To determine the proportion of men with completely negative multiparametric magnetic resonance imaging (MRI) scans and which individual sequence-T2-weighted imaging (T2WI) or diffusion-weighted imaging (DWI)-best predicts an overall negative examination result.

This was a single-center retrospective study evaluating 492 MRI scans compliant with Prostate Imaging Reporting and Data System (PI-RADS), version 2.1. Radiology reports described the absence of lesions or suspicious lesions with PI-RADS scores of 3-5, signifying positive T2WI or DWI results. Positivity on a dynamic contrast-enhanced (DCE) study was determined by early or simultaneous focal enhancement consistent with lesions on T2WI or DWI. All scans reported as negative were prospectively reviewed to ensure that each sequence truly met the criteria for negativity according to the PI-RADS guidelines. Descriptive statistics were employed to summarize the data, and the chi-square test was employed to assess the relationship between a negative T2WI result and a negative DWI/DCE result, as well as that between a negative DWI result and a negative DWI/DCE result, with logistic regression models identifying predictors of such combined results.

Among the patients evaluated, approximately one-third of those with suspected prostate cancer and 10% of those with known cancer could have concluded their examination after a single negative sequence. A negative T2WI result predicted negative DWI/DCE findings in 62.4% of scans (95% CI: 55.3-68.9), with an odds ratio of 245.3 (p < 0.001). Similarly, a negative DWI result predicted negative T2WI/DCE findings in 88.9% of scans (95% CI: 83.1-92.7) with an odds ratio of 76.4 (p < 0.001). These associations remained robust after adjustment for age, prostate-specific antigen level, prostate-specific antigen density, cancer status, and radiologist.

Findings from T2WI or DWI may serve as preliminary indicators for the subsequent diagnostic yield of other sequences, with DWI appearing to hold a slight advantage. Although the accuracy of this approach is not yet sufficient for clinical implementation, these results are promising and merit further investigation.

Gastric neuroendocrine neoplasms (G-NENs) are rare tumors categorized into subtypes, each exhibiting unique characteristics, levels of aggressiveness and prognostic implications. This study aimed to describe the experience on G-NEN management at the Brazilian National Cancer Institute.

Retrospective analysis involving all patients diagnosed with G-NEN from July 2000 to October 2022.

116 patients with G-NEN were identified; histopathological classification was possible in only 97 patients. Of these, 85 (87.6%) cases were of gastric neuroendocrine tumors (G-NETs) and 12 (12.4%) cases were of gastric neuroendocrine carcinoma (NEC). According to the WHO classification, 51 were classified as NET-G1, 31 as NET-G2, three as NET-G3 and 12 as NEC. Among the G-NETs, type 1 was most prevalent with 60 cases, followed by type 3 (eleven cases) and type 2 (five cases). Nonmetastatic patients were initially treated with endoscopic resection (59 patients), endoscopic surveillance (18 patients) and upfront surgical intervention (18 patients). For metastatic cases, treatment regimens included platinum-based chemotherapy, somatostatin analogs, peptide receptor radionuclide therapy and palliative surgical options. The median overall survival was 84.5 months for NET-G1, 73.4 months for NET-G2, 17.4 months for NET-G3 and 6.2 months for NEC.

This report presents the largest cohort of G-NEN in Brazil. While type 1 small G-NET generally exhibits indolent behavior, NEC is characterized by extreme aggressiveness. The survival outcomes observed in this treated population align with those reported in oncology centers from higher-income regions. This underscores the necessity for establishing reference centers dedicated to neuroendocrine tumors in low- to middle-income countries.

Adrenocortical carcinoma (ACC) is an uncommon and highly aggressive tumor with a grim prognosis. Numerous investigations have elucidated a close association between the dysregulated expression of multiple genes within tumors and the initiation as well as progression of neoplasms. These dysregulated genes not only exert pivotal roles in tumorigenesis but also harbor significant potential as prognostic biomarkers.

This study utilized transcriptomic data from public databases of ACC and normal tissue samples to screen for differentially expressed genes (DEGs). Subsequently, univariate Cox regression and receiver operating characteristic (ROC) curve were employed to identify potential prognostic biomarkers for ACC. Immunohistochemistry and in vitro cell experiments were conducted to validate the expression and potential functions of Cell division cycle 20 (CDC20) in ACC cells. Additionally, we analyzed the relationship between CDC20 and CD8+ T cells, immunotherapy response, somatic mutations, and copy number variations.

CDC20 has emerged as an independent adverse prognostic factor in ACC, with significantly elevated expression levels. In vitro cell experiments have demonstrated that downregulation of CDC20 expression suppresses proliferation and migration of ACC cells. Notably, our study has identified CDC20 expression as most closely associated with TP53 mutation. Additionally, CDC20 expression levels exhibit a negative correlation with infiltration of CD8+ T cells. Patients with low CDC20 expression may show improved response to anti-PD-1 immunotherapy.

CDC20 serves as a reliable and robust biomarker in ACC, playing a crucial role in predicting survival outcomes and assessing immunotherapy response in adult and childhood ACC patients.

The oncologic benefits of adjuvant chemotherapy for resected ampulla of Vater cancer (AoVCa) remain contentious. This study aimed to evaluate the long-term oncologic effects of postoperative adjuvant chemotherapy (PACT) in patients who underwent radical surgery for AoVCa.

From 2005 to 2019, clinical and pathological data of 306 AoVCa patients who underwent pancreatoduodenectomy were retrospectively reviewed. Patients were divided into the PACT (+) and PACT (-) groups. Propensity score matching (PSM) was conducted to adjust for clinical factors.

The PACT (+) group (n = 124) and PACT (-) group (n = 182) showed significant differences in cancer stage, lymph node metastasis, perineural invasion, lymphovascular invasion, and cancer differentiation. Lower overall survival (OS) (P < 0.001) and disease-free survival (DFS) (P < 0.001) were observed in the PACT (+) group. After PSM, no significant differences in OS or DFS were found between the groups. Multivariate analysis identified lymph node metastasis and perineural invasion as significant prognostic factors, while PACT did not significantly impact long-term survival. Paradoxically, PACT was associated with worse outcomes in patients with favorable prognostic factors.

This study suggests that PACT does not provide a clear oncologic benefit for resected AoVCa patients and may even be detrimental for those with favorable prognostic factors. There is an urgent need to develop effective anticancer treatments and consider tailored therapeutic approaches based on individual patient profiles. Future research should focus on long-term follow-up and the integration of precision medicine to improve outcomes for AoVCa patients.

Globally, gastric cancer (GC) stands as the fifth most prevalent form of malignant neoplasm and represents a significant contributor to mortality associated with oncological conditions. Despite advancements in therapeutic strategies for GC, the outcomes for patients with advanced stages of the disease continue to be unfavorable, largely due to tumor heterogeneity and the challenges posed by resistance to therapeutic agents. Metabolic reprogramming is pivotal in driving the advancement of GC, contributing to the development of resistance to pharmacological treatments and facilitating the cancer's ability to evade immune surveillance. Developing multi-target comprehensive treatment strategies by integrating tumor microenvironment (TME) modulation holds promise for significantly improving therapeutic efficacy.

The study analyzed GC and identified key cell subtypes by integrating data derived from single-cell RNA-sequencing (scRNA-seq) alongside spatial transcriptomics information. Cell type identification was accomplished using the tool of Seurat, and the spatial distribution of cell types was revealed through the Robust Cell Type Decomposition technique. CellChat was used to analyze the interactions between key cell subtypes and other cells, and the "StLearn" package was employed to investigate spatial cell communication in depth. Additionally, the functional role of the key molecule ELK4 was validated through in vitro experiments.

This research utilized scRNA-seq combined with spatial transcriptomics to comprehensively analyze GC, identifying the C1 NDUFAB1+ subtype, which exhibited high proliferative activity, metabolic reprogramming capabilities, and immune evasion properties. It was found that the C1 NDUFAB1+ subtype closely interacted with fibroblasts and pericytes via the PARs signaling pathway. Additionally, in vitro experiments confirmed that knockdown of ELK4 substantially curbed tumor cell proliferation, migration, and invasion.

This study revealed the main significance of the C1 NDUFAB1+ subtype in GC, elucidating its core mechanisms in tumor progression, metabolic reprogramming, and immune evasion. ELK4 was identified as a key regulatory factor that markedly enhanced the proliferation, migratory capacity, and invasive potential of tumor cells, while changes in the TME were a driving force behind immune suppression and drug resistance. The findings underscored the importance of developing specific therapeutic targets, targeting metabolic reprogramming, and overcoming immune evasion, providing new theoretical foundations.

Radiotherapy, as a key component of the comprehensive treatment system for malignant tumors, not only facilitates precise tumor destruction but also necessitates the strategic use of radioprotective agents to regulate immune responses and mitigate toxicity in normal tissues. Revealing the molecular biological mechanisms of ionizing radiation damage, such as DNA double-strand breaks, oxidative stress responses, and abnormal cell cycle regulation is critical for the development of clinically effective radioprotective drugs. Such advancements hold dual significance in enhancing patient outcomes and improving clinical efficacy. This paper explores the classification of radioprotective agents, and their diverse mechanisms of action, including free radical scavenging, regulation of redox enzyme systems, suppression of ionizing radiation-induced inflammation, and apoptosis-related immune damage. And, it also examines the challenges and prospects of their clinical translation. This study aims to provide important theoretical framework for the development of radioprotective agents to contribute to future advancements in radiation therapy.

Breast cancer (BC) is the leading cause of cancer death in women, partly because of the significant toxicity and low specificity associated with chemotherapy drugs. Photothermal therapy (PTT) provides a new paradigm for the precise treatment of BC through local thermal ablation and immune regulation. PTT utilizes the heat generated by laser irradiation to kill tumor cells. Notably, PTT can activate the innate and adaptive immune systems by releasing antigens, which are then presented by antigen-presenting cells (APCs). These antigens are primarily released through various forms of tumor cell death induced by the thermal effects of PTT. The process of PTT-activated anti-immunity involves T cells, dendritic cells (DCs), B cells, natural killer (NK) cells, and macrophages. Therefore, regulation of the immune system by PTT in BC is considered as a promising therapeutic approach. This review elucidates the mechanisms by which PTT regulates anti-tumor immune responses through processes such as antigen release, antigen presentation, and immune cell activation. We also focus on the latest advancements and challenges in nanomaterials research, preclinical studies, and translational trials for PTT in BC treatment. This review is expected to improve our understanding of the anti-tumor effects of PTT based on the immune cycle of BC. It is expected to address critical gaps in PTT-based immunotherapy for BC, such as insufficient antigen release, the immunosuppressive microenvironment, and the transformation of cold tumors.

The 5-year survival rate in muscle-invasive bladder cancer (MIBC) is approximately 50%, cross over computed tomography (CT) stage in chemo-naive patients. Studies indicate lower survival rates in females when compared to males. The theories that explain the sex disparity are hormonal factors and delayed diagnosis for females. New investigations suggest that neoadjuvant chemotherapy (NAC) might be a possible method for bridging the gender survival gap. The aim of this study was to investigate whether complete treatment with NAC (≥3 cycles) prior to cystectomy reduces the gender gap in survival rates for MIBC and improves the surrogate marker of downstaging.

A multicenter retrospective cohort from five Swedish urological centers, from 1st January 2005 to 17th July 2023 based on NAC-eligible patients divided in NAC-receiving and non-NAC-receiving subgroups and further divided by sex (males and females). Survival was analyzed based on the Kaplan-Meier method, using log-rank test and adjusted analyses were made with the Cox regression model. Outcome measurements were overall survival (OS), disease-free survival (DFS), and downstaging.

In the analysis of the total cohort (n=412), we could not detect any statistically significant differences in OS between NAC and non-NAC, nor between sexes, in the unadjusted analysis. In the adjusted analysis, we did not observe any significant differences in OS between sexes, either in total or within the NAC subgroups. Further analyzing the NAC group, we could see a significant increased downstaging rate in the NAC group compared to the non-NAC group (P<0.001) which indicates an increased survival in those receiving NAC treatment. There was no relationship between sexes and downstaging (P=0.72). Neither could we see any significant difference in downstaging between males and females in the NAC/non-NAC subgroups (P=0.41 and P=0.92, respectively).

NAC-eligible female and male MIBC patients who underwent radical cystectomy (RC) after at least three cycles of NAC, demonstrated similar OS and DFS. NAC seems to obliterate survival differences between genders in MIBC patients.

Colon cancer is a leading neoplasm worldwide, with 35% to 45% of colorectal cancer (CRC) patients exhibiting mutations in the Kirsten rat sarcoma oncogene (KRAS). This mutation affects disease development and serves as a biomarker for early detection, prognosis, and treatment. The objective of the present study was to identify the clinicopathological characteristics of colon cancer patients with KRAS mutations.

An analytical cross-sectional study involving patients with CRC was conducted. The study variables included sex, age, tumor location, KRAS and B-Raf proto-oncogene (BRAF) mutations, and the presence of metastases.

The study involved 51 patients, with a mean (standard deviation) age of 61.4 ± 11.0 years. The most common tumor location was the sigmoid colon (35.3%), and 45.1% of patients were classified as tumor, node, metastasis (TNM) stage III with lymph node dissemination. Genetic analysis revealed that 35% of patients had KRAS mutations, while 32% had BRAF mutations. Notably, 61.1% of KRAS-positive patients also had BRAF mutations compared to 15.1% of KRAS-negative patients (P = 0.02).

KRAS-positive patients predominantly had tumors in the sigmoid colon. The coexistence of KRAS and BRAF mutations suggests a potential molecular interaction influencing disease progression. These findings highlight a distinct genomic pattern and the need for further research into its clinical implications.

Sulfur metabolism plays a crucial role in the initiation and progression of cancer. Our objective is to elucidate the molecular diversity inherent in breast cancer and to develop a predictive index grounded in sulfur metabolism-related genes (SMRGs).

We acquired transcriptomic and clinical datasets pertaining to breast cancer from publicly accessible repositories. Consensus clustering analysis was used to classify SMRGs in breast cancer into molecular subtypes. To pinpoint characteristic genetic markers and assemble a risk stratification model, we executed differential expression profiling, along with univariate and Least Absolute Shrinkage and Selection Operator (LASSO) Cox regression analyses. Supplementary assessments encompassed gene set enrichment studies, scrutiny of somatic mutations, examination of the immune milieu, and exploration of chemotherapeutic responsiveness. Additionally, a nomogram model was constructed.

Through the categorization of SMRGs in breast neoplasms, two distinctive molecular phenotypes emerged, each harboring substantial disparities in clinical outcome. Among the nine SMRGs linked to prognosis, eight key players-notably TSTD1, SULT1A2, MPST, GOT2, ENOPH1, CSAD, CHST12, and CDO1-served as the foundation for developing a predictive risk profile dedicated to breast carcinomas. This novel signature adeptly partitioned subjects into high- and low-risk strata, wherein the latter exhibited markedly superior overall survival relative to the former. Comparative analysis unveiled that the low-risk cohort featured diminished tumoral mutational load, elevated stromal and immune indices, and reduced tumoral purity. Notably, this subgroup showcased attenuated infiltration by M2 and M0 macrophages, contrasted with augmented infiltration by B and T lymphocytes. Furthermore, heightened responsiveness to paclitaxel and docetaxel was observed in the high-risk population compared to the low-risk counterpart. Conclusively, amalgamation of the risk metric, chemotherapeutic record, disease stage, and nodal status culminated in the construction of a nomogram aimed at breast cancer management. The dysregulation of SMRGs in the signature were further validated in external cohort.

SMRGs contribute to the heterogeneity of breast cancer, and a molecular classification and prognostic evaluation can be achieved based on SMRGs.