, predominantly imatinib. Median hospital stay was 8 days (1-60). Over a median follow-up of 35.5 months, disease-free survival (DFS) was 82.3%. A total of 10.6% were alive with recurrence or metastases, and 7.1% died. Incidental GIST detection during bariatric surgery occurred in 8.9% of cases. The surgical approach, both laparoscopic [hazard ratio (HR) 2.454, 95% confidence interval (CI): 1.604-3.754, P < 0.001] and robotic resections (HR 2.936, 95%CI: 1.682-5.124, P < 0.001), were significantly associated with improved DFS compared with open surgery. CONCLUSION This study found that most GISTs were gastric in origin. Over three decades, the region showed a shift toward MIS, more molecularly guided and risk-adapted therapy, and improved outcomes. High rates of complete resection and favorable DFS underscore the effectiveness of multidisciplinary care. These region-specific findings provide important benchmarks to shape practice and future collaboration across centers.
BACKGROUND Alpha-fetoprotein-producing gastric cancer (AFPGC) is an aggressive subtype with frequent liver and nodal metastases and poor outcomes. Resistance to standard chemotherapy is common. Compound Muji Granules (CMG), a traditional multi-component herbal formulation reported to reduce serum alpha-fetoprotein, has shown antitumor activity in solid tumors. AIM To evaluate the effects of CMG combined with cisplatin in AFPGC cells and investigated the role of the epidermal growth factor receptor (EGFR)-phosphatidylinositol 3-kinase (PI3K)-protein kinase B (AKT)-mammalian target of rapamycin (mTOR) pathway. METHODS The human AFPGC cell line FU97 was treated with CMG, cisplatin, or both. Proliferation (cell counting kit-8), alpha-fetoprotein secretion, cell-cycle distribution and apoptosis (flow cytometry), and migration and invasion (Transwell assays) were assessed. Expression of EGFR, PI3K, AKT, and mTOR was measured by quantitative real-time-polymerase chain reaction and Western blotting. Network pharmacology and molecular docking were used to identify putative CMG targets. An EGFR-overexpressing FU97 model was generated to test pathway dependence. RESULTS CMG reduced FU97 cell proliferation, migration, and invasion; lowered alpha-fetoprotein secretion; and induced G0-G1 arrest and apoptosis as compared with control. The combination of CMG and cisplatin produced greater growth inhibition and apoptosis than either agent alone (P < 0.05). Combination therapy down-regulated EGFR, PI3K, AKT, and mTOR at the transcript and protein levels, consistent with suppression of the EGFR-PI3K-AKT-mTOR pathway. In EGFR-overexpressing FU97 cells, CMG plus cisplatin retained antiproliferative and proapoptotic activity, indicating efficacy in an EGFR-driven context. CONCLUSION CMG suppresses AFPGC cell growth, induces cell-cycle arrest and apoptosis, enhances cisplatin activity, and inhibits the EGFR-PI3K-AKT-mTOR pathway, supporting further evaluation of CMG combined with chemotherapy in AFPGC.
The recent study by Zweig et al published in the World Journal of Clinical Oncology highlights the promising role of reovirus in modulating key signaling pathways and cytokine profiles in metastatic colorectal cancer patients with KRAS mutations. Their findings demonstrate significant alterations in gene expression (e.g. , signal transducer and activator of transcription 3, glycogen synthase kinase 3 beta) and cytokine dynamics (e.g. vascular endothelial growth factor suppression, interferon-gamma elevation), suggesting reovirus-induced antitumor immunity. While these results underscore reovirus’s potential as a therapeutic adjuvant, critical questions remain regarding its long-term efficacy, optimal dosing, and synergy with existing therapies. This letter discusses the translational implications of these findings, emphasizing the need for larger clinical cohorts, tumor microenvironment-focused analyses, and combinatorial strategies with immune checkpoint inhibitors to maximize therapeutic impact. Addressing these gaps could accelerate reovirus’s integration into personalized oncology regimens for KRAS-driven malignancies.
Diabetes mellitus (DM), particularly type 2 diabetes and ovarian cancer (OC) intersect through a complex network of metabolic, inflammatory, and hormonal disturbances that influence tumorigenesis, disease progression, and clinical outcomes. Epidemiologic evidence consistently associates pre-existing DM with higher OC incidence and poorer survival; however, the mechanistic underpinnings remain incompletely defined and substantive knowledge gaps persist. Central to this intersection is the diabetic metabolic milieu, characterized by chronic hyperglycemia, compensatory hyperinsulinemia, and low-grade inflammation, which promotes cellular proliferation, genomic instability, and metastatic potential. Mechanistically, dysregulated insulin and insulin-like growth factor-1 signaling activates the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin axis, driving anti-apoptotic signaling, angiogenesis, and metabolic reprogramming. In parallel, diabetes-associated oxidative stress contributes to DNA damage, defective repair mechanisms, and epigenetic alterations that may accelerate malignant transformation of ovarian or fallopian tube precursor lesions. Despite these insights, critical gaps also remain regarding the influence of contemporary antidiabetic pharmacotherapies - such as metformin, receptor agonist-1 receptor agonists, and sodium-glucose cotransporter-2 inhibitors - on tumor metabolism, chemoresponsiveness, and survival outcomes. The interplay between reproductive hormonal signaling, diabetic metabolic alterations, and immune-stromal remodeling in the ovarian tumor microenvironment is similarly understudied. This review integrates epidemiologic, molecular, and clinical evidence linking DM and OC, evaluates the potential modifying effects of antidiabetic treatments, and highlights priorities for future investigation. Clarifying these intersecting pathways is essential for advancing risk stratification, informing precision therapies, and improving outcomes in this vulnerable population.
The recent article by Zari et al published in World Journal of Clinical Oncology on bone metastases patterns in stage IV breast cancer offers valuable insight by stratifying anatomical distribution according to histological subtypes. However, some important clinical and biological aspects remain insufficiently addressed. For instance, the lack of data on diagnostic imaging methods, prior systemic therapies, and metastatic burden limits the interpretation of survival outcomes. Moreover, the prognostic implications of specific skeletal sites, such as spinal vs appendicular involvement are not fully discussed. We believe that integrating anatomical findings with clinical history and biological markers would offer a more complete understanding and greater translational value.
