Mechanical behavior and particle crushing of irregular granular material under high pressure using discrete element method.

This study investigated the influence of stress levels on the mechanical behavior and particle crushing of irregular granular materials. Granular materials with irregular sides were modelled using the discrete element method. A new method of using a shear fracture zone to characterize the deformation of irregular granular materials under high pressure was proposed. The crushing energy is analysed based on the first law of thermodynamics. The shear strength of irregular granular materials shows significantly nonlinear behavior due to particle crushing. The deformation behavior can be characterized with the help of particle rotation under low confining pressure, and can be characterized with the help of particle breakage under high confining pressure. Granular materials easily break into many single fine particles under high confining pressure. The breakage degree can be represented by the value of crushing energy. Irregular granular materials have a large breakage degree under high confining pressures. It weakens the stability of engineered structures constructed from granular materials.

Arsenic Trioxide Promotes Tumor Progression by Inducing the Formation of PGCCs and Embryonic Hemoglobin in Colon Cancer Cells.

Arsenic trioxide (ATO) has been used to treat acute promyelocytic leukemia. However, it is not effective in treating solid tumors such as colorectal cancer. We have previously reported that polyploid giant cancer cells (PGCCs) exhibiting the characteristics of cancer stem cells can be generated by various inducers. In this study, ATO was used to induce the formation of PGCCs in LoVo and Hct116 colon cancer cell lines. The migration, invasion, and proliferation abilities of colon cancer cells with and without ATO treatment were assessed by wound-healing, transwell, and plate colony formation assays. The expression of epithelial to mesenchymal transition-related proteins and erythroid differentiation-related proteins in colon cancer cells was further evaluated by western blot and immunocytochemical assays. LoVo and Hct116 cells were transfected with a eukaryotic expression vector for green fluorescent protein (GFP), red fluorescent protein (RFP), H2B-GFP, and H2B-mCherry to study PGCCs formation via cell fusion. WB and ICC assays were performed to assess the expression of cell fusion-related proteins. MG132, small interfering RNA-glial cell missing 1 (GCM1), and chromatin immunoprecipitation-polymerase chain reaction assays were performed to study the role of GCM1/syncytin-1-mediated cell fusion. Clinically, the significance of cell fusion-related proteins and erythroid differentiation-related proteins expression in human colorectal cancer tissues was evaluated. Results of our study showed that ATO induced the formation of PGCCs, and the daughter cells derived from PGCCs gained a mesenchymal phenotype and exhibited strong migration, invasion, and proliferation abilities. PGCCs also produced embryonic hemoglobin-delta and -zeta with strong oxygen-binding ability and erythroid differentiation-related proteins after ATO treatment. In addition, cell fusion was observed during the formation of PGCCs, indicated by the presence of yellow fluorescence via the GCM1/syncytin-1 signaling pathway. Clinically, the expression of cell fusion-related and erythroid differentiation-related proteins gradually increased with the progression of human colorectal cancer tissues. In conclusion, ATO can promote tumor progression by inducing the formation of PGCCs via GCM1/syncytin-1-mediated cell fusion. PGCCs can produce daughter cells with high invasion and migration abilities and embryonic hemoglobin with strong oxygen binding ability, promoting survival of tumor cells in a hypoxic microenvironment.

High Migration and Invasion Ability of PGCCs and Their Daughter Cells Associated With the Nuclear Localization of S100A10 Modified by SUMOylation.

Our previous studies have confirmed that cobalt chloride (CoCl2) or chemoradiotherapy could induce the formation of polyploid tumor giant cells (PGCCs). Polyploid giant cancer cells are a special subpopulation of cancer cells that contribute to solid tumor heterogeneity. The size of PGCC was at least three times larger than regular diploid cancer cells. PGCCs have the properties of cancer stem cells (CSCs) and can express CSC markers CD44 and CD133. Daughter cells derived from PGCCs have strong proliferation, infiltration and migration abilities. However, the detailed molecular mechanism of daughter cells expressing mesenchymal phenotype and displaying strong abilities of proliferation and migration is unclear. As a plasminogen receptor, S100A10 which is closely associated with the invasion and metastasis of malignant tumors, was highly expressed in PGCCs with their daughter cells. In this study, CoCl2 was used to induce the formation of PGCCs in LoVo and HCT116 CRC cells. Cell functional experiments, co-immunoprecipitation, MG132 and ginkgolic acid treatment, western blot, and ChIP-Seq were used to identify the mechanism of S100A10 nuclear location. The proliferation and migration abilities of PGCCs and their daughter cells decreased significantly after S100A10 knockdown. In the control cells, S100A10 was mainly ubiquitinated, while in PGCCs and daughter cells, S100A10 was mainly SUMOylated, which was associated with S100A10 nuclear location. After SUMO1 was inhibited, the nuclear S100A10 in PGCCs and daughter cells decreased, and their proliferation and migration abilities significantly decreased. ChIP-Seq combined with real-time fluorescent quantitative PCR showed that S100A10 regulated the expression of neutrophil defensin 3 (DEFA3), receptor-type tyrosine-protein phosphatase N2 (PTPRN2), and rho guanine nucleotide exchange factor 18 (ARHGEF18), which were associated with actin dynamics and cytoskeleton remodeling. The expression of S100A10 in the nuclei and cytoplasm of rectal cancer after neoadjuvant chemoradiation (nCRT) and liver metastases increased compared with that in rectal cancer without nCRT. Taken together, the expression and nuclear localization of S100A10 modified by SUMOylation were associated with the high proliferation and migration of PGCCs and their daughter cells, and the differentiation, metastases, and relapse of CRCs by regulating the expression of ARHGEF18, PTPRN2, and DEFA3.

The Function of SUMOylation and Its Role in the Development of Cancer Cells under Stress Conditions: A Systematic Review.

Malignant tumors still pose serious threats to human health due to their high morbidity and mortality. Recurrence and metastasis are the most important factors affecting patient prognosis. Chemotherapeutic drugs and radiation used to treat these tumors mainly interfere with tumor metabolism, destroy DNA integrity, and inhibit protein synthesis. The upregulation of small ubiquitin-like modifier (SUMO) is a prevalent posttranslational modification (PTM) in various cancers and plays a critical role in tumor development. The dysregulation of SUMOylation can protect cancer cells from stresses exerted by external or internal stimuli. SUMOylation is a dynamic process finely regulated by SUMOylation enzymes and proteases to maintain a balance between SUMOylation and deSUMOylation. An increasing number of studies have reported that SUMOylation imbalance may contribute to cancer development, including metastasis, angiogenesis, invasion, and proliferation. High level of SUMOylation is required for cancer cells to survive internal or external stresses. Downregulation of SUMOylation may inhibit the development of cancer, making it an important potential clinical therapeutic target. Some studies have already begun to treat tumors by inhibiting the expression of SUMOylation family members, including SUMO E1 or E2. The tumor cells become more aggressive under internal and external stresses. The prevention of tumor development, metastasis, recurrence, and radiochemotherapy resistance by attenuating SUMOylation requires further exploration. This review focused on SUMOylation in tumor cells to discuss its effects on tumor suppressor proteins and oncoproteins as well as classical tumor pathways to identify new insights for cancer clinical therapy.

Role of Transmembrane 4 L Six Family 1 in the Development and Progression of Cancer.

Transmembrane 4 L six family 1 (TM4SF1) is a protein with four transmembrane domains that belongs to the transmembrane 4 L six family members (TM4SFs). Structurally, TM4SF1 consists of four transmembrane domains (TM1-4), N- and C-terminal intracellular domains, two extracellular domains, a smaller domain between TM1 and TM2, and a larger domain between TM3 and TM4. Within the cell, TM4SF1 is located at the cell surface where it transmits extracellular signals into the cytoplasm. TM4SF1 interacts with tetraspanins, integrin, receptor tyrosine kinases, and other proteins to form tetraspanin-enriched microdomains. This interaction affects the pro-migratory activity of the cells, and thus it plays important roles in the development and progression of cancer. TM4SF1 has been shown to be overexpressed in many malignant tumors, including gliomas; malignant melanomas; and liver, prostate, breast, pancreatic, bladder, colon, lung, gastric, ovarian, and thyroid cancers. TM4SF1 promotes the migration and invasion of cancer cells by inducing epithelial-mesenchymal transition, self-renewal ability, tumor angiogenesis, invadopodia formation, and regulating the related signaling pathway. TM4SF1 is an independent prognostic indicator and biomarker in several cancers. It also promotes drug resistance, which is a major cause of therapeutic failure. These characteristics make TM4SF1 an attractive target for antibody-based immunotherapy. Here, we review the many functions of TM4SF1 in malignant tumors, with the aim to understand the interaction between its expression and the biological behaviors of cancer and to supply a basis for exploring new therapeutic targets.

Solitary vertebral metastatic glioblastoma in the absence of primary brain tumor relapse: a case report and literature review.

BACKGROUND: Metastatic glioblastoma presenting as a solitary osteolytic cervical vertebral mass without primary brain tumor relapse is extremely rare with only 1 reported case in the literature. Because of its rarity, it can be easily overlooked and misdiagnosed, posing a diagnostic dilemma. CASE PRESENTATION: A 51-year-old man with right temporal glioblastoma was initially treated by tumor resection, radiotherapy and chemotherapy. Eighteen months after surgery, he was readmitted with complaints of neck pain for 2 weeks. Follow-up magnetic resonance imaging (MRI) and fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) revealed a solitary FDG-avid osteolytic lesion in the 4th cervical vertebral body without other abnormal FDG-uptake in the body and in the absence of local recurrence at the resection cavity. Because of the sudden worsening situation and intractable neck pain, the patient underwent tumor resection. Postoperatively, the pain was obviously reduced and the situation was improved. Interestingly, the immunohistochemical findings of glial fibrillary acidic protein (GFAP) indicated the characteristic of metastatic glioblastoma, despite that the histopathological findings of Hematoxylin & Eosin (H&E) staining was suspicious of osteoclastoma. According to the clinical history, imaging findings, pathological and immunohistochemical results, a final diagnosis of solitary vertebral metastasis from glioblastoma without central nervous system (CNS) relapse was confirmed. Then, the patient received radiotherapy on spine and adjuvant chemotherapy with temozolomide. However, he died suddenly 2 months after the tumor resection, nearly 21 months after the initial diagnosis. CONCLUSION: We emphasize that metastatic glioblastoma should be considered in the differential diagnosis of a solitary FDG-avid osteolytic vertebral mass on PET/CT. And the diagnosis of extracranial metastasis (ECM) from glioblastoma can be achieved through clinical history, imaging findings, pathological examination, and immunohistochemical staining with GFAP.

Molecular Mechanism of Stem Cell Differentiation into Adipocytes and Adipocyte Differentiation of Malignant Tumor.

Adipogenesis is the process through which preadipocytes differentiate into adipocytes. During this process, the preadipocytes cease to proliferate, begin to accumulate lipid droplets, and develop morphologic and biochemical characteristics of mature adipocytes. Mesenchymal stem cells (MSCs) are a type of adult stem cells known for their high plasticity and capacity to generate mesodermal and nonmesodermal tissues. Many mature cell types can be generated from MSCs, including adipocyte, osteocyte, and chondrocyte. The differentiation of stem cells into multiple mature phenotypes is at the basis for tissue regeneration and repair. Cancer stem cells (CSCs) play a very important role in tumor development and have the potential to differentiate into multiple cell lineages. Accumulating evidence has shown that cancer cells can be induced to differentiate into various benign cells, such as adipocytes, fibrocytes, osteoblast, by a variety of small molecular compounds, which may provide new strategies for cancer treatment. Recent studies have reported that tumor cells undergoing epithelial-to-mesenchymal transition can be induced to differentiate into adipocytes. In this review, molecular mechanisms, signal pathways, and the roles of various biological processes in adipose differentiation are summarized. Understanding the molecular mechanism of adipogenesis and adipose differentiation of cancer cells may contribute to cancer treatments that involve inducing differentiation into benign cells.

The role of CDC25C in cell cycle regulation and clinical cancer therapy: a systematic review.

One of the most prominent features of tumor cells is uncontrolled cell proliferation caused by an abnormal cell cycle, and the abnormal expression of cell cycle-related proteins gives tumor cells their invasive, metastatic, drug-resistance, and anti-apoptotic abilities. Recently, an increasing number of cell cycle-associated proteins have become the candidate biomarkers for early diagnosis of malignant tumors and potential targets for cancer therapies. As an important cell cycle regulatory protein, Cell Division Cycle 25C (CDC25C) participates in regulating G2/M progression and in mediating DNA damage repair. CDC25C is a cyclin of the specific phosphatase family that activates the cyclin B1/CDK1 complex in cells for entering mitosis and regulates G2/M progression and plays an important role in checkpoint protein regulation in case of DNA damage, which can ensure accurate DNA information transmission to the daughter cells. The regulation of CDC25C in the cell cycle is affected by multiple signaling pathways, such as cyclin B1/CDK1, PLK1/Aurora A, ATR/CHK1, ATM/CHK2, CHK2/ERK, Wee1/Myt1, p53/Pin1, and ASK1/JNK-/38. Recently, it has evident that changes in the expression of CDC25C are closely related to tumorigenesis and tumor development and can be used as a potential target for cancer treatment. This review summarizes the role of CDC25C phosphatase in regulating cell cycle. Based on the role of CDC25 family proteins in the development of tumors, it will become a hot target for a new generation of cancer treatments.

Different p53 genotypes regulating different phosphorylation sites and subcellular location of CDC25C associated with the formation of polyploid giant cancer cells.

BACKGROUND: Our previous studies have confirmed that cobalt chloride (CoCl2) can induce the formation of polyploid giant cancer cells (PGCCs), which is the key to the heterogeneity of solid tumors. PGCC formation is closely related to the abnormal expression of cell cycle-related proteins and cell fusion. In this study, we investigated the molecular mechanism of PGCCs formation by detecting the expression of cell cycle-related proteins in mutant and wild-type p53 cancer cell lines. METHODS: HEY, BT-549, SKOv3 and MDA-MB-231 cells were treated with CoCl2 and the cell cycle was detected by flow cytometry. The expression and subcellular localization of cell cycle-related proteins, kinases, and P53 were compared before and after CoCl2 treatment. Immunoprecipitation was used to analyze the interacting proteins of pCDC25C-Ser216 and pCDC25C-Ser198. The clinicopathologic significances of these cell cycle-related proteins and protein kinases expression were studied. RESULTS: CoCl2 induced the formation of PGCCs and G2/M arrest. CDC25C, cyclin B1, and CDK1 expressions after CoCl2 treatment were lower than that in control cells. Cytoplasmic CDC25C was degraded by ubiquitin-dependent proteasome. The expression of P53 and phosphokinases including CHK1, CHK2, PLK1, and Aurora A increased after CoCl2 treatment. The expression of pCDC25C-Ser216 and pCDC25C-Ser198 depended upon the genotype of p53. The expressions of cell cycle-related proteins and kinases gradually increased with the development of ovarian cancer and breast cancer. CONCLUSION: CHK1, CHK2-pCDC25C-Ser216-cyclin B1-CDK1, and Aurora A-PLK1-pCDC25C-Ser198-cyclin B1-CDK1 signaling pathways may participate in the formation of PGCCs and different phosphorylation sites of CDC25C may be associated with the genotype of p53.

FGFR2/STAT3 Signaling Pathway Involves in the Development of MMTV-Related Spontaneous Breast Cancer in TA2 Mice.

The Tientsin Albino 2 (TA2) mouse has a high incidence of spontaneous breast cancer (SBC) in the absence of external inducers or carcinogens. The initiation of SBC is related to mouse mammary tumor virus (MMTV) infection and pregnancy. Pathologic analysis showed that breast cancer cells in TA2 mice are triple negative. Our previous study confirmed that fibroblast growth factor receptor 2 (FGFR2) expression increased in SBC tissue compared to that in their corresponding normal breast tissues of TA2 mice. The present study focused on the function of the FGFR2/STAT3 signaling pathway in the initiation of SBC. In this study, the expression of FGF3, FGFR2, STAT3, p-STAT3Tyr705, and p-STAT3Ser727 was detected in serum and normal mammary gland tissues of TA2 mice with different number of pregnancies and SBC. The proliferation, invasiveness, and migration abilities of MA-891 cells from TA2 SBC were compared before and after cryptotanshinone and Stattic treatment. Transient siRNA transfection was used to detect the invasiveness, and migration abilities to avoid the off-targets effects. Downstream protein expression of STAT3 was also detected in MA-891 cells and TA2 xenografts from MA-891 inoculation. In addition, STAT3 expression was analyzed in 139 cases of human breast cancer including 117 cases of non-triple negative breast cancer (non-TNBC) (group I) and 22 cases of triple-negative breast cancer (TNBC) (group II). Results of our study confirmed that MMTV-LTR amplification, and FGFR2, p-STAT3Tyr705, p-STAT3Ser727 expression increased with the number of pregnancies in the breast tissue of TA2 mice and were the highest in SBC. Serum FGF3 expression of SBC was higher than it of TA2 mice with different number of pregnancies. After STAT3 was inhibited, the abilities of proliferation, invasiveness, and migration in MA-891 decreased and the expression levels of STAT3, p-STAT3Ser727, p-STAT3Tyr705, Bcl2, cyclin D1, and c-myc in MA-891 and animal xenografts were also down-regulated. In human breast cancer, STAT3 expression was significantly higher in TNBC than that in non-TNBC. Our results showed that the FGFR2/STAT3 signaling pathway may be related to SBC initiation in TA2 mice. Inhibition of STAT3 can decrease proliferation, invasiveness, and migration in MA-891 cells and the growth of TA2 xenografts.

Critical role and its underlying molecular events of the plasminogen receptor, S100A10 in malignant tumor and non-tumor diseases.

S100A10 is a small molecular weight protein expressed in the cytoplasm of many cells and one of the members of the S100 protein family that binds calcium and forms the largest subgroup of EF-hand proteins. The regulatory processes of S100A10 are complicated. S100A10 participates in the regulation of a variety of tumor and non-tumor diseases through cascade reactions with multitudinous signaling molecules. In malignant tumors, such as acute promyelocytic leukemia (APL) and lung cancer, S100A10 is likely involved in their progression, including invasion and metastasis through the regulation of plasmin production and subsequent plasmin-dependent stimulation of other proteases, such as matrix metalloproteinase (MMP)-2 and -9. Both the plasmin and MMPs are capable of inducing degradation of the extracellular matrix (ECM) and basement membrane, which is a critical step for tumor progression. In non-tumor diseases, the distribution of S100A10 in the brain and its interaction with 5-hydroxytryptamine 1B (5-HT1B) receptor, an important mediator in the central nervous system that maintains a dynamic balance of the neurotransmitters, correlates with depression-like behavior. S100A10 also participates in inflammatory responses through the regulation of peripheral macrophage migration to the inflammatory sites, which depends on the generation of plasmin and other proteinases at the surface of macrophages. Considerable attention should be paid to understand the significant role of S100A10 in the modulation of malignant tumor and non-tumor diseases.

Clinicopathological Significances of Cancer Stem Cell-Associated HHEX Expression in Breast Cancer.

Aberrant expression of the transcription factor hematopoietic ally expressed homeobox/proline-rich homeodomain (HHEX/PRH) is implicated in numerous cancers. However, the association of HHEX with breast cancer (BC) remains unclear. In this study, HHEX mRNA and protein expression were analyzed using the Oncomine, UALCAN, GEPIA, TCGAportal, and HPA databases. We evaluated the effect of HHEX on clinicopathological parameters using Kaplan-Meier plotter, OncoLnc, TCGAportal, PROGgeneV2, and BC-GenExMiner. Western blotting was performed to compare the level of HHEX in breast samples of Tientsin Albino 2 mice, human breast precancerous lesions, benign breast tumors, and BC. The correlation between HHEX and cancer stem cells was investigated using the GEO (GSE52327 and GSE94865) and GEPIA datasets. Networks between HHEX and survival-related gene marker sets and microRNAs were analyzed using GEPIA, StarBase, and Cytoscape. Results of this study showed that HHEX expression in BC was significantly lower than those in breast precancerous lesions and benign breast tumors at both mRNA and protein levels. BC patients with lower HHEX expression had significantly worse overall survival and disease-free survival. Moreover, HHEX significantly affected the clinicopathology of BC. Specifically, low HHEX expression was correlated with the following groups of patients: age ≤51 years, ER-negative or PR-negative patients, HER-2 positive, triple-negative breast cancer, and basal-like BC. Immunohistochemical analysis of the breast samples showed significant differences of HHEX staining index (P < 0.001) among the three groups. To further investigate the mechanism, we determined the intersection of differentially expressed genes related to BC stem cells and those genes after HHEX expression was altered. This led to the identification of four potentially regulated genes-CXL12, BLNK, PAG1, and LPXN. Using StarBase and km-plotter, the negative regulation of HHEX expression and survival trends, including miR-130b, miR-30e, and miR-301b were joined into miRNA-HHEX-mRNA potential regulatory network. The abilities of proliferation, migration and invasion increased in MDA-MB-231 and BT-549 breast cancer cell lines after HHEX down expression and decreased after HHEX overexpression compared them in the control cells. In conclusion, these data suggest that HHEX expression is downregulated in BC and HHEX may regulate the development of BC through the stem cell-related genes.

Extracranial bone metastases from recurrent anaplastic astrocytoma on FDG PET/CT: A case report a care-compliant article.

OBJECTIVE: Extracranial bone metastases from astrocytoma are rare and frequently detected as part of multiorgan metastases. It is extremely rare for astrocytoma to have extracranial bone metastases alone. The importance of whole-body fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT) imaging in evaluating extracranial metastasis (ECMs) has not been described effectively due to the rarity of this event. The purpose of our case report is to emphasize the role of FDG PET/CT in the assessment of tumor recurrence and extracranial bone metastases from anaplastic astrocytoma. METHODS AND MATERIALS: A 25-year-old woman was firstly admitted with a 4-month history of progressive blurred vision, and 2-month history of intermittent headache. Presurgical MRI imaging revealed a large mass in the left trigone of lateral ventricle. Subsequently, she underwent tumor resection, radiotherapy and chemotherapy. A final pathological diagnosis of anaplastic astrocytoma (WHO III) was made. Nearly 12 months after the surgery, the follow-up brain MR imaging revealed a contrast-enhanced lesion in the site of operative region. Whole-body FDG PET/CT imaging was performed to evaluate the situation. RESULTS: Postoperative brain FDG PET/CT showed an abnormal focal FDG uptake corresponding to the contrast-enhanced lesion in the operative area, suggesting a tumor recurrence. Whole-body FDG PET/CT also showed multiple FDG-avid osteosclerotic lesions in the body. It was highly suggestive of extracranial bone metastases. A subsequent open bone biopsy of FDG-avid lesion in right iliac crest was performed. Histopathological and immunohistochemical findings indicated characteristic of glioma. The patient died 1 month later, nearly 13 months after the initial diagnosis. CONCLUSIONS: ECMs from anaplastic astrocytoma are extremely rare but they do occur. Whole-body FDG PET/CT imaging with inclusion of brain was valuable in differentiating tumor recurrence from radiation necrosis and in detecting uncommon extracranial bone metastases from anaplastic astrocytoma, which were closely related to prognosis of this disease.

Solitary Choroidal Metastasis From Lung Adenocarcinoma on FDG PET/CT.

Solitary choroidal metastasis as an initial presentation of lung cancer is rare. A 67-year-old woman who initially presented with a 3-month history of blurred vision in the right eye was suggestive of choroidal melanoma on MRI. Preoperatively, a pulmonary mass was found on x-ray. She was referred for an FDG PET/CT imaging, which revealed a choroidal lesion with minimal FDG uptake in right eye and increased FDG activity in the known lung mass. A pathological diagnosis of metastatic lung adenocarcinoma was made after enucleation of the right eyeball.

FDG-Avid Keloid on PET/CT Imaging.

Keloid is a benign fibroproliferative growths resulting from an overexuberant healing response. A 51-year-old man with a 20-year history of keloid formation presented with a 1-year history of unexplained progressive weakness of both lower limbs. He was clinically suspected of having paraneoplastic neurologic syndrome. FDG PET/CT was performed to exclude underlying malignancy. FDG PET/CT revealed a giant FDG-avid keloid in the anterior chest wall without any other abnormal FDG uptake in the body. We emphasize that a benign FDG-avid keloid should be considered in the differential diagnosis of FDG-avid cutaneous lesions on PET/CT.

Blastic Plasmacytoid Dendritic Cell Neoplasm Evaluated by FDG PET/CT.

Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and aggressive hematological malignancy. A 34-year-old man with a biopsy-proven BPDCN underwent FDG PET/CT for staging. FDG PET/CT revealed multiple mild FDG-avid cutaneous lesions on the chest and back, involvement of left inguinal lymph node, and a markedly increased FDG-avid subcutaneous mass in the left lower leg.

Polysplenia Syndrome With Splenic and Skeletal Muscle Metastases From Thyroid Carcinoma Evaluated by FDG PET/CT: Case Report and Literature Review: A Care-Compliant Article.

Polysplenia syndrome (PSS) is a rare congenital abnormality. Metastases to spleen and skeletal muscle from differentiated thyroid cancer (DTC) are also extremely rare. Our case report aims to present an interesting case of PSS associated with splenic metastasis (SM) and skeletal muscle metastasis (SMM) from advanced papillary thyroid carcinoma which was evaluated on fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT). An 84-year-old Chinese man was admitted with the history of multiple enlarged masses in bilateral neck, right axillary, and inguinal areas for >2 months. The results of ultrasonography examination were highly suggestive of malignancy. The histological results of the following biopsy were consistent with papillary thyroid carcinoma with involvement of multiple regional lymph nodes. He was referred for an FDG PET/CT imaging to evaluate the situation. FDG PET/CT showed that an intense FDG-avid thyroid mass with widespread regional lymph node involvement and distant metastases in the body. Unexpected sites of metastases were detected in the spleens and skeletal muscles. Most interestingly, FDG PET/CT imaging also described the typical imaging findings of PSS including the 2 right-sided spleens, azygos and hemiazygos continuation of inferior vena cava (IVC), right-sided stomach, middle line liver, a short pancreas, preduodenal portal vein (PPV), and malrotation of gut. Whole body FDG PET/CT imaging can accurately evaluate the situation of DTC by detecting regional lymph node involvement, common and rare sites of distant metastases which are closely related to staging, management, and prognosis of this disease. Whole-body FDG PET/CT is also valuable in demonstrating the typical imaging features of PSS.

Extensive invasive extramammary Paget disease evaluated by F-18 FDG PET/CT: a case report.

Extramammary Paget disease (EMPD) is a rare cutaneous, intraepithelial adenocarcinoma. Because of its rarity, little is known about the value of fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) in evaluating this disease. Our case report aims to increase current knowledge of FDG PET/CT in EMPD as a noninvasive imaging tool for assessing the extension of the disease and detecting distant metastases.We reported a 64-year-old Chinese man who presented with a slowly progressive, ill-margined erythematous lesion with a crusted, eroded, and scaly surface involving multiple sites of penis, scrotum, left pelvic wall, hip, groin, and thigh for >4 years, which became extensive in the past 1 year. He was referred for an FDG PET/CT examination to further evaluate the lesions. A following skin biopsy was performed to obtain a definitive histological diagnosis.FDG PET/CT imaging revealed mild FDG uptake at the extensive cutaneous lesion with subcutaneous invasion, involvement of lymph nodes, and multiple intense FDG-avid of skeletal metastases. According to the appearance of FDG PET/CT, a provisional diagnosis of advanced cutaneous malignancy was made. Histopathology findings indicated characteristic of EMPD. The patient was treated with radiation therapy and died from complications 2 months after the last dose of radiotherapy.Our case highlighted that a whole-body FDG PET/CT should be incorporated into the diagnostic algorithm of EMPD to give a comprehensive assessment of this disease.

Primary anorectal melanoma on FDG PET/CT.

Primary anorectal melanoma is an extremely rare, aggressive malignancy with a poor prognosis. A 76-year-old man with a 2-month history of rectal bleeding, anal pain, and tenesmus was referred for an F-FDG PET/CT examination, which revealed an abnormal focal FDG uptake on the lower rectum with multiple other intense FDG-avid regions in locoregional pelvic lymph nodes, bones, liver, and lung. It was highly suggestive of malignancy, and a provisional diagnosis of advanced rectal carcinoma was made. However, a following tissue biopsy of the lesion on the lower rectum performed by colonoscopy histopathologically indicated primary anorectal melanoma.

[Cerebral glucose metabolism in Parkinson's disease with dementia].

OBJECTIVE: To assess the regional cerebral glucose utilization and the imaging characteristic of Parkinson's disease with dementia (PDD) with (18)F-fluorodeoxyglucose (FDG) positron emission tomography (PET). METHODS: Questionnaire survey, mini-mental state examination (MMSE), physical examination, and FDG PET on brain at rest state were performed on 20 patients with PDD, 13 males and 7 females, aged (70 +/- 6), and sex- and age-matched 8 patients with non-demented PD, and 30 healthy parsons. Visual inspection and statistical parametric mapping (SPM) were used to investigate the regional cerebral metabolic rate of glucose (rCMRglc) and the distribution of the tracer. RESULTS: The MMSE score of the PDD group was (27.5 +/- 2.4), (10 - 24), significantly lower than those of the non-PDD group [(27.5 +/- 2.4) (22 - 30)] and control group [(27.9 +/- 2.2) (21 - 30)] (F = 60.31, P = 0.000). There were no significant differences in Hoehn-Yahr staging and disease courses between the two PD groups (P > 0.05). Visual inspection showed that there were no significant focal hypometabolic areas in the imaging of the non-demented PD patients, while compared to the controls, the rCMRglc levels of the PDD patients decreased in bilateral superior parietal lobules (BA 7), inferior parietal lobules (BA 40, 39), superior frontal gyri (BA 6), middle frontal gyri (BA 6, 8, 9), middle temporal gyri (BA 21), cuneate lobes (BA 17, 18, 19), cingulate cortices (BA 31), lingual gyri (BA 19) basal ganglia, and thalamus. According to the severity of memory impairment and the onset of hallucination, the subtype of PDD was classified into memory impairment dominant group (MD) and hallucination dominant group (HD). The rCMRglc of MD subgroup decreased significantly in the parietotemporal association cortex, especially in the precuneus lobe. The rCMRglc of the HD subgroup decreased significantly in the occipital cortex. There were no significant differences in MMSE score and Hoehn-Yahr staging between the MD and HD groups (both P > 0.05), while the age of the HD subgroup was significantly lower, and the disease duration of the HD subgroup was significantly longer than those toe MD group (both P < 0.05). CONCLUSIONS: (18)F-FDG/PET imaging is helpful to the diagnosis of PDD and may help investigate the potential pathophysiology of PDD.