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Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies, presenting a persisting global health burden. Neutrophils have a double-edged role in tumor progression exhibiting both pro-tumor and anti-tumor functions. CD71, also known as transferrin receptor 1, performs a critical role in cellular iron uptake and is highly expressed on proliferating cells, and especially on activated immune cells. CD71 is known to be elevated in various types of solid cancers and is associated with poor prognosis, however, the expression of CD71 on neutrophils in PDAC and its potential clinical impact is still unknown. Therefore, we analyzed CD71 on circulating neutrophils in PDAC and clinical control patients and found a significant increased expression in PDAC patients. High expression of CD71 on neutrophils in PDAC patients was associated with reduced outcome compared to low expression. CD71 on neutrophils correlated positively with the levels of proinflammatory cytokines IL-6, IFN-γ, and growth factor ligands CD40-L, and BAFF in plasma of PDAC patients. Finally, we have demonstrated that high expression of CD71 on neutrophils was also associated with an increased expression of CD39 and CD25 on circulating T-cells. Based on our findings, we hypothesize that CD71 on neutrophils is associated with tumor progression in PDAC. Further studies are required to investigate the distinct functionality of CD71 expressing neutrophils and their potential clinical application. [ABSTRACT FROM AUTHOR]

Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies, presenting a persisting global health burden. Neutrophils have a double-edged role in tumor progression exhibiting both pro-tumor and anti-tumor functions. CD71, also known as transferrin receptor 1, performs a critical role in cellular iron uptake and is highly expressed on proliferating cells, and especially on activated immune cells. CD71 is known to be elevated in various types of solid cancers and is associated with poor prognosis, however, the expression of CD71 on neutrophils in PDAC and its potential clinical impact is still unknown. Therefore, we analyzed CD71 on circulating neutrophils in PDAC and clinical control patients and found a significant increased expression in PDAC patients. High expression of CD71 on neutrophils in PDAC patients was associated with reduced outcome compared to low expression. CD71 on neutrophils correlated positively with the levels of proinflammatory cytokines IL-6, IFN-γ, and growth factor ligands CD40-L, and BAFF in plasma of PDAC patients. Finally, we have demonstrated that high expression of CD71 on neutrophils was also associated with an increased expression of CD39 and CD25 on circulating T-cells. Based on our findings, we hypothesize that CD71 on neutrophils is associated with tumor progression in PDAC. Further studies are required to investigate the distinct functionality of CD71 expressing neutrophils and their potential clinical application.

The overexpression of polysialic acid (polySia) on neural cell adhesion molecules (NCAM) promotes hypersialylation, and thus benefits cancer cell migration and invasion. It has been proposed that the binding between the polysialyltransferase domain (PSTD) and CMP-Sia needs to be inhibited in order to block the effects of hypersialylation. In this study, CMP was confirmed to be a competitive inhibitor of polysialyltransferases (polySTs) in the presence of CMP-Sia and triSia (oligosialic acid trimer) based on the interactional features between molecules. The further NMR analysis suggested that polysialylation could be partially inhibited when CMP-Sia and polySia co-exist in solution. In addition, an unexpecting finding is that CMP-Sia plays a role in reducing the gathering extent of polySia chains on the PSTD, and may benefit for the inhibition of polysialylation. The findings in this study may provide new insight into the optimal design of the drug and inhibitor for cancer treatment. [ABSTRACT FROM AUTHOR]

The subject of lymphatics and cancer had been in the air for a lot of time. The Editor, Paolo Zamboni, came up at first with the idea of writing about this issue and was good enough to ask me to attempt this work after I provided him with images of mesenteric, intestinal and hepatic metastases from a young patient I treated for a malignant melanoma of the skin, in the last year of my surgical practice.

The overexpression of polysialic acid (polySia) on neural cell adhesion molecules (NCAM) promotes hypersialylation, and thus benefits cancer cell migration and invasion. It has been proposed that the binding between the polysialyltransferase domain (PSTD) and CMP-Sia needs to be inhibited in order to block the effects of hypersialylation. In this study, CMP was confirmed to be a competitive inhibitor of polysialyltransferases (polySTs) in the presence of CMP-Sia and triSia (oligosialic acid trimer) based on the interactional features between molecules. The further NMR analysis suggested that polysialylation could be partially inhibited when CMP-Sia and polySia co-exist in solution. In addition, an unexpecting finding is that CMP-Sia plays a role in reducing the gathering extent of polySia chains on the PSTD, and may benefit for the inhibition of polysialylation. The findings in this study may provide new insight into the optimal design of the drug and inhibitor for cancer treatment.

Background: Secondary rectal linitis plastica (RLP) from prostatic adenocarcinoma is a rare and poorly understood form of metastatic spread, characterized by a desmoplastic response and concentric rectal wall infiltration with mucosal preservation. This complicates endoscopic diagnosis and can mimic gastrointestinal malignancies. This case series underscores the critical role of magnetic resonance imaging (MRI) in identifying the distinct imaging features of RLP and highlights the importance of considering this condition in the differential diagnosis of patients with a history of prostate cancer., Case Summary: Three patients with secondary RLP due to prostatic adenocarcinoma presented with varied clinical features. The first patient, a 76-year-old man with advanced prostate cancer, had rectal pain and incontinence. MRI showed diffuse prostatic invasion and significant rectal wall thickening with a characteristic "target sign" pattern. The second, a 57-year-old asymptomatic man with elevated prostate-specific antigen levels and a history of prostate cancer exhibited rectoprostatic angle involvement and rectal wall thickening on MRI, with positron emission tomography/computed tomography PSMA confirming the prostatic origin of the metastatic spread. The third patient, an 80-year-old post-radical prostatectomy, presented with refractory constipation. MRI revealed a neoplastic mass infiltrating the rectal wall. In all cases, MRI consistently showed stratified thickening, concentric signal changes, restricted diffusion, and contrast enhancement, which were essential for diagnosing secondary RLP. Biopsies confirmed the prostatic origin of the neoplastic involvement in the rectum., Conclusion: Recognizing MRI findings of secondary RLP is essential for accurate diagnosis and management in prostate cancer patients., Competing Interests: Conflict-of-interest statement: The authors declare that they have no conflict of interest to disclose., (©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.)

Purpose: Integrins may be involved in the metastatic spread of high-grade serous ovarian cancer (HGSOC) which determines the therapeutical approach and prognosis. We investigated the integrin expression in primary tumor and metastases of advanced HGSOC. Methods: The expression of integrin α2, α4, α5, α6, and β1 was assessed by immunostaining in tumor samples of the ovary, omentum, and peritoneum of each patient. Differences in integrin expression among tumor localizations and their association with clinicopathological parameters were examined by Fisher's exact test. The impact of integrin expression on progression-free survival (PFS) and overall survival (OS) was examined by Cox regression and Kaplan–Meier analyses. Results: Hundred and thirteen tumor samples of 40 HGSOC patients were examined. The expression of the integrins did not differ between the three tumor localizations (all p values > 0.05) with the exception of high expression of integrin α4 in primary tumor and omentum (52.5% versus 47.5%, p = 0.008) and primary tumor and peritoneum (52.5% versus 47.5%, p = 0.050). High expression of integrin α4 in peritoneum was associated with poorer PFS (HR 2.02 95% CI 1.01–4.05, p = 0.047), younger age (p = 0.047), and death (p = 0.046). Median PFS in patients with high expression of integrin α4 was 13.00 months, whereas median PFS in patients without high expression of integrin α4 was 21.00 months (p = 0.040). Expression of other integrins did not correlate with PFS or OS. Conclusion: Expression of integrin α4 may be altered during the metastatic spread of HGSOC and affect prognosis, whereas expression of integrin α2, α5, α6, and β1 did not reveal any prognostic value. [ABSTRACT FROM AUTHOR]

In this paper, we consider the following system { u t = Δ u − χ ∇ ⋅ (u ∇ ω) , v t = d v Δ v − ξ ∇ ⋅ (v ∇ ω) , m t = d m Δ m + u − m , ω t = − (γ 1 u + m) ω , in two dimensional space with zero-flux boundary conditions. This model was proposed by Franssen et al. [7] to characterize the invasion and metastatic spread of cancer cells. We first establish the global existence of uniformly bounded global strong solutions. Then using the decay of ECM and the positivity of MDE, we further improve the regularity of obtained solutions, and achieve the uniform boundedness of solutions in the classical sense. Subsequently, we also prove the uniqueness of solutions. After that, we turn our attention to the large time behavior of solutions, and show that the global classical solution strongly converges to a semi-trivial steady state in the large time limit. [ABSTRACT FROM AUTHOR]

Gastric cancer (GC) is the fifth-most prevalent and second-most deadly cancer worldwide. Due to the late onset of symptoms, GC is frequently treated at a mature stage. In order to improve the diagnostic and clinical decision-making processes, it is necessary to establish more specific and sensitive indicators valuable in the early detection of the disease whenever a cancer is asymptomatic. In this work, we gathered information about CXC chemokines and GC by using scientific search engines including Google Scholar, PubMed, SciFinder, and Web of Science. Researchers believe that GC chemokines, small proteins, class CXC chemokines, and chemokine receptors promote GC inflammation, initiation, and progression by facilitating angiogenesis, tumor transformation, invasion, survival, metastatic spread, host response safeguards, and inter-cell interaction. With our absolute best professionalism, the role of CXC chemokines and their respective receptors in GC diagnosis and prognosis has not been fully explained. This review article updates the general characteristics of CXC chemokines, their unique receptors, their function in the pathological process of GC, and their potential application as possible indicators for GC. Although there have only recently been a few studies focusing on the therapeutic efficacy of CXC chemokine inhibitors in GC, growing experimental evidence points to the inhibition of CXC chemokines as a promising targeted therapy. Therefore, further translational studies are warranted to determine whether specific antagonists or antibodies designed to target CXC chemokines alone or in combination with chemotherapy are useful for diagnosing advanced GC. [ABSTRACT FROM AUTHOR]

Meningiomas are generally slow-growing extra-axial benign tumours and in rare cases they can metastasize both neural and extra-neural. Intracranial meningiomas with leptomeningeal dissemination are extremely rare and the exact pathogenesis still remains unknown. The aim of this review is to analyse the pathways of intracranial and spinal metastatic spread of intracranial meningiomas and to discuss their particular clinical and pathological features. We highlight the fact that there is a possibility of leptomeningeal dissemination, even if cerebrospinal fluid cytology is negative, in patients with a medical history of a resected meningioma. We identified three possible ways of dissemination: haematogenous, through the CSF, or during surgery. From a histopathological point of view, the more malignant the meningioma, the more likely its leptomeningeal dissemination.

Meningiomas are generally slow-growing extra-axial benign tumours and in rare cases they can metastasize both neural and extra-neural. Intracranial meningiomas with leptomeningeal dissemination are extremely rare and the exact pathogenesis still remains unknown. The aim of this review is to analyse the pathways of intracranial and spinal metastatic spread of intracranial meningiomas and to discuss their particular clinical and pathological features. We highlight the fact that there is a possibility of leptomeningeal dissemination, even if cerebrospinal fluid cytology is negative, in patients with a medical history of a resected meningioma. We identified three possible ways of dissemination: haematogenous, through the CSF, or during surgery. From a histopathological point of view, the more malignant the meningioma, the more likely its leptomeningeal dissemination. [ABSTRACT FROM AUTHOR]

Infants and young children with neuroblastoma (NB) may present with metastases. The primary tumor most commonly originates in the abdomen and metastasizes to lymph nodes, liver, and bone marrow. Infants and young children presenting with multiple skull metastases are rare. We present a rare case of a 20-month-old child who presented with metastatic neuroblastoma and multiple skull lesions. The child responded well to induction chemotherapy followed by myeloablative busulfan/melphalan consolidation. The child had substantial tumor reduction after chemotherapy was started. There was a significant decrease in tumor sizes and uptake, as seen in the metaiodobenzylguanidine study. The 6-month follow-up examination showed complete remission, and the remission continues. Infants and young children with neuroblastoma rarely present with metastatic lesions to the skull. Even large lesions involving the skull base may be successfully treated with chemotherapy. The use of myeloablative busulfan/melphalan consolidation after induction chemotherapy can decrease the overall metastatic tumor burden. Craniofacial specialists should be aware of treatment options for these young children. [ABSTRACT FROM AUTHOR]

The human prolyl isomerase PIN1, best known for its association with carcinogenesis, has recently been indicated in the disease of pancreatic ductal adenocarcinoma (PDAC). However, the functions of PIN1 and the feasibility of targeting PIN1 in PDAC remain elusive. For this purpose, we examined the expression of PIN1 in cancer, related paracarcinoma and metastatic cancer tissues by immunohistochemistry and analyzed the associations with the pathogenesis of PDAC in 173 patients. The functional roles of PIN1 in PDAC were explored in vitro and in vivo using both genetic and chemical PIN1 inhibition. We showed that PIN1 was upregulated in pancreatic cancer and metastatic tissues. High PIN1 expression is significantly association with poor clinicopathological features and shorter overall survival and disease‐free survival. Further stratified analysis showed that PIN1 phenotypes refined prognostication in PDAC. Inhibition of PIN1 expression with RNA interference or with all trans retinoic acid decreased not only the growth but also the migration and invasion of PDAC cells through regulating the key molecules of multiple cancer‐driving pathways, simultaneously resulting in cell cycle arrest and mesenchymal‐epithelial transition in vitro. Furthermore, genetic and chemical PIN1 ablation showed dramatic inhibition of the tumorigenesis and metastatic spread and then reduced the tumor burden in vivo. We provided further evidence for the use of PIN1 as a promising therapeutic target in PDAC. Genetic and chemical PIN1 ablation exerted potent antitumor effects through blocking multiple cancer‐driving pathways in PDAC. More potent and specific PIN1 targeted inhibitors could be exploited to treat this aggressive cancer. [ABSTRACT FROM AUTHOR]

Cancer is a complex disease that starts with mutations of key genes in one cell or a small group of cells at a primary site in the body. If these cancer cells continue to grow successfully and, at some later stage, invade the surrounding tissue and acquire a vascular network, they can spread to distant secondary sites in the body. This process, known as metastatic spread, is responsible for around 90% of deaths from cancer and is one of the so-called hallmarks of cancer. To shed light on the metastatic process, we present a mathematical modelling framework that captures for the first time the interconnected processes of invasion and metastatic spread of individual cancer cells in a spatially explicit manner—a multigrid, hybrid, individual-based approach. This framework accounts for the spatiotemporal evolution of mesenchymal- and epithelial-like cancer cells, membrane-type-1 matrix metalloproteinase (MT1-MMP) and the diffusible matrix metalloproteinase-2 (MMP-2), and for their interactions with the extracellular matrix. Using computational simulations, we demonstrate that our model captures all the key steps of the invasion-metastasis cascade, i.e. invasion by both heterogeneous cancer cell clusters and by single mesenchymal-like cancer cells; intravasation of these clusters and single cells both via active mechanisms mediated by matrix-degrading enzymes (MDEs) and via passive shedding; circulation of cancer cell clusters and single cancer cells in the vasculature with the associated risk of cell death and disaggregation of clusters; extravasation of clusters and single cells; and metastatic growth at distant secondary sites in the body. By faithfully reproducing experimental results, our simulations support the evidence-based hypothesis that the membrane-bound MT1-MMP is the main driver of invasive spread rather than diffusible MDEs such as MMP-2. [ABSTRACT FROM AUTHOR]

Keywords: pituitary carcinoma; metastatic spread; seed and soil theory; systemical spread; craniospinal spread EN pituitary carcinoma metastatic spread seed and soil theory systemical spread craniospinal spread N.PAG N.PAG 3 01/09/21 20210105 NES 210105 Pituitary carcinomas (PCs) are defined as tumors of adenohypophyseal origin that show craniospinal and/or systemic metastases ([1]). In one series, PRL-secreting PCs spread systemically more often (71%) than ACTH-secreting PCs (57%); in contrast, growth hormone (GH)-secreting carcinomas present more commonly with cerebrospinal metastasis ([10]). In addition to intra-cranial, the metastasis of ACTH-secreting carcinomas has a predilection for the liver and spinal ([10], [15], [16]), and the metastasis of PRL-secreting carcinomas exhibits preferences for lymph nodes and bones ([9]-[11], [16], [17]). [Extracted from the article]

Purpose: To create and validate an evidence-based prediction rule to optimize use of follow-up chest CT for ovarian cancer.Methods: In this Institutional Review Board-approved retrospective study performed at two academic medical centers, electronic medical records from January through December 2013 at center 1 (USA) and January 2012 through December 2013 at center 2 (South Korea) were searched to identify consecutive chest CTs performed within 5 years of initial cytoreductive surgery in patients with pathologically proven ovarian cancer. Three separate study cohorts were created: cohort 1, 316 CTs (in 150 patients) with high-grade serous ovarian cancer (HGSC) from center 1; cohort 2, 374 CTs (81 patients) with HGSC from center 2; and cohort 3, 87 CTs (56 patients) with non-HGSC histologies from center 1. A radiologist blinded to outcome of CT, using a prediction rule that utilized previously available information, categorized each CT into "high-risk" (stage 4 at presentation and/or preexisting abdominal disease [disease below diaphragmatic dome, visualized on abdominal CT]) or "low-risk" (neither of above). A blinded radiologist then reviewed chest CTs in random order to record thoracic metastases above the diaphragmatic dome, and outcome was compared with prediction rule risk category.Results: Among the three cohorts and in the total population, the prediction rule identified 94 of 316 (30%), 170 of 374 (45%), 53 of 87 (61%), and 317 of 777 (41%) CTs as "low-risk," respectively. The sensitivity, specificity, positive predictive value, negative predictive value, positive likelihood ratio, and negative likelihood ratio were as follows: cohort 1: 95%, 35%, 24%, 97%, 1.46, 0.14; cohort 2: 88%, 53%, 29%, 95%, 1.87, 0.22; cohort 3: 88%, 66%, 21%, 98%, 2.59, 0.18; total population: 91%, 47%, 26%, 96%, 1.72, 0.19. False-negative rate in the three cohorts and in total population was 3 of 94 (3%), 8 of 170 (5%), 1 of 53 (2%), and 12 of 317 (4%); however, in each of these cases there was concurrent new abdominal disease.Conclusions: The easy-to-use prediction rule helps avoid unnecessary chest CTs in patients with ovarian cancer with high sensitivity and negative predictive value, and with minimal risk of missing thoracoabdominal metastases. [ABSTRACT FROM AUTHOR]

Purpose: The development of metastases is the most aggressive attribute of breast cancer. In this retrospective multicenter study, we evaluated if and how the different pathological breast cancer subtypes influence the spreading of tumor cells, the development of metastasis and the survival of breast cancer patients.Methods: This retrospective German multicenter study is based on the BRENDA collective including 9625 breast cancer patients treated in the adjuvant setting. We used the χ 2 tests for the analysis of the categorical variables between groups of patients with different sites of metastasis. Survival distributions and median survival times were estimated using the Kaplan-Meier product-limit method. The log-rank test was applied to compare survival rates. The Cox proportional hazards model was used to estimate the hazard ratio and confidence intervals.Results: 886 women developed metastases during a time interval of 53 months after primary diagnosis. Luminal A tumor patients were more likely to get bone metastases than lung, liver or CNS metastases. Patients with a triple-negative subtype were, however, the least affected by metastasis in the skeleton. They were most likely to develop visceral metastases. Location, numbers of metastases herein and the subtype influenced the overall survival (OAS). Altogether, the best OAS was found in patients with the luminal A subtype, the worst in patients with the triple-negative subtype.Conclusions: Knowledge of the typical metastatic pattern of the subtypes of breast cancer will help to personalize therapeutic options and follow-up examinations of cancer patients. [ABSTRACT FROM AUTHOR]

Objectives: Melanomas arising from mucosa are rare and associated with a poor prognosis. This study aims to provide an analysis of metastatic pathways, time intervals, factors influencing metastatic spread and organs for distant metastases.Methods: A total of 116 patients with mucosal melanomas of different sites were included. The mean follow-up interval was 47 ± 52 months. Patients were assigned to two different metastatic pathways, either presenting loco-regional lymph node metastases as first spread or direct distant metastases. The distribution of distant metastases was assessed.Results: Twenty-six patients presented with a pre-existing metastatic spread and were not assigned to pathways. Of the included patients, 44 developed metastases after treatment of the primary tumour; 25 patients directly developed distant metastases; 16 patients developed regional lymph node metastases prior to distant metastases. Location of the primary tumour in the upper airway or GI tract and advanced T stage were significant risk factors of direct distant metastases. Distant metastases are mainly located in the lung, the liver and non-regional lymph nodes.Conclusions: Mucosal melanomas show a high rate of direct distant metastases rather than regional lymph node metastases. Thus the follow-up should always include a whole-body cross-sectional imaging in high-risk tumours.Key Points: • Mucosal melanomas show a high rate of direct distant metastases. • T stage and primary location are predictors for direct distant metastases. • Distant metastases were mainly found in lung, liver and lymph nodes. • Follow-up of a high-risk mucosal melanoma should include whole-body imaging. [ABSTRACT FROM AUTHOR]

The resistance of cancer cells to chemotherapeutic drugs (MDR) is a major problem to be solved. A supramolecular DEAE-dextran-MMA copolymer (DDMC)/paclitaxel (PTX) complex was obtained by using PTX as the guest and DDMC as the host having 50-300 nm in diameter. The drug resistance of B16F10 melanoma cells to paclitaxel was observed, but there is no drug resistance of melanoma cells to the DDMC/PTX complex in vitro. The cell death rate was determined using Michaelis-Menten kinetics, as the DDMC/PTX complex promoted allosteric supramolecular reaction to tubulin. The DDMC/PTX complex showed a very superior anti-cancer activity to paclitaxel alone in vivo. The median survival time (MST) of the saline, PTX, DDMC/PTX4 (particle size, 50 nm), and DDMC/PTX5 (particle size, 290 nm) groups were 120 h (T/C, 1.0), 176 h (T/C, 1.46), 328 h (T/C, 2.73), and 280 h (T/C, 2.33), respectively. The supramolecular DDMC/PTX complex showed the twofold effectiveness of PTX alone ( p < 0.036). Histochemical analysis indicated that the administration of DDMC/PTX complex decreased distant metastasis and increased the survival of mice. A mouse of DDMC/PTX4 group in vivo was almost curing after small dermatorrhagia owing to its anti-angiogenesis, and it will be the hemorrhagic necrotic symptom of tumor by the release of 'tumor necrosis factor alpha (TNF-α)' cytokine. As the result, the medicinal action of the DDMC/PTX complex will suppress the tumor-associated action of M2 macrophages and will control the metastasis of cancer cells. [ABSTRACT FROM AUTHOR]

There is growing evidence about differences in metastatic spread among breast cancer (BC) biologic subtypes (BS). Aim of this study was to analyze the pattern of metastasization according to BS and to explore the corresponding prognosis. A series of 544 consecutive patients receiving anticancer therapy for metastatic BC from 2004 to 2013, was analyzed. BS were defined by immunohistochemistry according to St Gallen 2013 criteria. Association between BS and the different distant localizations was analyzed. Prognosis was described in terms of overall survival (OS), progression free survival (PFS) and post progression survival (PPS). Results were reported taking luminal A BC as reference. Triple negative BC showed a higher tropism for lung (OR 4.30 95 % CI 1.41-13.1), while non luminal HER2 subtype was associated with a higher rate of liver metastases (OR 3.61 95 % CI 1.36-9.58). All subtypes were associated with a lower risk of bone-only localization. Central nervous system (CNS) involvement was more common in HER2 positive BC (OR 6.3, 95 % CI 1.08-36.66). Liver, lung and CNS involvement influenced negatively OS (HR 1.64, 95 % CI 1.29-2.07; HR 1.49, 95 % CI 1.18-1.90; HR 2.891, 95 % CI 1.85-4.51, respectively) and PFS (HR 1.39, 95 % CI 1.13-1.71; HR 1.26, 95 % CI 1.02-1.55; HR 1.75, 95 % CI 1.12-2.71, respectively). Multivariate analysis confirmed liver involvement as independent predictor of worse OS (HR 1.64, 95 % CI 1.15-2.34). Stratification by metastatic pattern showed significant differences in terms of PPS but not in terms of PFS. The study suggests that BS may be characterized by typical patterns of metastatic spread and have different impact on clinical outcome. [ABSTRACT FROM AUTHOR]

Objective: To study the CT appearance and histopathology of mass-forming intrahepatic cholangiocarcinoma (IHCC) at presentation and correlate these features with metastatic disease and patient survival. Materials and methods: In this IRB-approved, HIPAA compliant retrospective study, we reviewed pathology database of 459 patients with cholangiocarcinoma seen from 2004 through 2013 to identify 92 patients with IHCC (48 women, 44 men, mean age 61 years) who had CT scans of primary tumor available for review. All baseline and follow-up CT's were reviewed by two radiologists in consensus to record imaging characteristics and metastatic patterns. Clinical and histopathology data were obtained from electronic medical records. Imaging patterns and histopathology were analyzed for associations with metastatic spread and survival. Results: Three distinct CT patterns of IHCC at presentation were identified: solitary dominant mass (type I IHCC, n = 34), dominant mass with satellite nodules in same segment (type II IHCC, n = 19), and multiple scattered hepatic lesions (type III IHCC, n = 39). Distant metastases developed in 49/92 patients (53%); 39 (42%) of which were present at diagnosis. Lungs (22/92; 24%), peritoneum (17/92; 18%), and bones (13/92; 14%) were most common metastatic sites. Type I IHCC had smaller size, lowest incidence of metastases at presentation, and best overall survival, while type III IHCC had shortest survival ( p < 0.017). Poorly differentiated IHCC had higher proportion of osseous metastases ( p = 0.042) and worse survival ( p = 0.027). Conclusion: IHCC has three distinct CT patterns at presentation with different prognoses. Knowledge of these patterns can help radiologists to detect the extrahepatic disease and predict prognosis. [ABSTRACT FROM AUTHOR]

Introduction: Fine needle aspiration biopsy (FNAB) is an easy method with an option of repetitive withdrawal of cell material. Methods: First, mice were inoculated with mouse T-lymphoma, after 10 d the samples from tumor, lymph nodes and spleen gained by FNAB and excision were analyzed by flow cytometry. Tumor progression was compared to the control group simultaneously. Then, 10 d after tumor cell inoculation free doxorubicin (DOX) or different PHPMA DOX conjugates were injected. Cell material was analyzed to detect subpopulations of lymphocyte infiltrate, and levels of cytokines in correlation with progression or regression of the disease. Results: FNAB has no influence on the tumor's growth or survival of experimental animals. After treatment with PHPMA conjugates there was a significant increase of T-lymphocyte subpopulations in tumor microenvironment compared to controls or free DOX, but only in mice with confirmed macroscopic regression of tumor within two weeks. Mice treated with conjugates showed significantly lower cancer infiltration of lymph nodes and spleen. Conclusion: FNAB provides a great benefit to in vivo monitoring of cell changes directly in the tumor after treatment. The number of infiltrating T-lymphocytes increases in correlation with consecutive tumor eradication after treatment with PHPMA. This proves that not only direct cytotoxic but also imunostimulating effect are necessary for successful treatment. [ABSTRACT FROM AUTHOR]

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Epithelioid hemangioendothelioma (EHE) is a rare tumor of the vascular origin. It was first described in its pulmonary form by Dail and Leibow in 1975. and named »intravascular bronhioalveolar tumor« (IVBAT). Since then, reports of occurences of the tumor have been made for number of locations, but most often tumor can be found in soft tissues, liver, lungs, bone and skin. It is considered to be a low or borderline malignant tumor with, usually, slow progression, but aggressive forms have been descrided.We here report a case of a 46-year old female patient with multifocalmalignant tumor spreading to lungs, liver, spleen and with synchronous involvement of lumbal vertebrae, illiac bones and central nervous system dissemination. To the best of the authors knowledge, no case of malignant EHE with multiorgan involvement of this proportions and synchronous central nervous system and bone involvement in one patient has been reported to this date in English-speaking literature. [ABSTRACT FROM AUTHOR]

Interleukin-13 (IL-13) is an anti-inflammatory cytokine produced in cells of hematopoetic origin. It is not known whether pancreatic cancer cells produce IL-13 or whether IL-13 can modulate pancreatic cancer cell growth and influence the frequency of lymph node metastases. Cell growth and signaling were analyzed by cell counting, colorimetric proliferation assays, fluorescent-activated cell sorting, and in vitro kinase activity assays. IL-13 expression and secretion were determined by Northern blot analysis and enzyme-linked immunosorbent assay, respectively. Localization of IL-13 and its transmembrane receptor (IL-4R) in primary pancreatic ductal adenocarcinoma (PDAC) was characterized by immunohistochemistry. IL-13 enhanced the growth of ASPC-1, CAPAN-1, and COLO-357 cells. This was associated with enhanced p44/42 mitogen-activated protein kinase (MAPK) phoshorylation. In contrast to p44/42 MAPK, phosphatidylinositol 3-kinase activity was also induced in IL-13-unresponsive MIA PaCa-2, PANC-1, and T3M4 cells. All cells expressed and secreted IL-13. Neutralizing IL-13 antibodies inhibited the growth of ASPC-1 and CAPAN-1 cells. Immunohistochemical analysis of resected primary ductal adenocarcinoma specimens revealed high levels of IL-13 in 30 of 70 cases and its transmembrane receptor (IL-4R) in 28 of 70 cases, respectively. Fifteen of 16 specimens (94%) exhibiting high IL-13 and IL-4R coexpression had lymph node metastases, while only 30 of the remaining 54 samples (56%) had positive lymph nodes ( p = 0.0134). IL-13 can act as an autocrine growth factor in PDAC. Endogenous expression of IL-13 in conjunction with IL-4R in the cancer cells seems to facilitate lymph node metastasis. [ABSTRACT FROM AUTHOR]

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Purpose:Adenoid cystic carcinoma (ACC) is one of the most common malignant tumours of the salivary glands characterized by multiple recurrences and distant metastasis resulting in significantly worsening prognosis. Galectin-3, a member of the β-galactoside-binding lectin family, has been implicated in tumour progression, metastasis, and found to have prognostic value. The aim of the study was to determine galectin-3 expression in ACC and correlate it with clinicopathological features and patient survival. Methods: Galectin-3 expression was investigated in paraffin sections of 35 ACC of the head and neck. Patients were divided into two groups based on a threshold of 5% positivity in the tumour cell population. The mean follow-up period for all patients was 90.1 months (range 3–300.1 months). Results: Seventeen (48.6%) tumour specimens were considered galectin-3-positive. Galectin-3 reactivity was significantly associated with regional and distant metastasis ( P=0.045 and P<0.001, respectively). There was no statistical significance in the correlation of galectin-3 expression and disease-free survival and overall survival rate ( P=0.095 and 0.102, respectively). Conclusion: Galectin-3 may be used as an indicator in the prediction of metastatic spread in ACC. [ABSTRACT FROM AUTHOR]

Chiasmatic gliomas with metastatic spread are rare in children and are usually associated with diencephalic syndrome. They are mostly pilocytic astrocytomas and their transformation to high-grade astrocytomas has never previously been reported in the pediatric population. We report leptomeningeal spread of a chiasmatic pilocytic astrocytoma in a child presenting with diencephalic syndrome. He was treated with chemotherapy and radiation. The tumor recurred with transformation into a high-grade astrocytoma. Radiation therapy may have played a role in transformation of the tumor, but more research is needed to further clarify the biological behavior of this tumor. [ABSTRACT FROM AUTHOR]