Tumor Behavior Research Articles

‘What is this brain’s story?’ Healthcare professionals’ perspectives of managing brain tumour related personality and behaviour changes

‘What is this brain’s story?’ Healthcare professionals’ perspectives of managing brain tumour related personality and behaviour changes

Leveraging Single-Cell Multi-Omics to Decode Tumor Microenvironment Diversity and Therapeutic Resistance

Leveraging Single-Cell Multi-Omics to Decode Tumor Microenvironment Diversity and Therapeutic Resistance

Germ cell tumors in children.

Pediatric germ cell tumors represent a rare but biologically diverse group of neoplasms arising from pluripotent primordial germ cells. The 2022 edition of the WHO Classification of Pediatric Tumors introduced the first organ independent classification of germ cell tumors, reflecting advances in molecular biology, histopathology, and clinical practice. This review highlights the key changes, including the refined distinctions between the different subtypes. These updates enhance diagnostic accuracy and provide a framework for understanding age-dependent differences in tumor biology and behavior. Emphasis is placed on integrating the new classification into multidisciplinary care, particularly in addressing diagnostic challenges in pre- and post-pubertal-type germ cell tumors. By bridging the gap between histopathology and oncology, the updated classification represents a pivotal step forward in improving outcomes for children with germ cell tumors.

Glucose Metabolism Reprogramming of Immune Cells in the Microenvironment of Pancreatic and Hepatobiliary Cancers.

Pancreatic and hepatobiliary cancers are increasing in prevalence and contribute significantly to cancer-related mortality worldwide. Emerging therapeutic approaches, particularly immunotherapy, are gaining attention for their potential to harness the patient's immune system to combat these tumors. Understanding the role of immune cells in the tumor microenvironment (TME) and their metabolic reprogramming is key to developing more effective treatment strategies. This review aims to explore the relationship between immune cell function and glucose metabolism in the TME of pancreatic and hepatobiliary cancers. This review synthesizes current research on the metabolic adaptations of immune cells, specifically focusing on glucose metabolism within the TME of pancreatic and hepatobiliary cancers. We examine the mechanisms by which immune cells influence tumor progression through metabolic reprogramming and how these interactions can be targeted for therapeutic purposes. Immune cells in the TME undergo significant metabolic changes, with glucose metabolism playing a central role in modulating immune responses. These metabolic shifts not only affect immune cell function but also influence tumor behavior and progression. The unique metabolic features of immune cells in pancreatic and hepatobiliary cancers provide new opportunities for targeting immune responses to combat these malignancies more effectively. Understanding the complex relationship between immune cell glucose metabolism and tumor progression in the TME of pancreatic and hepatobiliary cancers offers promising therapeutic strategies. By modulating immune responses through targeted metabolic interventions, it may be possible to improve the efficacy of immunotherapies and better combat these aggressive cancers.

Recurrence-free survival after hepatectomy using propofol-based total intravenous anaesthesia and sevoflurane-based inhalational anaesthesia: a randomised controlled study.

While evidence from preclinical and observational cohort studies have suggested potential disparities in tumour behaviour associated with the choice of intra-operative anaesthetics, clinical evidence of tumour recurrence and metastasis remains inconclusive. We aimed to compare the impact of intra-operative anaesthesia on oncologic outcomes following hepatectomy for hepatocellular carcinoma. Adult patients scheduled for elective hepatectomy for hepatocellular carcinoma were assigned randomly (1:1) to either propofol-based total intravenous anaesthesia or sevoflurane-based inhalational anaesthesia. For recurrence-free survival, overall survival, intrahepatic recurrence-free survival and extrahepatic recurrence-free survival, the survival curves of the two groups were estimated using the Kaplan-Meier method and compared with the log-rank test. The primary outcome was one-year recurrence-free survival. Among the 536 patients enrolled, primary analysis comprised 228 and 226 patients in the total intravenous anaesthesia and sevoflurane-based inhalational anaesthesia groups, respectively. The probability of recurrence-free survival at one year was 79.1% (47 events) and 77.7% (50 events) in the total intravenous anaesthesia and sevoflurane-based inhalational anaesthesia groups, respectively (adjusted hazard ratio 1.04, 95%CI 0.72-1.52). The probability of intrahepatic and extrahepatic recurrence-free survival, as well as overall survival at one year, was not significantly different between total intravenous anaesthesia and sevoflurane-based inhalational anaesthesia: 81.3% (42 events) vs. 81.7% (41 events); 91.5% (19 events) vs. 88.8% (25 events); 99.1% (2 events) vs. 100.0% (no event), respectively. Subgroup analyses revealed that in patients undergoing open hepatectomy, total intravenous anaesthesia was associated with a significantly lower hazard of tumour recurrence or death (hazard ratio 0.49, 95%CI 0.25-0.95, p = 0.034), while in patients undergoing laparoscopic surgery, no significant difference was observed (hazard ratio 1.14, 95%CI 0.73-1.80, p = 0.558). Intra-operative anaesthesia technique did not affect postoperative recurrence and overall survival in patients with hepatocellular carcinoma undergoing hepatectomy.

Precision medicine in gynecological cancer (Review).

The advent of personalized and precision medicine has revolutionized oncology and treatment of gynecological cancer. These innovative approaches tailor treatments to individual patient profiles beyond genetic markers considering environmental and lifestyle factors, thereby optimizing therapeutic efficacy and minimizing adverse effects. Precision medicine uses advanced genomic technologies such as next-generation sequencing to perform comprehensive tumor profiling. This allows identification of distinct genetic mutations, expression patterns and signaling pathway alterations, revealing the complex molecular landscape of gynecological cancer such as ovarian, cervical and uterine cancer. A major challenge in treating these cancers is their inherent molecular heterogeneity, which can influence tumor behavior, therapy response and prognosis. Precision medicine aims to overcome this by identifying biomarkers and molecular drivers for targeted therapy selection. For example, the identification of breast cancer (BRCA) gene mutations in ovarian cancer has guided the use of poly (ADP-ribose) polymerase inhibitors, leading to more effective treatments with fewer side effects. Similar targeted therapies and immunotherapies have also been developed for cervical and uterine cancer, marking progress toward personalized care. Future directions in gynecological oncology emphasize the importance of molecular profiling and development of targeted therapies. By understanding the unique molecular features of each patient, clinicians can select the most effective personalized treatment strategies to improve patient outcomes and quality of life.

Insulin-like Growth Factor 1 (IGF1) and Its Isoforms: Insights into the Mechanisms of Endometrial Cancer.

Endometrial cancer (EC) is a common gynaecological malignancy associated with metabolic dysfunctions such as obesity, diabetes and insulin resistance, as well as hormonal imbalances, particularly involving oestrogen and progesterone. These factors disrupt normal cellular metabolism, heightening the risk of developing endometrioid EC (EEC), the most prevalent subtype of EC. The insulin-like growth factor-1 (IGF1) pathway, a key regulator of growth, metabolism, and organ function, is implicated in EC progression. Recent research highlights the distinct roles of IGF1 isoforms, including IGF1-Ea, IGF1-Eb, and IGF1-Ec, in promoting tumour growth, metastasis, and hormone signalling interactions, particularly with oestrogen. This review examines the function and clinical significance of IGF-1 isoforms, emphasising their mechanisms in gynaecological physiology and their contributions to EC pathogenesis. Evidence from other cancers further underscores the relevance of IGF1 isoforms in driving tumour behaviours, offering valuable insights into their potential as biomarkers and therapeutic targets. Understanding these mechanisms provides opportunities for novel approaches to the prevention, diagnosis, and treatment of EC, improving patient outcomes and advancing the broader field of hormone-driven cancers.

Cushing Disease Clinical Phenotype and Tumor Behavior Vary With Age: Diagnostic and Perioperative Implications

Abstract Context Little is known about presenting clinical characteristics, tumor biology, and surgical morbidity of Cushing disease (CD) with aging. Objective Using a large multi-institutional data set, we assessed diagnostic and prognostic significance of age in CD through differences in presentation, laboratory results, tumor characteristics, and postoperative outcomes. Methods Data from the Registry of Adenomas of the Pituitary and Related Disorders (RAPID) were reviewed for patients with CD treated with transsphenoidal tumor resection at 11 centers between 2003 and 2023. Outcomes assessed included comorbidities, presenting features, preoperative endocrine evaluations, perioperative characteristics, postoperative endocrine laboratory values, and complications. Results Of the 608 patients evaluated, 496 (81.6%) were female; median age at surgery was 44 years (range, 10-78 years). Increasing age was associated with increasing comorbidities, frailty, rates of postoperative thromboembolic disease, Knosp grade, tumor size, and postoperative cortisol and adrenocorticotropin nadirs. Conversely, increasing age was associated with decreased hallmark CD features, preoperative 24-hour urinary free cortisol, Ki-67 indices, and arginine vasopressin deficiency. Younger patients presented more frequently with weight gain, facial rounding/plethora, abdominal striae, hirsutism, menstrual irregularities, dorsocervical fat pad, and acne. Obstructive sleep apnea and infections were more common with increasing age. Conclusion There are age-dependent differences in clinical presentation, tumor behavior, and postoperative outcomes in patients with CD. Compared to younger patients, older patients present with a less classic phenotype characterized by fewer hallmark features, more medical comorbidities, and larger tumors. Notably, age-related differences suggest a more indolent tumor behavior in older patients, potentially contributing to delayed diagnosis and increased perioperative risk. These findings underscore the need for tailored diagnostic and therapeutic approaches across age groups, with a focus on managing long-term comorbidities and optimizing surgical outcomes.

Evaluation of Epigenetic Markers in the Diagnosis and Prognosis of Colorectal Cancer

Introduction: colorectal cancer (CRC) is one of the leading causes of cancer-related death worldwide. Epigenetic factors play a significant role in its development and are increasingly used as tools for early diagnosis and prognosis of this disease. Method: a literature review was conducted on studies published in the last 10 years, available in databases such as PubMed, Cochrane, and SciELO. The selected studies analyze the effectiveness of epigenetic markers, such as DNA methylation and microRNAs, in CRC detection and prognosis. Results: out of 112 articles reviewed, 45 studies met the inclusion criteria, excluding duplicates and those that did not align with the objectives of this review. The analyzed studies highlight that epigenetic marker, particularly the methylation of genes such as SEPT9, NDRG4, and BMP3, are effective in detecting colorectal cancer (CRC) in its early stages, thus enhancing early intervention opportunities. Key microRNAs, such as miR-21, miR-92a, and miR-29a, were also identified, with their alteration associated with CRC progression and aggression prediction. Conclusions: epigenetic markers provide valuable insights into tumor behavior, metastatic potential, and response to various treatment modalities. Some of the most recent studies suggest that the combined use of epigenetic biomarkers and traditional screening methods, such as colonoscopy, may optimize diagnostic accuracy.

Superior Classification of Brain Cancer Types Through Machine Learning Techniques Applied to Magnetic Resonance Imaging

Brain cancer remains one of the most challenging medical conditions due to its intricate nature and the critical functions of the brain. Effective diagnostic and treatment strategies are essential, particularly given the high stakes involved in early detection. Magnetic Resonance (MR) imaging has emerged as a crucial modality for the identification and monitoring of brain tumors, offering detailed insights into tumor morphology and behavior. Recent advancements in artificial intelligence (AI) and machine learning (ML) have revolutionized the analysis of medical imaging, significantly enhancing diagnostic precision and efficiency. This study classifies three primary brain tumor types—glioma, meningioma, and general brain tumors—utilizing a comprehensive dataset comprising 15,000 MR images obtained from Kaggle. We evaluated the performance of six distinct machine learning models: K-Nearest Neighbors (KNN), Neural Networks, Logistic Regression, Support Vector Machine (SVM), Decision Trees, and Random Forests. Each model's effectiveness was assessed through multiple metrics, including classification accuracy (CA), Area Under the Curve (AUC), F1 score, precision, and recall. Our findings reveal that KNN and Neural Networks achieved remarkable classification accuracies of 98.5% and 98.4%, respectively, significantly surpassing the performance of other evaluated models. These results underscore the promise of ML algorithms, particularly KNN and Neural Networks, in improving the diagnostic process for brain cancer through MR imaging. Future research will focus on validating these models with real-world clinical data, aiming to refine and enhance diagnostic methodologies, thus contributing to the development of more accurate, efficient, and accessible tools for brain cancer diagnosis and management.

High Intelectin‐1 Expression Associated with Aggressive Tumor Behavior and Worse Survival in Rectal Cancer

High Intelectin‐1 Expression Associated with Aggressive Tumor Behavior and Worse Survival in Rectal Cancer

The Prognostic Impact of SIRT1, STAT3, and YAP1 in Colorectal Carcinoma.

Colorectal cancer (CRC) is the most common gastrointestinal malignancy with a complicated behavior including relapse, metastasis, and development of resistance to chemotherapeutic drugs. Silent information regulator 2 homologue 1 (SIRT1), signal transducer and activator of transcription 3 (STAT3), and yes-associated protein (YAP) are cancer-related genes that have unclarified actions and even controversial roles in many human cancers including CRC. The current study aimed to evaluate the prognostic roles of SIRT1, STAT3, and YAP in CRC. Hundred and 13 CRC archival blocks were processed by TMA technique and immunostained with SIRT1, STAT3, and YAP antibodies. SIRT1, STAT3, and YAP are expressed in both tumor and stromal cells. SIRT1 expression in both the epithelial and stromal compartments was associated with favorable prognostic parameters, including longer overall and recurrence-free survival. In contrast, the epithelial and stromal expression of both STAT3 and YAP1 was associated with poor prognostic parameters, including short overall and recurrence-free survival. STAT3 and YAP epithelial expression showed a positive correlation with one another, but a negative correlation with epithelial SIRT1. While SIRT1 stromal expression was inversely correlated with stromal YAP expression, STAT3 and YAP concurrent stromal expression demonstrated a positive correlation with one another. There is crosstalk between CRC tumor and stromal cells by the coparallel expression of molecules such as SIRT1, STAT3, and YAP. There is a synergism between the STAT3 and YAP pathways in CRC at the level of the tumor and stroma. The tumor microenvironment of CRC could modulate tumor behavior by expressing markers suppressing invasion, such as SIRT1 or enhancing invasion, such as STAT3 and YAP.

Risk Factors for the Development of Neurological Deficits in Metastatic Spinal Disease: An International, Multicenter Delphi Study.

Delphi study. The objective of this study was to identify risk factors associated with the development and/or progression of neurological deficits in patients with metastatic spinal disease. A three-round Delphi study was conducted between January-May 2023 including AO Spine members, comprising mainly neurosurgeons and orthopedic surgeons. In round 1, participants listed radiological factors, patient characteristics, tumor characteristics, previous cancer-related treatment factors and additional factors. In round 2, participants ranked the factors on importance per category and selected a top 9 from all factors. Kendall's W coefficient of concordance was calculated as a measure of consensus. In the final round, participants provided feedback on the rankings resulting from round 2. Lastly, the highest-ranking factors were more clearly defined and operationalized by an expert panel. Over two hundred physicians and researchers participated in each round. The factors listed in the first round were collapsed into 12 radiological factors, 14 patient characteristics, 6 tumor characteristics and 12 previous cancer-related treatment factors. High agreement was found in round 3 on the top-half lists in each category and the overall top 9, originating from round 2. Kendall's W indicated strong agreement between the participants. 'Epidural spinal cord compression', 'aggressive tumor behavior' and 'mechanical instability' were deemed most influential for the development of neurological deficits. This study provides factors that may be related to the development and/or progression of neurological deficits in patients with metastatic spinal disease. This list can serve as a basis for future directions in prognostication research.

Pan-cancer association of a mitochondrial function score with genomic alterations and clinical outcome

Mitochondria are pivotal in cellular energy metabolism and have garnered significant attention for their roles in cancer progression and therapy resistance. Despite this, the functional diversity of mitochondria across various cancer types remains inadequately characterized. This study seeks to fill this knowledge gap by introducing and validating MitoScore—a novel metric designed to quantitatively assess mitochondrial function across a wide array of cancers. Our investigation evaluates the capacity of MitoScore not only to distinguish between tumor and adjacent normal tissues but also to serve as a predictive marker for clinical outcomes. We analyzed gene expression data from 24 cancer types and corresponding normal tissues using the TCGA database. MitoScore was calculated by summing the normalized expression levels of six mitochondrial genes known to be consistently altered across multiple cancers. Differential gene expression was assessed using DESeq2, with a focus on identifying significant changes in mitochondrial function. MitoScore’s associations with tumor proliferation, hypoxia, aneuploidy, and clinical outcomes were evaluated using Spearman’s correlation, linear regression, and Kaplan–Meier survival analyses. MitoScore was significantly higher in tumor tissues compared to normal tissues across most cancer types (p < 0.001). It positively correlated with tumor proliferation rates (r = 0.46), hypoxia scores (r = 0.61), and aneuploidy (r = 0.44), indicating its potential as a marker of aggressive tumor behavior. High MitoScore was also associated with poorer prognosis in several cancer types, suggesting its utility as a predictive biomarker for clinical outcomes. This study introduces MitoScore, a metric for mitochondrial activity often elevated in tumors and linked to poor prognosis. It correlates positively with hypoxia and negatively with stromal and immune infiltration, highlighting mitochondria’s role in the tumor microenvironment. MitoScore’s association with genomic instability, such as aneuploidy, suggests mitochondrial dysfunction contributes to cancer progression. Despite challenges in mitochondrial-targeted therapies, MitoScore may identify tumors responsive to such treatments, warranting further research for clinical application.

Platelet stimulation-regulated expression of ILK and ITGB3 contributes to intrahepatic cholangiocarcinoma progression through FAK/PI3K/AKT pathway activation

ObjectiveIntrahepatic cholangiocarcinoma (iCCA) is a highly lethal hepatobiliary malignancy with an increasing incidence annually. Extensive research has elucidated the existence of a reciprocal interaction between platelets and cancer cells, which promotes tumor proliferation and metastasis. This study aims to investigate the function and mechanism underlying iCCA progression driven by the interplay between platelets and tumor cells, aiming to provide novel therapeutic strategies for iCCA.MethodsThe associations between platelets and cancer development were investigated by analyzing the peripheral blood platelet count, degree of platelet activation and infiltration in the microenvironment of patients with iCCA. By co-culturing tumor cells with platelets, the influence of platelet stimulation on the epithelial-mesenchymal transition (EMT), proliferation, and metastasis of iCCA cells was assessed through in vitro and in vivo experiments. Quantitative proteomic profiling was conducted to identify key downstream targets that were altered in tumor cells following platelet stimulation. The RNA interference technique was utilized to investigate the impacts of gene silencing on the malignant biological behaviors of tumor cells.ResultsCompared with healthy adults, patients with iCCA presented significantly higher levels of peripheral blood platelet counts, platelet activation and infiltration degrees, which were also found to be correlated with patient prognosis. Platelet stimulation greatly facilitated the EMT of iCCA cells, leading to enhanced proliferative and metastatic capabilities. Mechanistically, proteomic profiling identified a total of 67 up-regulated and 40 down-regulated proteins in iCCA cells co-cultured with platelets. Among these proteins, two elevated targets ILK and ITGB3, were further demonstrated to be partially responsible for platelet-induced iCCA progression, which might depend on their regulatory effects on FAK/PI3K/AKT signaling transduction.ConclusionsOur data revealed that platelet-related indices were abnormally ascendant in iCCA patients compared to healthy adults. Co-culturing with platelets enhanced the progression of EMT, and the motility and viability of iCCA cells in vitro and in vivo. Proteomic profiling discovered that platelets promoted the development of iCCA through FAK/PI3K/AKT pathway by means of elevating the expression of ILK and ITGB3, indicating that both proteins are promising therapeutic targets for iCCA with the guidance of platelet-related indices.

Personalized Vascularized Tumor Organoid-on-a-Chip for Tumor Metastasis and Therapeutic Targeting Assessment.

While tumor organoids have revolutionized cancer research by recapitulating the cellular architecture and behaviors of real tumors in vitro, their lack of functional vasculature hinders their attainment of full physiological capabilities. Current efforts to vascularize organoids are struggling to achieve well-defined vascular networks, mimicking the intricate hierarchy observed in vivo, which restricts the physiological relevance particularly for studying tumor progression and response to therapies targeting the tumor vasculature. An innovative vascularized patient-derived tumor organoids (PDTOs)-on-a-chip with hierarchical, tumor-specific microvasculature is presented, providing a versatile platform to explore tumor-vascular dynamics and antivascular drug efficacy. It is found that highly metastatic tumor cells induced vessel angiogenesis and simultaneously migrated toward blood vessels via the Notch pathway. The evident association between the angiogenic and migratory capacities of PDTOs and their clinical metastatic outcomes underscores the potential of the innovative platform for evaluating tumor metastasis, thus offering valuable insights for clinical decision-making. Ultimately, the system represents a promising avenue for advancing the understanding of tumor metastasis and developing personalized treatment strategies based on patient-specific tumor characteristics.

The Therapeutic Potential of Physical Exercise in Cancer: The Role of Chemokines

The global increase in cancer cases and mortality has been associated with inflammatory processes, in which chemokines play crucial roles. These molecules, a subfamily of cytokines, are essential for the migration, adhesion, interaction, and positioning of immune cells throughout the body. Chemokines primarily originate in response to pathogenic stimuli and inflammatory cytokines. They are expressed by lymphocytes in the bloodstream and are divided into four classes (CC, CXC, XC, and CX3C), playing multifaceted roles in the tumor environment (TME). In the TME, chemokines regulate immune behavior by recruiting cells such as tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs), which promote tumor survival. Additionally, they directly influence tumor behavior, promoting pathological angiogenesis, invasion, and metastasis. On the other hand, chemokines can also induce antitumor responses by mobilizing CD8+ T cells and natural killer (NK) cells to the tumor, reducing pro-inflammatory chemokines and enhancing essential antitumor responses. Given the complex interaction between chemokines, the immune system, angiogenic factors, and metastasis, it becomes evident how important it is to target these pathways in therapeutic interventions to counteract cancer progression. In this context, physical exercise emerges as a promising strategy due to its role modulating the expression of anti-inflammatory chemokines and enhancing the antitumor response. Aerobic and resistance exercises have been associated with a beneficial inflammatory profile in cancer, increased infiltration of CD8+ T cells in the TME, and improvement of intratumoral vasculature. This creates an environment less favorable to tumor growth and supports the circulation of antitumor immune cells and chemokines. Therefore, understanding the impact of exercise on the expression of chemokines can provide valuable insights for therapeutic interventions in cancer treatment and prevention.

Pooled clinical trial analyses evaluating outcomes of HER2-low vs HER2-0 expression in patients with metastatic breast cancer following chemotherapy.

The therapeutic importance of subsetting patients with HER2-negative breast cancer according to their tumors' cellular HER2 expression (e.g., HER2-low vs. HER2-0) is relatively new, stemming from the dramatic results of the DESTINY-04 trial which established HER2-low expression as actionable. Most prior observational research of traditionally HER2-negative patients suggests that tumor behavior and biology do not vary according to HER2-low vs. HER2-0 expression, though some studies suggest otherwise. Here we studied this question in women with metastatic breast cancer (MBC) who were treated with standard single agent chemotherapy in the setting of clinical trials carried out in the pre-DESTINY-04 era. After pooling data from 142 female patients with MBC across historic clinical trials and categorizing them according to HER2 expression (i.e., HER2-0 or HER2-low), we evaluated associations between HER2 expression and the outcomes of both progression-free survival (PFS) and overall survival (OS) with both Kaplan-Meier and Cox proportional hazards methods. Studying data from an era when quantifying amounts of tumor HER2 expression in HER2-negative patients was neither standardized nor clinically actionable, we found no meaningful clinical differences in PFS or OS according to HER2-low vs. HER2-0 status, supporting prior findings of no biologic differences.

The Immune Contexture in Canine Anal Sac Adenocarcinoma: Immunohistochemical Quantification of Tumor-Infiltrating Lymphocytes and Tumor-Associated Macrophages with Image Analysis.

Canine anal sac gland adenocarcinomas (ASACs) are locally aggressive and highly metastatic to regional lymph nodes. Tumor-infiltrating lymphocytes (TILs) and tumor-associated macrophages (TAMs) can be effective prognostic and predictive markers in numerous human neoplasms and are increasingly investigated in dogs. The aim of this study was to characterize immune cells in canine ASACs and their relationship with tumor size, histologic metastatic status, and tumor clinical stage. Thirty ASACs with known tumor size, metastatic status, and clinical stage were immunolabeled for Iba1 (macrophages), CD20 (B cells), CD3 (T cells), and Foxp3 (regulatory T cells). With image analysis, two areas of 1 mm2 were analyzed for each case at the tumor core (TC) and invasive margin (IM) and immune cells were counted. Eighteen patients had metastasis at the time of diagnosis, of which fifteen were nodal only, and three were both distant and nodal. The median tumor size was 32.5 mm (range 11-70). The clinical stage was I in five cases, II in seven cases, III in fifteen cases, and IV in three cases. T cells and macrophages were the most abundant immune cells in all tumors. Tumor size did not influence the number or type of infiltrating immune cells. By contrast, significantly higher numbers of TC T lymphocytes were found in patients without metastasis, while significantly higher numbers of TC macrophages were found in dogs with metastasis. Immune cell infiltrate did not differ according to clinical stage. The results indicate that the tumor immune microenvironment, specifically TILs and TAMs, contribute to tumor behavior and may influence metastatic potential; in particular, high CD3 infiltration may prevent tumor progression, while increased macrophage infiltration could promote it.

Pathological Spectrum of Melanoma: A Nine-Year Retrospective Analysis of Tumor Characteristics Across Diverse Anatomic Sites.

Melanoma is a highly aggressive malignancy originating from melanocytes, characterized by its potential to arise in various anatomic locations, both common and rare. The incidence of melanoma has been steadily increasing globally, with variations in clinical presentation, tumor behavior, and prognosis depending on the anatomical site involved. Understanding the diverse pathological spectrum of melanoma is critical for optimizing diagnostic and therapeutic strategies. This retrospective study provides a comprehensive analysis of melanoma tumor characteristics in 25 patients diagnosed and treated over a nine-year period at Meenakshi Mission Hospital. The study spans a wide spectrum of anatomical sites, including both typical cutaneous locations, such as the thigh and arm, and less common locations, such as the rectum, anal canal, esophagus, and glans penis. The patient cohort, predominantly male (92%, n=23), had a median age of 64 years (range 32-81 years). Tumor sizes varied from 1.2 cm to 5.1 cm, and ulceration was observed in all cases. Histologically, malignant melanoma was the most frequent diagnosis, with subtypes such as balloon cell melanoma, spindle cell melanoma, and superficial spreading melanoma also represented. Mitotic rates ranged from 5 to 22 mitoses per 10 high-power fields (HPF), reflecting varying levels of tumor aggressiveness. Lymphovascular invasion was noted in 12% of cases (n=3), highlighting the metastatic potential in some patients. This study underscores the pathological diversity of melanoma, highlighting the importance of thorough diagnostic evaluation and tailored therapeutic approaches. The findings contribute to a better understanding of melanoma's clinical and tumor characteristics across both typical and atypical anatomical sites, with implications for improving diagnostic accuracy and patient management.