Abstract: A type II cadherin, Cadherin-19 (CDH19), plays a vital role in neural crest development. CDH19 regulates cell–cell junctions and migration by forming catenin-cytoskeleton complexes. Although anti-CDH19 monoclonal antibodies (mAbs) are used for specific applications such as Western blotting and immunohistochemistry (IHC), suitable anti-CDH19 mAbs for flow cytometry are limited. Here, novel anti-human CDH19 mAbs (Ca19Mabs) were developed through flow cytometry-based high-throughput screening. One clone, Ca19Mab-8 (IgG1, κ), specifically recognized CDH19-overexpressing Chinese hamster ovary-K1 cells but did not bind to other 21 CDHs (including both type I and type II) in flow cytometry. Additionally, Ca19Mab-8 recognized endogenous CDH19 in the human glioblastoma cell line LN229. The dissociation constant (KD) of Ca19Mab-8 for LN229/CDH19 was 9.0 × 10⁻⁹ M. Ca19Mab-8 can detect CDH19 in Western blotting and IHC. These findings suggest that Ca19Mab-8 is versatile for basic research and has potential applications in clinical diagnosis and tumor therapy.

Abstract: Background: Oncology medication costs are increasing internationally; patient attitudes towards these costs remain unclear. Methods: A three-part cross-sectional questionnaire was distributed to patients with breast cancer to determine their attitudes towards oncology medication costs and to ex-plore potential patient acceptable methods to reduce these costs. Results: 321 patients were eligible for inclusion and 180 fully completed the questionnaire (56.1% response rate). Overall, 67.8% (N = 122/180) of patients found the costs presented in the questionnaire to be unacceptable. 92.2% (N = 166/180), 87.8% (N = 158/180) and 68.9% (N = 124/180) of participants found the costs of pembrolizumab, palbociclib and trastuzumab respectively to be unacceptable. 72.8% (N = 131/180) of patients indicated that they would like to be better informed about the societal costs of their cancer treatment and 81.1% (N = 146/180) of patients believed that reducing the costs of cancer treatment to society is important. There was a statistically significant difference in patient desires to be better informed of societal drug costs between those with early-stage breast cancer and those with metastatic disease (75.8% vs 47.4%, χ2 = 6.923, p = 0.009). Conclusion: These findings indicate that many Irish patients with breast cancer find the societal costs of oncology medications to be unacceptable, and many patients have a de-sire to be better informed of these costs.

Abstract: Glioblastoma (GBM) remains among the most treatment-refractory human malignancies, shaped by profound molecular heterogeneity, extensive genomic instability and an immunosuppressive tumor microenvironment. Radiotherapy represents a cornerstone of current management; however, its therapeutic benefit is frequently limited by adaptive resistance and ineffective antitumor immunity. Emerging evidence indicates that ionizing radiation acts not only as a cytotoxic modality, but also as a potent immunological trigger through the release of damage-associated molecular patterns (DAMPs) and the induction of immunogenic cell death (ICD). In this review, we synthesize recent advances describing how canonical DAMPs—including HMGB1, ATP, calreticulin exposure, mitochondrial and nuclear DNA fragments—coordinate innate and adaptive immune activation via TLR-, RAGE- and cGAS–STING-dependent pathways. We further discuss the dual nature of DAMP signaling, which can either promote durable antitumor immunity or foster chronic inflammation, myeloid reprogramming and tumor tolerance, depending on radiation dose, fractionation, tumor context and concomitant therapies. Special emphasis is placed on how different radiation qualities, particularly proton versus photon irradiation, differentially modulate DAMP release, ICD dynamics and microenvironmental remodeling. Finally, we highlight translational opportunities to exploit DAMP-related signatures as liquid-biopsy biomarkers of response, as rational selectors for combination strategies (including immunotherapy and radiosensitizers), and as biological guides for personalized and adaptive radiotherapy in GBM. Collectively, DAMP-centered radiobiology provides a conceptual framework to integrate immunity into radiation planning and may enable a new generation of biologically informed treatment strategies for glioblastoma.

Abstract: Immunotherapy has transformed cancer management. Patients receiving immune checkpoint inhibitors frequently experience concurrent pain and sleep disturbances that affect quality of life, treatment adherence, and overall survival. Nursing interventions addressing both symptoms remain poorly defined. This scoping review searched the Scopus, ScienceDirect, PubMed, and CINAHL for updates from 2019 to 2025 following PRISMA-ScR guidelines; ten studies were included (randomized controlled trials, systematic reviews, and observational studies for all cancers since focusing on melanoma alone would not give enough results. Nurse-led interventions included education, physical therapies (massage, reflexology, acupressure), behavioral approaches, and digital platforms (telehealth, electronic patient-reported outcomes). The patients achieved moderate short-term pain reductions, significantly improved quality of life, enhanced treatment adherence, and reduced emergency department visits by up to 45%. However, only 2/10 studies used validated instruments to measure sleep quality, and none designed primary interventions specifically targeting sleep disturbances in patients receiving immunotherapy. Long-term sustainability of pain interventions was questionable, with most effects attenuating beyond eight weeks except for psycho-educational approaches. Future research should develop integrated, nurse-delivered interventions addressing pain and sleep as interconnected symptoms, with extended follow-up periods and enhanced accessibility across diverse healthcare settings. Validated instruments to measure sleep quality should be employed.

Abstract:

Background: Accurate prognostic assessment remains crucial in metastatic renal cell carcinoma (mRCC), especially as treatment options have expanded beyond vascular endothelial growth factor (VEGF)–targeted therapies to include immune checkpoint inhibitors (ICIs) and ICI–TKI combinations. The widely used IMDC classification shows important limitations in the modern therapeutic era, highlighting the need for complementary prognostic tools. In this context, the Meet-URO and CANLPH scores—incorporating clinical, inflammatory, and nutritional markers have emerged as promising alternatives. Objective: To evaluate and compare the prognostic performance of the Meet-URO and CANLPH scoring systems in a real-world mRCC cohort predominantly treated with first-line tyrosine kinase inhibitor (TKI) monotherapy due to limited access to ICI-based combinations. Methods: This retrospective single-center study included 112 patients with mRCC. The Meet-URO score was calculated for all patients, while the CANLPH score was assessed in 56 patients with complete laboratory data. CAR, NLR, and PHR were computed using baseline pre-treatment measurements. Overall survival (OS) and progression-free survival (PFS) the latter defined exclusively for first-line therapy—were estimated using the Kaplan–Meier method. Correlations between inflammatory markers and survival outcomes were analyzed using Spearman’s rho. Results: Meet-URO demonstrated clear prognostic stratification across all five categories, with the most favorable outcomes in score group 2 and progressively poorer OS and PFS in higher-risk groups. CANLPH also showed meaningful survival discrimination, with the highest inflammatory group (score 3) exhibiting markedly reduced OS and PFS. CAR was the strongest individual predictor of survival, while NLR and PHR showed weaker associations. Conclusion: Both Meet-URO and CANLPH provide strong, complementary prognostic information in mRCC, even in a cohort largely treated with TKI monotherapy. Their integration into routine risk assessment may enhance clinical decision-making, particularly in resource-limited settings.

Abstract: Background/Objectives: Nutritional risk screening is critical in the management of gynaecologic oncology (GO) surgical patients. Malnutrition is prevalent in this population and is associated with poorer surgical outcomes, including increased morbidity, prolonged hospital stays, and reduced survival rates. Nevertheless, the optimal nutritional screening tools for this patient group remain undefined. Methods: We conducted a narrative review to critically appraise commonly used nutritional screening and assessment tools in surgical GO patients. To highlight practical challenges in accurately identifying at-risk individuals, we incorporated findings from our recent clinical audit. Results: Several nutritional screening and assessment tools were identified. The results varied considerably between tools. The presence of ascites and rapid deterioration in oral intake were frequently overlooked, leading to under-recognition of malnutrition. These issues were corroborated by our audit findings. Emerging strategies including determining body composition from routine preoperative CT scans show promise. Conclusions: Accurate nutritional assessment is imperative to improve surgical outcomes in surgical GO patients. As currently no gold standard currently exists for this population, bespoke approaches to address disease-specific nutritional considerations are urgently needed to identify those at risk and allow for timely nutritional interventions. Integrating CT-based body composition analysis can provide an objective solution, thus requiring further investigation.

Abstract:

Background/Objectives: The anti-CLDN18.2 antibody zolbetuximab has emerged as a novel therapeutic option for advanced gastric adenocarcinoma. However, robust predictive biomarkers for its efficacy remain an unmet need. Methods: Utilizing the Japanese Center for Cancer Genomics and Advanced Therapeutics database, we retrospectively analyzed the clinical and genomic profiles of 49 patients with gastric adenocarcinoma who received zolbetuximab-containing regimens. Due to Japanese health insurance regulations, these patients were deemed to have CLDN18.2-positive tumors. We explored the association between objective response rate (ORR) and concurrent genomic alterations, focusing on tumor mutational burden (TMB) and major mutations (TP53, ARID1A, CDH1). Results: The ORR to zolbetuximab-based therapy in this cohort was 22.2%. Statistical analysis revealed a trend toward higher clinical response in patients with lower TMB (median 1.82 in responders vs. 4.0 in non-responders; p=0.050). Furthermore, patients without a CDH1 single nucleotide variant also showed a suggestive trend toward better response (p=0.086). No significant associations were found with TP53 or ARID1A alterations (p=0.787 and p=0.239, respectively). Conclusions: Our findings suggest that low TMB and the absence of CDH1 variants may serve as potential predictive biomarkers for response to zolbetuximab in CLDN18.2-positive gastric cancer. Prospective validation is warranted to maximize patient selection for this targeted therapy.

Abstract: Cancer remains a leading cause of morbidity and mortality worldwide, and effective strategies for cancer prevention are urgently needed to complement therapeutic ad-vances. While dietary factors are known to influence cancer risk, the molecular mecha-nisms that mediate inter-individual responses to nutritional exposures remain poorly defined. Emerging evidence identifies long non-coding RNAs (lncRNAs) as pivotal regulators of gene expression, chromatin organization, metabolic homeostasis, immune signaling, and cellular stress responses, core processes that drive cancer initiation and progression and are highly sensitive to nutritional status. In parallel, advances in pre-cision nutrition have highlighted how variability in genetics, metabolism, microbiome composition, and epigenetic landscapes shapes dietary influences on cancer susceptibility. This review integrates these rapidly evolving fields by positioning lncRNAs as molecular conduits that translate dietary exposures into transcriptional and epigenetic programs governing cancer development, progression, and therapeutic vulnerability. We provide mechanistic evidence demonstrating how dietary bioactive compounds and micronu-trients, including polyphenols (curcumin, resveratrol, EGCG), flavonoids, alkaloids such as berberine, omega-3 fatty acids, folate, vitamin D, probiotic metabolites (such as bu-tyrate and propionate), and trace elements (such as selenium, and zinc), modulate on-cogenic and tumor-suppressive lncRNAs. These nutrient-lncRNA interactions influence cancer-relevant pathways controlling proliferation, epithelial-mesenchymal transition, inflammation, oxidative stress, and metabolic rewiring. We further discuss emerging lncRNA signatures that reflect nutritional and metabolic states, their potential utility as biomarkers for individualized dietary interventions, and their integration into liquid biopsy platforms. Leveraging multi-omics datasets and systems biology, we outline AI-driven frameworks to map nutrient-lncRNA regulatory networks and identify tar-getable nodes for cancer chemoprevention. Finally, we address translational challenges, including compound bioavailability, inter-individual variability, and limited clinical validation, and propose future directions for incorporating lncRNA profiling into preci-sion nutrition-guided cancer prevention trials. Together, these insights position lncRNAs at the nexus of diet and cancer biology and establish a foundation for mechanistically informed precision nutrition strategies in cancer chemoprevention.

Abstract: Background: Head and neck squamous cell carcinomas (HNSCC) are aggressive malignancies with high mortality and poor prognosis. Pseudogenes with altered expression during HNSCC progression may serve as potential biomarkers for early detection, prognosis, and therapy selection. Methods: In this report, we analyzed the expression of ANXA2P2 and PA2G4P4 pseudogenes in HNSCC patients using data from The Cancer Genome Atlas. Clinical correlations were assessed through UALCAN and cBioPortal. Functional enrichment was investigated using REACTOME, ESTIMATE, and Gene Set Enrichment Analysis. Statistical analyses were performed with GraphPad Prism 8. Results: Both ANXA2P2 and PA2G4P4 were significantly upregulated in HNSCC compared to normal tissue. Their expression varied based on HPV status and was negatively correlated with overall survival. High pseudogene expression was associated with dysregulated oncogenic pathways, while low expression was linked to distinct immunological profiles. Conclusions: ANXA2P2 and PA2G4P4 exhibit oncogenic properties in HNSCC and hold potential as diagnostic and prognostic biomarkers.

Abstract: Background/Objectives: WHO grade II meningiomas exhibit heterogeneous clinical behavior that cannot be predicted by conventional histology. This study examined the relationship between the tumor immune microenvironment (TIME) and tumor growth kinetics in order to establish a biological basis for more precise risk stratification. Methods: A retrospective cohort of 15 patients was evaluated. Serial preoperative magnetic resonance imaging (MRI) scans were used to calculate the relative growth rate (RGR) and minimize the baseline tumor size. The densities of Iba1-positive macrophages (TAMs) and B7-H3-positive tumor cells were quantified using a deep learning-based image analysis system. Results: Linear correlation analysis showed no significant associations between individual immune components and RGR. However, median-based stratification revealed distinct associations. Tumors with low TAM density or high B7-H3-positive tumor cell density exhibited significantly higher RGR (P = 0.0401). Additionally, a significant inverse relationship was identified between TAM and that of B7-H3-positive tumor cell densities (Spearman’s R = -0.911, P < 0.001). Conclusions: We identified a proliferative "immune-cold" phenotype in WHO grade II meningiomas, which is characterized by low TAM density and high B7-H3-positive tumor cell density. This study extends established molecular frameworks by suggesting that high B7-H3-positive tumor cells proactively contribute to rapid tumor growth. These findings highlight the importance of targeting B7-H3-positive tumor cells when treating malignant meningiomas.

Abstract:

Cadherin-5 (CDH5), also known as vascular endothelial cadherin (VE-cadherin), plays essential roles in endothelial cell adhesion, vascular barrier function, and signaling. CDH5 coordinates endothelial cell–cell junction during vascular remodeling, which is indispensable for both vascular homeostasis and adaptive responses to pathological stimuli. Although anti-CDH5 monoclonal antibodies (mAbs) can be used for individual applications including flow cytometry, western blotting, and immunohistochemistry (IHC), highly sensitive and versatile anti-CDH5 mAbs for all applications remain limited. Here, novel anti-human CDH5 mAbs, designated Ca₅Mabs, were developed using a flow cytometry-based high-throughput screening. Among them, a clone Ca₅Mab-8 (IgG_2a, κ) recognized CDH5-overexpressed Chinese hamster ovary-K1 (CHO/CDH5) cells in flow cytometry. Furthermore, Ca₅Mab-8 also recognized endogenous CDH5-expressing human endothelial cell lines (HUVEC/TERT2 and HDMVEC/TERT164-B) and a cervical cancer cell line (Hela). These reactivities were superior to a commercially available anti-CDH5 mAb (clone BV9). The dissociation constant value of Ca₅Mab-8 for CHO/CDH5 was determined as 6.1 × 10⁻⁹ M. Ca₅Mab-8 can detect endogenous CDH5 in Western blotting. Moreover, Ca₅Mab-8, but not BV9, is available for IHC to detect endothelial cells in formalin-fixed paraffin-embedded tissues. These results indicate that Ca₅Mab-8 is versatile for research and are expected to contribute to clinical applications, such as tumor diagnosis and therapy.

Abstract: FLASH radiotherapy (FLASH-RT) sounds cool -- it's a way of blasting tumors with radiation super fast (over 40 Gy/s). Early tests are showing that it might be easier on healthy tissue while still killing cancer cells. Scientists have a few ideas about why this might be the cases, like maybe it drains oxygen quickly, messes with how cells make bad stuff, or protects cell parts. Animal tests on lungs, brains, skin, guts, and blood stuff seem to say FLASH-RT can shield normal tissue. Some early human tests look acceptable with only a few bad side effects. Still, getting it into clinics is tricky. We need better machines, ways to measure doses right, and plans for treatment. It also helps to learn how it works and getting past rules and money stuff. Doctors, scientists, and engineers working together can help find the best methods to do it, figure out how it works and show it is safe and it works in human trials. If we can find a way to make it work, it could be a game-changer for cancer treatment.

Abstract: Algal carotenoids play a promising role in handling chronic disease due to their diverse bioactive properties, including anti-inflammatory, antioxidant, and anticancer effects. This study assesses the activity of the antioxidant xanthophyll diatoxanthin (Dt), derived from marine diatoms, against triple-negative breast cancer (TNBC) cells using in vitro models, gene expression evaluation and explorings its role in potentiating the cytotoxic effect of chemotherapy. Dt exhibited selective activity against MDA-MB-231 and BT-549 TNBC cells and when combined with doxorubicin synergistically enhanced anti-tumor efficacy in both TNBC cell lines by further reducing cell viability. Dt also exerted its activity in inhibiting migration, chemotaxis, and suppressing 3D-tumor spheroid growth, and downregulating angiogenesis-related genes. Notably, secretome analysis revealed that Dt-induced changes in inflammatory, oxidative and angiogenic mediators, highlighting its ability to modulate the TNBC microenvironment. Dt also downregulated key pro-survival, proangiogenic and pro-tumorigenic genes in both TNBC cell lines, supporting its role in disrupting oncogenic pathways. Angiogenesis-related genes were significantly reduced. Dt also decreased the expression of angiogenic mediators in HUVEC cells, supporting Dt’s role in inhibiting tumor vascularization. Results on gene expression regulation were confirmed by RNAseq analysis. These findings pose Dt as a multifaceted candidate for contrasting TNBC, capable of targeting inflammation, angiogenesis, tumor cell growhth, and cell migration. Given its selective activity against TNBC cells, ability to enhance chemotherapy efficacy, and modulation of the tumor microenvironment, Dt holds promise as complementary drug for cancer prevention and interception. Future studies should focus on validating these effects in vivo and exploring Dt’s potential in combinatorial treatment strategies for cancer.

Abstract: Psychological trauma and chronic stress are increasingly acknowledged as relevant contributors to the onset and progression of somatic illness, including cancer. This integrative narrative review examines the potential role of prolonged and unresolved psychological conflicts, such as early-life adversity, toxic relational dynamics, chronic grief, and emotional invalidation, in modulating oncological vulnerability. Drawing from the fields of psycho-oncology, psychoneuroimmunology, and developmental psychopathology, we outline the psychobiological mechanisms through which chronic stress may impair immune surveillance, dysregulate the hypothalamic–pituitary–adrenal (HPA) axis, and promote low-grade systemic inflammation. These alterations can increase susceptibility to oncogenic infections (e.g., persistent Human Papillomavirus (HPV), reduce the body’s capacity to repair cellular damage, and contribute to tumorigenesis. We further discuss how trauma-related disorders, including posttraumatic stress disorder (PTSD), may negatively affect treatment adherence, reduce responsiveness to chemotherapy and immunotherapy, and increase cancer recurrence risk. Moreover, we introduce the model of trauma–cancer–retraumatization, highlighting how a cancer diagnosis can both reactivate unresolved psychological trauma and amplify emotional distress. Empirical studies suggest that trauma-informed psychotherapeutic interventions targeting emotional processing, attachment security, and perceived agency may improve both psychological well-being and clinical outcomes in oncology patients. Based on this evidence, we recommend integrating systematic screening for adverse childhood experiences (ACEs) and trauma history into cancer care pathways. Recognizing and addressing the hidden burden of psychological conflict in oncology may support a more holistic approach to cancer prevention, treatment, and survivorship.

Abstract:

Background and Clinical Significance: Breast cancer is the most frequent malignancy in women. Advanced metastatic breast cancer is considered a treatable but incurable condition, with a median overall survival of only 2-3 years. Among its subtypes, triple-negative breast cancer (TNBC) accounts for a high proportion of breast cancer–related deaths. It is characterized by an aggressive clinical course, early recurrence, and a strong propensity for visceral and brain metastases. Case Presentation :We report the case of a Caucasian woman who, two years after being initially diagnosed and treated for TNBC, developed disease relapse with lung and mediastinal lymph node metastases. The patient received three months of chemotherapy combined with an adjuvant integrative protocol consisting of melatonin, cannabidiol, and oxygen–ozone therapy. This combined approach led to the complete disappearance of the lung nodules. Subsequently, stereotactic radiotherapy was performed and, in association with the ongoing integrative treatment, resulted in a significant reduction of mediastinal adenopathy. Introduction of immunotherapy, supported continuously by the same adjuvant strategy, achieved a complete and durable remission. Strikingly, the patient remained disease-free five years after the diagnosis of lung and mediastinal metastases. Conclusions: This clinical case highlights the potential benefit of using melatonin, cannabidiol, and oxygen–ozone therapy as part of an integrative approach in patients with aggressive metastatic TNBC. While it is not possible to establish causality from a single case, the sustained remission observed suggests that such unconventional adjuvant strategies could play a supportive role in enhancing the efficacy of standard oncologic therapies.

Abstract:

Pancreatic cancer (PC) and colorectal cancer (CRC) are among the most lethal malignancies, with growing evidence pointing to the gut microbiota role in their progression. This study explores the anticancer potential of two microbiota-derived postbiotics, N-acetylcysteine (NAC) and tetrahydro β-carboline carboxylic acid (THC), in targeting some hallmark traits of PC and CRC, both as standalone agents and in combination with standard chemotherapeutics (gemcitabine for PC and 5-fluorouracil (5-FU) for CRC). Here, we found that NAC selectively reduced the viability of PC cells BxPC-3 without triggering apoptosis, while effectively inducing apoptosis in PC cells Panc-1 and in CRC cell lines. THC exhibited stronger anticancer activity, inhibiting proliferation and promoting apoptosis in all tested PC and CRC cells, even at lower concentrations. Combination treatments yielded promising synergistic effects. NAC enhanced the cytotoxicity of gemcitabine in Panc-1 cell through increased apoptosis. NAC when combined with 5-FU also increase apoptosis of CRC cells. THC further potentiated gemcitabine impact on Panc-1 cells by increasing apoptosis and by inducing cell cycle changes in BxPC-3. In CRC model, THC co-treatment with 5-FU reduced cell viability and increased apoptosis in all cells. These findings underscore the therapeutic potential of integrating microbiota-derived postbiotics with conventional chemotherapy, offering a novel avenue to improve outcomes in PC and CRC treatment.

Abstract: High-grade serous ovarian cancer (HGSOC) is the most prevalent and aggressive form of epithelial ovarian cancer, characterized by high recurrence rates and poor clinical outcomes. In this study, we identify molecular signatures associated with recurrence by conducting integrative transcriptomic and proteomic analyses on paired primary and recurrent HGSOC tissues from 34 patients. RNA sequencing and proteomic profiling revealed 185 differentially expressed genes (DEGs) and 36 differentially expressed proteins (DEPs) linked to recurrence. Pathway Enrichment and Ingenuity Pathway Analysis highlighted the involvement of immune cell trafficking, cell signaling, and MAPK pathway activation in recurrent tumors. Survival analysis identified seven DEGs significantly correlated with recurrence-free survival; among these, IL7R, IRF8, and PTPRC were upregulated in recurrent tumors and associated with poor prognosis, while NSG1 was downregulated and linked to favorable outcomes. Immunohistochemistry validated the differential expression of these markers at the protein level. Proteomic analysis demonstrated that recurrent tumor-specific DEGs are functionally linked to MAPK signaling. Co-expression analyses revealed dynamic regulatory interactions between DEGs and DEPs, suggesting context-dependent molecular shifts during recurrence. This integrative multi-omics approach reveals key molecular alterations underlying HGSOC recurrence and identifies IL7R, IRF8, PTPRC, and NSG1 as potential prognostic biomarkers and therapeutic targets. Our findings provide a foundation for targeted strategies to improve outcomes for patients with recurrent HGSOC.

Abstract: Background: This study analyzed the epidemiological profile of patients with non-melanoma skin cancer, female breast cancer, prostate cancer, colon and rectum cancer, lung cancer, and stomach cancer in southeastern Brazil (Espírito Santo, São Paulo, Minas Gerais, and Rio de Janeiro), covering the pre-pandemic period (2017 to 2019) and the pandemic period (2020 to 2022). Methods: The DATASUS database was used to assess possible impacts of percentage differences between these periods through point regression analysis and comparisons between the pre-pandemic and pandemic periods, as well as between the sexes using the Student's t-test. Results: The results suggest that sex-specific characteristics impose varying impacts and incidences on each gender. In Espírito Santo, there was a growing trend in stomach and non-melanoma skin cancers, while in São Paulo, only stomach cancer showed a statistically significant upward trend. Regarding staging, it was observed that during the pandemic period, the highest incidence was in stage IV, whereas in the pre-pandemic period, the highest incidences were in stages 0 and I, with medium and small effect sizes. Furthermore, the loss of pre-pandemic data was 11.46% (54,080 cases), while during the pandemic, the loss was 27.52% (129,869 cases), both statistically significant values of considerable magnitude. Conclusion: It can be concluded that there was a significant increase in the temporal trend only for stomach cancer in the states of São Paulo and Espírito Santo; for the other cancers and states, the trends were stationary. The high rate of missing data during the pandemic suggests a considerable impact on the results, highlighting the importance of additional prospective studies to better understand the effects of COVID-19 on oncology.

Abstract: The clinical management of Pancreatic Neuroendocrine Neoplasms (Pan-NENs) is complicated by the disease's intrinsic variability, which creates significant hurdles for accurate risk profiling and the standardization of treatment protocols. Recently, Artificial Intelligence (AI) has offered a promising avenue to address these challenges. By integrating and processing high-dimensional multimodal datasets (encompassing clinical history, radiomics, and pathology), these computational tools can refine survival forecasts and support the development of personalized medicine. However, the transition from experimental success to routine clinical use is currently obstructed by reliance on limited, retrospective cohorts that lack external validation, alongside unresolved concerns regarding algorithmic transparency and ethical governance. This review evaluates the current landscape of AI-driven prognostic modeling for Pan-NENs and critically examines the pathway towards their reliable integration into clinical practice.

Abstract: Immunotherapy has shown much promise for blood cancers, which may all be treatable or curable soon, especially if hematopoietic stem cells are harvested and frozen ahead of time for each individual. However, solid tumors are still extremely difficult to treat. Immunotherapy has helped in some instances for solid tumors, e.g., melanoma, and may eventually be able to cure all solid tumors for reasons that are a bit unclear currently. There may be a more direct way to treat solid tumors, though. I have written multiple articles about targeting truncal, i.e., clonal, mutations in solid tumors as a means of eliminating them. This would be a treatment specific to each patient. However, in my earlier work, I was under the impression that there may only be a handful of clonal mutations in an average solid tumor patient. After further investigation, it seems that instead of just several, there could be thousands of clonal mutations on average in a solid tumor patient. This may essentially ensure that all of a solid tumor patient’s cancer cells could be targeted.