Different Stages Of Tumor Research Articles

Microfluidic Device-Based In Vivo Detection of PD-L1-Positive Small Extracellular Vesicles and Its Application for Tumor Monitoring.

Liquid biopsy is of great significance in tumor early diagnosis and treatment stratification. PD-L1-positive small extracellular vesicles (PD-L1+ sEVs) are closely related to tumor growth and immunotherapy response, which are considered valuable liquid biopsy biomarkers. In contrast to conventional in vitro detection, in vivo detection has the ability to improve the detection efficiency and enable continuous or real-time dynamic monitoring. However, in vivo detection of PD-L1+ sEVs has multiple difficulties, such as high cell background, complex blood environments, and lack of a specific and stable detection method. Herein, the in vivo detection of PD-L1+ sEVs method was constructed, which efficiently separated sEVs based on the microfluidic device and quantitatively analyzed PD-L1+ sEVs by aptamer recognition and hybridization chain reaction. The concentration of PD-L1+ sEVs was continuously monitored, and significant differences at different stages of tumor as well as a correlation with tumor volume were found. Diseased and healthy individuals could also be effectively distinguished based on the concentration of PD-L1+ sEVs. The method with good stability, biocompatibility, and detection performance provided a powerful means for in vivo detection of PD-L1+ sEVs, contributing to the clinical diagnosis and treatment of tumor.

Abstract IA027: Role of stress-survival pathways and transcriptomic alterations in progression of colorectal cancer: A Hispanic health disparities perspective

Abstract Essential to improving treatment, prognosis, and detection strategies are the identification and validation of new ethnicity-specific genomic profiles in cellular stress and survival pathways as effective predictors of colorectal cancer (CRC). These pathways are increasingly implicated in tumorigenesis of CRC and in providing resistance to chemotherapy-induced cell death. In this study, we have explored the role of these pathways in the biological significance of the expression of stress-survival pathway-associated genes in CRC progression and their role in promoting tumor aggressiveness from the Hispanic health disparities perspective. Transcript expression of oxidative stress and apoptosis-associated gene was evaluated in CRC gene microarray and RNAseq datasets to obtain 28 target genes. These genes were screened for transcript-level expression in six CRC cell lines and cDNA arrays containing the tumor (n=40) from different stages, and control (n=8) samples. The protein expression was evaluated by immunohistochemistry (IHC) in CRC microarrays (TMAs) containing different stages of tumor (n = 108) and control (n = 12) tissues. Target genes were also analyzed in Hispanic and Non-Hispanic White (NHWs) tissues at the transcript level. The analysis of target genes FOXM1, CDK1, CDK4, Chek1, and MCM10 showed consistent upregulation in CRC cell lines, cDNA arrays, and TMAs. The differential expression was also associated with the tumor stages. Among the target genes, Chek1, MCM10, and FOXM1 were found to be differentially expressed in Hispanic tissues when compared to the NHW samples. No significant difference was observed in the expression levels of CDK1 and CDK4 between the Hispanic and NHW tissues. Eight genes that did not show differential expression in CRC cell lines, were also seen to be upregulated in the Hispanic tissues, suggesting the influence of ethnicity-specific genetic makeup on the expression of these genes. The genes identified to be upregulated in Hispanic tissues may be used as potential biomarkers or as therapeutic targets in the Hispanic population. Citation Format: Aditi Kulkarni, Urbashi Basnet, Frances Rangel, Sourav Roy. Role of stress-survival pathways and transcriptomic alterations in progression of colorectal cancer: A Hispanic health disparities perspective [abstract]. In: Proceedings of the 15th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2022 Sep 16-19; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2022;31(1 Suppl):Abstract nr IA027.

The pivotal regulatory factor circBRWD1 inhibits arsenic exposure-induced lung cancer occurrence by binding mRNA and regulating its stability

Multiple studies have indicated that circular RNAs (circRNAs) play a regulatory role in different stages of tumors by interacting with various molecules. With continuous in-depth research on the biological functions of circRNAs, increasing evidence has shown that circRNAs play important roles in carcinogenesis caused by environmental pollutants. However, the function and mechanism of circRNAs in arsenic exposure-induced lung cancer occurrence have not been reported. In this study, RNA sequencing and qPCR assays revealed that the expression of circBRWD1 was decreased in BEAS-2B-As cells and multiple lung cancer cell lines. Silencing circBRWD1 promoted cell viability and proliferation, inhibited cell apoptosis, and accelerated the G0/G1 phase transition in BEAS-2B-As cells; however, these functions were abrogated by circBRWD1 overexpression. Mechanistically, under arsenic exposure, expression of decreased circBRWD1 led to enhanced stability of the mRNA to which it directly binds (c-JUN, c-MYC, and CDK6 mRNA), increasing its expression. This mechanism promotes the malignant transformation of lung cells and ultimately leads to lung cancer. Our findings thus reveal the molecular mechanism of arsenic carcinogenesis.

Conditioned media of pancreatic cancer cells and pancreatic stellate cells induce myeloid-derived suppressor cells differentiation and lymphocytes suppression

As pancreatic cancer cells (PCCs) and pancreatic stellate cells (PSCs) are the two major cell types that comprise the immunosuppressive tumor microenvironment of pancreatic cancer, we aimed to investigate the role of conditioned medium derived from PCCs and PSCs co-culture on the viability of lymphocytes. The conditioned medium (CM) collected from PCCs and/or PSCs was used to treat peripheral blood mononuclear cells (PBMCs) to determine CM ability in reducing lymphocytes population. A proteomic analysis has been done on the CM to investigate the differentially expressed protein (DEP) expressed by two PCC lines established from different stages of tumor. Subsequently, we investigated if the reduction of lymphocytes was directly caused by CM or indirectly via CM-induced MDSCs. This was achieved by isolating lymphocyte subtypes and treating them with CM and CM-induced MDSCs. Both PCCs and PSCs were important in suppressing lymphocytes, and the PCCs derived from a metastatic tumor appeared to have a stronger suppressive effect than the PCCs derived from a primary tumor. According to the proteomic profiles of CM, 416 secreted proteins were detected, and 13 DEPs were identified between PANC10.05 and SW1990. However, CM was found unable to reduce lymphocytes viability through a direct pathway. In contrast, CM that contains proteins secreted by PCC and/or PSC appear immunogenic as they increase the viability of lymphocytes subtypes. Lymphocyte subtype treated with CM-induced MDSCs showed reduced viability in T helper 1 (Th1), T helper 2 (Th2), and T regulatory (Treg) cells, but not in CD8+ T cells, and B cells. As a conclusion, the interplay between PCCs and PSCs is important as their co-culture displays a different trend in lymphocytes suppression, hence, their co-culture should be included in future studies to better mimic the tumor microenvironment.

A spatiotemporal multi-scale computational model for FDG PET imaging at different stages of tumor growth and angiogenesis

A deeper understanding of the tumor microenvironment (TME) and its role in metabolic activity at different stages of vascularized tumors can provide useful insights into cancer progression and better support clinical assessments. In this study, a robust and comprehensive multi-scale computational model for spatiotemporal transport of F-18 fluorodeoxyglucose (FDG) is developed to incorporate important aspects of the TME, spanning subcellular-, cellular-, and tissue-level scales. Our mathematical model includes biophysiological details, such as radiopharmaceutical transport within interstitial space via convection and diffusion mechanisms, radiopharmaceutical exchange between intracellular and extracellular matrices by glucose transporters, cellular uptake of radiopharmaceutical, as well as its intracellular phosphorylation by the enzyme. Further, to examine the effects of tumor size by varying microvascular densities (MVDs) on FDG dynamics, four different capillary networks are generated by angiogenesis modeling. Results demonstrate that as tumor grows, its MVD increases, and hence, the spatiotemporal distribution of total FDG uptake by tumor tissue changes towards a more homogenous distribution. In addition, spatiotemporal distributions in tumor with lower MVD have relatively smaller magnitudes, due to the lower diffusion rate of FDG as well as lower local intravenous FDG release. Since mean standardized uptake value (SUVmean) differs at various stages of microvascular networks with different tumor sizes, it may be meaningful to normalize the measured values by tumor size and the MVD prior to routine clinical reporting. Overall, the present framework has the potential for more accurate investigation of biological phenomena within TME towards personalized medicine.

Abstract 3674: Differential expression of stress-survival pathway genes related to Hispanic colorectal cancer disparities

Abstract Colorectal cancer (CRC) accounts for 12% and 8% of all estimated new cases of cancer and 11% and 9% of all cancer deaths in Hispanic men and women, respectively. Stress-survival pathways have been implicated in tumorigenesis of CRC and in providing resistance to chemotherapy-induced cell-death by suppressing reactive oxygen species (ROS), repairing DNA damage, and by regulating cell signaling pathways. However, studies related to the role of these pathways in CRC from the Hispanic health disparities perspective, are limited. Essential to improving treatment, prognosis, and detection strategies is the identification and validation of new ethnicity-specific transcriptomic markers within the stress-survival pathways as effective predictors of CRC. In this study, we have explored the role of stress-survival pathway genes in Hispanic and Non-Hispanic White (NHW) CRC tissues. We have used microarray and RNA-seq datasets obtained from the gene expression omnibus (GEO) and the cancer genome atlas (TCGA) to identify 28 genes associated with CRC. These genes were screened for transcript level expression in one normal colon and two CRC cell lines, and in cDNA arrays containing tumor (n=40) from different stages, and control (n=8) samples. The protein level expressions were evaluated by immunohistochemistry (IHC) in CRC tissue microarrays (TMAs) containing different stages of tumor (n = 108) and control (n = 12) tissues. All 28 genes were also analyzed for their transcript level expressions in Hispanic and NHW tissues. Genes related to apoptosis like FOXM1, CDK1, CDK4, Chek1, and MCM10 showed consistent upregulation in CRC cell lines, cDNA arrays and TMAs when compared to normal samples. We could also detect a correlation between the differential expression of these genes and the tumor stages. CDK4, Chek1, FOXM1, and CDC25, were observed to be downregulated in the Hispanic CRC tissues. On the other hand, oxidative stress markers were not seen to be differentially expressed in the two CRC cell lines when compared to the normal cell line. However, some of the known oxidative stress markers like PRDX4, GPX1, and SOD2 were found to be upregulated in Hispanics when compared to NHW tissues. Our results suggest that some of these stress-survival pathway genes could be explored as interesting candidates for ethnicity-specific CRC biomarkers and as novel therapeutic targets in the future. Citation Format: Aditi Kulkarni, Urbashi Basnet, Abhijeet R. Patil, Rebecca DeJesus, Sourav Roy. Differential expression of stress-survival pathway genes related to Hispanic colorectal cancer disparities [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 3674.

Sequence Requirements for miR-424-5p Regulating and Function in Cancers.

MiRNAs (microRNAs) are the most abundant family of small noncoding RNAs in mammalian cells. Increasing evidence shows that miRNAs are crucial regulators of individual development and cell homeostasis by controlling various biological processes. Therefore, miRNA dysfunction can lead to human diseases, especially in cancers with high morbidity and mortality worldwide. MiRNAs play different roles in these processes. In recent years, studies have found that miR-424-5p is closely related to the occurrence, development, prognosis and treatment of tumors. This review discusses how miR-424-5p plays a role in different kinds of cancers from different stages of tumors, including its roles in (i) promoting or inhibiting tumorigenesis, (ii) regulating tumor development in the tumor microenvironment and (iii) participating in cancer chemotherapy. This review provides a deep discussion of the latest findings on miR-424-5p and its importance in cancer, as well as a mechanistic analysis of the role of miR-424-5p in various tissues through target gene verification and pathway analysis.

Duality of Interactions Between TGF-β and TNF-α During Tumor Formation.

The tumor microenvironment is essential for the formation and development of tumors. Cytokines in the microenvironment may affect the growth, metastasis and prognosis of tumors, and play different roles in different stages of tumors, of which transforming growth factor β (TGF-β) and tumor necrosis factor α (TNF-α) are critical. The two have synergistic and antagonistic effect on tumor regulation. The inhibition of TGF-β can promote the formation rate of tumor, while TGF-β can promote the malignancy of tumor. TNF-α was initially determined to be a natural immune serum mediator that can induce tumor hemorrhagic necrosis, it has a wide range of biological activities and can be used clinically as a target to immune diseases as well as tumors. However, there are few reports on the interaction between the two in the tumor microenvironment. This paper combs the biological effect of the two in different aspects of different tumors. We summarized the changes and clinical medication rules of the two in different tissue cells, hoping to provide a new idea for the clinical application of the two cytokines.

68Ga-FAPI-04 vs. 18F-FDG in a longitudinal preclinical PET imaging of metastatic breast cancer.

This longitudinal study aims to evaluate the performance of 68Ga-FAPI-04 and 18F-FDG and to profile the dynamic process of tumor metastasis in a preclinical 4T1 breast cancer model. Although both of these two radioligands are wildly used in clinic, no study was reported on their performance in the longitudinal monitoring of tumor metastasis. Also, no correlation between the expression level of fibroblast activation protein (FAP) and the development of tumor metastasis has been elucidated previously. In this study, we evaluated the performance of 68Ga-FAPI-04 and 18F-FDG PET during the entire process of tumor metastasis, and their potential for the early diagnosis of tumor metastasis. We also clarified the correlation of uptakes as well as the signal-to-background (S/B) ratios between these two probes at different stages of tumor metastasis. Forty 4T1 metastatic breast cancer murine models were established using female BALB/c mice, followed by the longitudinal imaging with 68Ga-FAPI-04 and 18F-FDG once a week for up to 6weeks. In vitro hematoxylin and eosin (H&E) and immunochemistry (IHE) staining were performed to evaluate FAP expression on the metastatic lesions. Further statistical analysis was performed to evaluate the correlation of 68Ga-FAPI-04 and 18F-FDG uptake (%ID/cc) at different stages of the metastasis. 68Ga-FPAI-04 holds an advantage over 18F-FDG with higher sensitivity at the early stage of tumor metastasis. However, with the progress of tumor metastasis, uptake of 68Ga-FAPI-04 decreases and becomes less sensitive than 18F-FDG. There is also no direct correlation between uptake or S/B ratios of 68Ga-FAPI-04 and 18F-FDG during this dynamic process. 68Ga-FAPI-04 is more sensitive than 18F-FDG in detecting the early stage of tumor metastasis, but becomes less sensitive than 18F-FDG at the late stage of tumor metastasis. We envision this result would be meaningful for the explanation of the 68Ga-FAPI-04 and 18F-FDG imaging both in the future clinic and preclinic studies.

An Analysis of Tumor Margin Shrinkage in the Surgical Resection of Squamous Cell Carcinoma of the Oral Cavity.

BackgroundSurgical resection of the oral cavity squamous cell carcinoma with clear surgical margins is the key to preventing local recurrence and avoiding the need for adjuvant treatment or margin re-resection. There is often a discrepancy observed between the clinically determined margins of the tumor when it is being resected and the histopathological result after the specimen has been processed.MethodsA total of six patients who underwent primary surgical resection of oral squamous cell carcinoma between June and October 2020 were included. Surgical margins of the tumor were measured and recorded at three stages of tumor resection: pre-incision, post-resection, and post-formalin fixation. The 1 cm pre-incision anterior margin was compared to both the anterior post-resection and post-formalin fixation margins to document any shrinkage between the different stages of tumor resection.ResultsThe overall mean surgical margin shrinkage was 26% (95% confidence interval {CI} 9.34-42.66, p=0.012). The greatest amount of margin shrinkage occurred between pre-incision and post-resection measurements, which is statistically significant at 19.7% (95% CI 7.49-31.83, p=0.009). To a lesser extent, tumor surgical margins also decreased by 12.7% (95% CI -2.66 to 28.09, p=0.083) between post-resection and post-formalin fixation.ConclusionDimensions of tumor surgical margins in oral cavity squamous cell carcinoma specimens decrease from surgical resection to histopathological processing. Most of this shrinkage occurs between the clinically determined pre-incision and immediately after tumor resection in the post-resection measurement. These findings suggest that it might be prudent to consider surgical margin shrinkage when outlining initial margins to ensure adequate and complete resection of the tumor.

Linking Metabolic Reprogramming, Plasticity and Tumor Progression.

Simple SummaryIn the present review, we discuss the role of metabolic reprogramming which occurs in malignant cells. The process of metabolic reprogramming is also known as one of the “hallmarks of cancer”. Due to several reasons, including the origin of cancer, tumor microenvironment, and the tumor progression stage, metabolic reprogramming can be heterogeneous and dynamic. In this review, we provide evidence that the usage of metabolic drugs is a promising approach to treat cancer. However, because these drugs can damage not only malignant cells but also normal rapidly dividing cells, it is important to understand the exact metabolic changes which are elicited by particular drivers in concrete tissue and are specific for each stage of cancer development, including metastases. Finally, the review highlights new promising targets for the development of new metabolic drugs. The specific molecular features of cancer cells that distinguish them from the normal ones are denoted as “hallmarks of cancer”. One of the critical hallmarks of cancer is an altered metabolism which provides tumor cells with energy and structural resources necessary for rapid proliferation. The key feature of a cancer-reprogrammed metabolism is its plasticity, allowing cancer cells to better adapt to various conditions and to oppose different therapies. Furthermore, the alterations of metabolic pathways in malignant cells are heterogeneous and are defined by several factors including the tissue of origin, driving mutations, and microenvironment. In the present review, we discuss the key features of metabolic reprogramming and plasticity associated with different stages of tumor, from primary tumors to metastases. We also provide evidence of the successful usage of metabolic drugs in anticancer therapy. Finally, we highlight new promising targets for the development of new metabolic drugs.

Investigating Receptor Expression in Response to Wnt5a Isoforms in Urothelial Carcinoma Cell Lines

Urothelial carcinoma (UC), the most common form of bladder cancer, has a high rate of recurrence and a low five‐year survival rate for high grade and metastatic tumors. Expression of Wnt5a, a protein that plays a role in many critical processes in cells and is involved in many different molecular signaling pathways, has been shown to correlate with UC development and pathological stage. Recently the Wnt5a gene has been shown to encode two different isoforms (Wnt5a‐L and Wnt5a‐S). Correlation of isoform expression with tumor cell phenotype suggests opposing roles, either as tumor‐promoting or tumor‐suppressing, depending on the cancer type. The effects of each Wnt5a isoform in UC, however, are not well understood.In order to understand how the Wnt5a isoforms function in the development of UC, it is important to understand which signaling pathways are being activated or inhibited by each isoform. This project aims to identify Wnt5a receptors that are differentially upregulated or downregulated in response to treatment with either Wnt5a‐L or Wnt5a‐S in several different UC cell lines derived from different stages of tumors, as well as in a primary human bladder cell line. The project will include identification and characterization of the Wnt5a receptors normally expressed in the untreated, basal state, information which is currently unknown. Wnt5a isoform treatment will be conducted using conditioned media collected from Chinese Hamster Ovary (CHO) cells that have been genetically modified to express either Wnt5a‐L or Wnt5a‐S. Using western blot analysis, we have already quantified the amount of each isoform present in the conditioned media so that equal amounts of each isoform can be used for cell treatments. We have also used western blot analysis to demonstrate that we can isolate membrane proteins from cell lysates. We will now be treating the cell lines with equal concentrations of Wnt5a‐L, Wnt5a‐S or commercially available Wnt5a as a positive control; isolating the membrane proteins from each cell line after treatment; and applying the isolated membrane proteins to custom antibody arrays in order to examine the expression of 17 different Wnt5a receptors. Results from these experiments will show what receptors are upregulated or downregulated in response to each Wnt5a isoform, which will help elucidate the signaling pathways regulated by each isoform in the pathogenesis of UC.Support or Funding InformationThis project was supported in part by funding from the Honors Tutorial College, Student Enhancement Award, and Heritage College of Osteopathic Medicine Research and Scholarly Activities Committee, all at Ohio University. Special thanks is given to Dr. Karl Willert, who provided the CHO cell lines expressing each Wnt5a isoform.

IPredCNC: Computational prediction model for cancerlectins and non-cancerlectins using novel cascade features subset selection

Lectins are special types of protein that play a crucial role in tumor cell differentiation due to their significant binding affinity to certain types of saccharide (carbohydrate) groups. They are also closely related to certain types of proteins that initiate tumor cell survival, growth, metastasis, carcinoma, and different stages of tumor. Differentiating the specific functions of proteins remains challenging in the post-genomic era. This endeavor is vital in therapeutic cancer studies, but web-lab experiments related to this issue are expensive and time-consuming. To cope with this situation, several computational sequence-based methods have been proposed to differentiate the specific functions of proteins. In the current study, we have developed a fast-accurate cascade feature selection-based machine learning model for cancer lectins using different sequence-based feature descriptive techniques. This model yielded 85.21% accuracy, 87.84% sensitivity, 81.92% specificity, and 0.922 AUC with a multilayer perceptron over k-fold, and stratified k-fold cross-validation tests. These concrete empirical results show the authenticity and robustness of the proposed study compared to all existing approaches. This proposed novel methodology would be a handy tool in cancer therapeutics research, drug design, and academic studies. All the source codes and data regarding this manuscript are freely available via http://www.github.com/zaheeerkhancs/iPredCNC.

Reactive oxygen species and cancer: A complex interaction.

Elevated levels of Reactive Oxygen Species (ROS), increased antioxidant ability and the maintenance of redox homeostasis can cumulatively contribute to tumor progression and metastasis. The sources and the role of ROS in a heterogeneous tumor microenvironment can vary at different stages of tumor: initiation, development, and progression, thus making it a complex subject. In this review, we have summarized the sources of ROS generation in cancer cells, its role in the tumor microenvironment, the possible functions of ROS and its important scavenger systems in tumor progression with special emphasis on solid tumors.

Integrated analysis of differentially expressed profiles and construction of a competing endogenous long non-coding RNA network in renal cell carcinoma.

BackgroundLong non-coding RNAs (lncRNAs) play crucial roles in the initiation and progression of renal cell carcinoma (RCC) by competing in binding to miRNAs, and related competitive endogenous RNA (ceRNA) networks have been constructed in several cancers. However, the coexpression network has been poorly explored in RCC.MethodsWe collected RCC RNA expression profile data and relevant clinical features from The Cancer Genome Atlas (TCGA). A cluster analysis was explored to show different lncRNA expression patterns. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses and gene set enrichment analysis (GSEA) were performed to analyze the functions of the intersecting mRNAs. Targetscan and miRanda bioinformatics algorithms were used to predict potential relationships among RNAs. Univariate Cox proportional hazards regression was conducted to determine the RNA expression levels and survival times.ResultsBioinformatics analysis revealed that the expression profiles of hundreds of aberrantly expressed lncRNAs, miRNAs, and mRNAs were significantly changed between different stages of tumors and non-tumor groups. By combining the data predicted by databases with intersection RNAs, a ceRNA network consisting of 106 lncRNAs, 26 miRNAs and 69 mRNAs was established. Additionally, a protein interaction network revealed the main hub nodes (VEGFA, NTRK2, DLG2, E2F2, MYB and RUNX1). Furthermore, 63 lncRNAs, four miRNAs and 31 mRNAs were significantly associated with overall survival.ConclusionOur results identified cancer-specific lncRNAs and constructed a ceRNA network for RCC. A survival analysis related to the RNAs revealed candidate biomarkers for further study in RCC.

Quantification of Radiation Exposure of Non-Dominant Index for the Surgeon Performing Sentinel Lymph-Node Removal Procedure.

Sentinel lymph-node scintigraphy is a useful method for accurate staging of different tumors and a helpful tool in personalized therapy for oncological patients. The radiation exposure for surgical staff has been a concern since the sentinel lymph-node detection method was developed. The objective of the study was to determine and quantify the exposure to radiation of the non-dominant index for the surgeon performing sentinel lymph-node removal and to determine, if there is an irradiation risk imposed during the surgical procedure. We performed a study over a period of one year, where we evaluated the exposure of surgeon's non-dominant index during 196 sentinel lymph-node removal procedures. The pharmaceutical was administrated via subcutaneous injection in four peritumoral or perilesional injection sites. The equipment we used consisted of EuroProbe3 for sentinel lymph-node detection and ring TLD dosimeter placed on the surgeon's non-dominant index. The clinical distribution was: 104 melanomas, 84 breast carcinomas, 6 vulvar carcinomas and 2 penial carcinomas. The administered activity showed an average of 39.55 MBq (SD ± 1.96) Tc-99m nanoalbumin compound. The non-dominant index exposure ranged between 0.10 mSv and 0.13 mSv/month with a cumulative dose of 1.31 mSv/year, thus 6.69 µSv per procedure. The surgeon received a minimal dose for the non-dominant index. The values we recorded did not pose any additional concerns or restrictions, the exposure being under the limits and constraints established by regulations, close to the detectability limit of the dosimeter. The procedure is safe in terms of radiation protection, respecting the limitation and optimization principles.

Limitations of dual time point FDG-PET imaging in the evaluation of focal abdominal lesions.

For the evaluation of the diagnostic potential of dual time point FDG positron emission tomography (PET) in patients with suspicious focal abdominal uptake, dual time point PET imaging was compared with clinical findings. In a prospective study, 56 patients exhibiting a solitary suspicious, intense abdominal FDG uptake, underwent dual time point PET imaging for staging or restaging of different malignant tumors, maximal standardized uptake value (SUVmax) measurements included. The first acquisition was started 64.8 +/- 19.5, the second 211.3 +/- 52.5 min after FDG injection. The final diagnosis based on CT or MRT imaging and a follow-up period of 12.6 +/- 2.8 months. Additionally, colonoscopy was done in 6 patients. In another 6 patients histopathology was obtained from CT guided biopsy. Malignant focal abdominal lesions with a SUVmax <2.5 (n = 4) showed an uptake increase of > or =30%. In the remaining malignant cases with an uptake of > or =2.5 (n = 11), uptake increased in 64% and decreased in 36%. Malignant lesions showing FDG uptake decrease (n = 4) had an initial SUVmax value > or =2.5 and remained with a SUVmax > or =2.5 in the second imaging. In benign lesions with an initial SUVmax > or =2.5 (n = 31), the uptake increased in 17 patients (55%) and decreased in 14 patients (45%). All lesions which changed configuration (33%) were confirmed as benign (n = 5). Using dual time point PET abdominal lesions show a very hetergenous uptake pattern regardless of their dignity. Malignancy can only be reliably excluded in lesions which change their configuration and in lesions with an initial SUVmax value <2.5 combined with an SUV decrease in the delayed imaging. Particularly abdominal lesions which show an initial SUVmax > or =2.5 combined with a SUV increase in the delayed imaging are suspicious for malignancy and need further clarification.

Isolation of circulating tumor cells in pancreatic cancer patients by immunocytochemical assay.

The patients diagnosed with pancreatic cancer have the possibilities of getting the cancer again even after resection. The tumor cells identified from blood can be related to different stages of tumor. In this study, we used an immunoassay to detect circulating tumor cells in blood and bone marrow samples. About 120 patients' blood and bone marrow samples were used in this study along with controls. The presence of tumor cells was evaluated with different stages of cancer classified by UICC. The survival rate at each stages of tumor was also analyzed. The tumor cells were isolated both in blood (29%) and bone marrow samples (25%). The prevalence of tumor cells increased with increase in stages of tumor in blood samples. The survival of the patients considerably related to different stages of tumor but it cannot be taken a parameter alone for the patients' survival.

КОРЕКЦІЯ ДИСБІОЗУ КИШЕЧНИКА У ХВОРИХ, ОПЕРОВАНИХ З ПРИВОДУ РАКУ ШЛУНКА

&lt;p&gt;РЕЗЮМЕ. У роботі представлені результати зміни показників кишкової мікрофлори товстої кишки на різних стадіях пухлинного процесу до та після лікування. Особливо важливі вчасне розпізнання та терапія кишкового кандидозу, як профілактика системного та генералізованого кандидозу у пацієнтів із груп ризику, до яких насамперед належать пацієнти, які отримують протипухлинну променеву та/або хіміотерапію. Після лікування у хворих на рак шлунка спостерігали зменшення дисбіозу товстої кишки, а також зменшення кишкового кандидозу, що дозволяє поліпшити якість життя пацієнтів.&lt;/p&gt;

Circulating tumor cells for precision medicine in cancer

Over the last two decades, we have seen many advances in the biological underpinnings of many kinds of cancers that have had a significant impact either directly or indirectly on the management and ultimately on the prognostic outcome of this disease. Next-generation sequencing studies have provided further evidence to support the notion4 that cancer is a disease characterized by Darwinian evolution. However, Ones often fail to obtain the information in different stages of the tumor before making treatment decision. This may be the major reason for treatment failures. Currently, circulating tumor cells (CTCs) is considered as aliquid biopsy. By detecting CTCs at different stages of tumor and obtaining the biological characteristics of CTCs, ones can get information about tumor evolution at different stages. It might provide effective basis for individual therapy to tumors, and promote the accuracy of tumor treatment. Key words: Neoplasm circulating cells; Neoplasms/TH; Review