ResearchPad - Oncology https://www.researchpad.co Default RSS Feed en-us © 2020 Newgen KnowledgeWorks <![CDATA[Paraneoplastic encephalitis with leukoencephalopathy in primary fallopian tube carcinoma]]> https://www.researchpad.co/product?articleinfo=Nd7171b94-7e20-41a9-8607-2a8e5ab6ece8 <![CDATA[Primary perirenal angiosarcoma: A preoperative diagnostic challenge]]> https://www.researchpad.co/product?articleinfo=N374636c1-be81-4ea8-8de5-28836dd78124 <![CDATA[ACAT2 Promotes Cell Proliferation and Associates with Malignant Progression in Colorectal Cancer]]> https://www.researchpad.co/product?articleinfo=Nd0c065e5-85fa-40b2-a9c5-f323541897cd

Background and Aims

Colorectal cancer (CRC) is a major disease that threatens human health. It has been reported that the acyl-coenzyme A (CoA): cholesterol acyltransferase 2 (ACAT2) gene can promote the progression of hepatocellular carcinoma, but its function in CRC is still unclear. In this study, we aimed to elucidate the function of ACAT2 in CRC.

Methods

Western blot and qPCR were used to detect the relative level of ACAT2 in CRC tissue and adjacent non-cancerous tissues, and then the association between ACAT2 expression and the clinicopathological features and survival of CRC patients were assessed. The expression of ACAT2 in CT26 and DLD1 cells was down-regulated by siRNA, and the effects of ACAT2 knockdown on cell proliferation were examined. The inhibitory effects of ACAT2 knockdown were further confirmed by tumor growth assays in vivo.

Results

Our data showed that the expression of ACAT2 in CRC tissues was markedly higher than in adjacent non-cancerous tissues. The high expression of ACAT2 was significantly associated with tumor size, lymph node metastasis and clinical stage. The increased expression of ACAT2 was also significantly associated with worse 5-year overall survival of CRC patients. siRNA-mediated ACAT2 knockdown strongly inhibited CT26 and DLD1 cells proliferation and induced G0/G1 phase cell cycle arrest and apoptosis in these cells. Knockdown of ACAT2 expression suppressed the growth of CRC and inhibited the expression of Ki67 in vivo.

Conclusion

Our study demonstrated that ACAT2 played a positive role in regulating the proliferation of CRC and may be useful as a potential biomarker and therapeutic target for this disease.

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<![CDATA[Evaluation of Concordance Between Deficient Mismatch Repair and Microsatellite Instability Testing and Their Association with Clinicopathological Features in Colorectal Cancer]]> https://www.researchpad.co/product?articleinfo=Na0d6574b-f661-4fe8-9af1-63f1bbea8800

Background

Microsatellite instability (MSI) is one of the most important molecular characteristics of colorectal cancer (CRC), which mainly results from defective DNA mismatch repair (MMR). This study was performed to investigate the concordance between deficient MMR and MSI testing, and to evaluate the association of these two results with clinicopathological characteristics in Chinese CRC patients.

Methods

A total of 738 CRC patients were included. Tumor tissues and paired peripheral blood specimens were obtained. Screening for MMR was investigated using immunohistochemical (IHC) technique, and multiple polymerase chain reaction-capillary electrophoresis (PCR-CE) method was performed to detect the MSI status. All clinicopathological data, immunohistochemistry and microsatellite instability analyses were then statistically analyzed.

Results

Of the 738 (17.75%) CRC patients, 131 expressed as deficient mismatch repair (dMMR) status, and postmeiotic segregation increased 2 (PMS2) deficiency was the most frequent deficiency among these four MMR proteins. MSI-high (MSI-H) status occurred in 74 of the 738 (10.03%) CRC patients, 55 of whom showed instability at all six mononucleotides repeat markers. dMMR was significantly associated with MSI-H and moderate concordance was observed between IHC and PCR-CE in evaluating deficient MMR/MSI through Kappa test. Statistically, dMMR was significantly associated with younger age, right-sided colon and poor differentiation. MSI-H was associated with younger age, right-sided colon, poor differentiation, mucinous type and tumor, node, metastasis (TNM) stage II.

Conclusion

A moderate concordance between deficient MMR and MSI testing indicates that both IHC and PCR-CE methods should be routinely tested to provide reliable data for clinical treatment decisions.

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<![CDATA[Mitofusin1 Is a Major Mediator in Glucose-Induced Epithelial-to-Mesenchymal Transition in Lung Adenocarcinoma Cells]]> https://www.researchpad.co/product?articleinfo=N740baced-cc25-4460-acf8-d6e46745ed29

Background

Epithelial-to-mesenchymal transition (EMT) has been considered a latent mediator of diverse biological processes in cancer. However, the mechanisms involved in high glucose-associated EMT in lung adenocarcinoma (LAD) have not been fully clarified. In this study, we aimed to investigate whether mitofusin1 (MFN1) is involved in the EMT of LAD cells induced by glucose and to identify the molecular mechanism involved in this process.

Materials and Methods

The expression of specific proteins was analysed by Western blotting, immunohistochemistry, co-immunoprecipitation and immunofluorescence analysis. The proliferation, migration and invasion of cells were assessed by Cell Counting Kit-8, bromodeoxyuridine incorporation, wound-healing and transwell assays. Lung tissues of adjacent normal regions and lung tissues from patients with LAD and LAD combined with diabetes mellitus were collected to determine the expression and significance of MFN1.

Results

Here, we showed that the expression of MFN1 was increased in LAD tissues compared with adjacent normal tissues and expression was even higher in lung tissues from patients with LAD combined with diabetes. In the lung cancer cell line A549, increased cell proliferation, invasion and EMT induced by high glucose were inhibited by MFN1 silencing. Mechanistic studies demonstrated that inhibiting autophagy reversed the abnormal EMT triggered by high glucose conditions. In addition, our data provide novel evidence demonstrating that PTEN-induced kinase (Pink) is a potential regulator involved in MFN1-mediated cell autophagy, which eventually leads to high glucose-induced proliferation, invasion and EMT of A549 cells.

Conclusion

Taken together, our data show that MFN1 interacts with Pink to induce the autophagic process and that the abnormal occurrence of autophagy ultimately contributes to glucose-induced pathological EMT in LAD.

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<![CDATA[Clinical Analysis and Prognostic Significance of Hepatitis B Virus Infections with Diffuse Large B-Cell Lymphoma]]> https://www.researchpad.co/product?articleinfo=Nef0eeb94-7b70-4011-ba39-68bae17d80eb

Background

China is a high endemic area for the hepatitis B virus (HBV). The studies established the epidemiology between HBV and diffuse large B-cell lymphoma (DLBCL), but further research is necessary to clarify the potential link between HBV and DLBCL.

Patients and Methods

A total of 319 patients diagnosed with DLBCL were recruited as cases at First Medical Centre of Chinese PLA General Hospital from September 2010 to December 2018. During the same time, two age- and sex-matched controls were selected for each case, and the control groups comprised of 319 patients with non-hematological malignancy and 319 subjects with non-malignant conditions. Relative risk of developing DLBCL among individuals tested positive for hepatitis B surface antigen was calculated. After that, we retrospectively analyzed clinical data from DLBCL patients with different HBV infection statuses.

Results

The HBV infection rate of patients with DLBCL (11.60%) was significantly higher than the other two control groups (5.02% and 4.08%), indicating the risk of DLBCL may increased in HBV infections. Meanwhile, this study demonstrated an independent association between HBV infection and poorer clinical outcomes.

Conclusion

Our study demonstrated that HBV infection may play an important role in the pathogenesis of DLBCL and show poor outcomes in HBV-endemic China.

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<![CDATA[Glycyrrhizic Acid Inhibits Proliferation of Gastric Cancer Cells by Inducing Cell Cycle Arrest and Apoptosis]]> https://www.researchpad.co/product?articleinfo=N3ce0f3fa-53ce-4509-946e-6e239fd5c49a

Purpose

Glycyrrhizic acid (GA) is the main active ingredient extracted from Chinese herb licorice root, and it shows anti-tumor effects in many cancer types, while its role in gastric cancer (GC) is still unknown. In this study, we evaluated the effects of GA on GC cells and explored the underlying mechanisms.

Methods

The anti-proliferation effect of GA on GC cells was assessed by CCK-8, colony formation, and EdU assay. The effects of GA on cell cycle and apoptosis were detected by flow cytometer. Western blotting was performed to explore the underlying mechanisms.

Results

Our results showed that GA had a time- and dose-dependent inhibitory effect on proliferation of GC cells. Flow cytometer analysis demonstrated that GA would lead to G1/S-phase arrest and apoptosis. GA treatment down-regulated the levels of G1 phase-related proteins, including cyclin D1, D2, D3, E1, and E2. In terms of apoptosis, GA treatment up-regulated the levels of Bax, cleaved PARP, and pro-caspase-3, -8, -9, but did not influence their cleavage patterns. The expression of Bcl-2, survivin and p65 was attenuated after treatment. Besides, GA would down-regulate the phosphorylation of PI3K/AKT pathway.

Conclusion

This study focused on inhibitory effect of GA on GC cells by inducing cell cycle arrest and apoptosis. Several important cyclins- and apoptosis-related proteins were involved in the regulation of GA to GC cells, and phosphorylated PI3K and AKT were attenuated. The results of this study indicated that GA is a potential and promising anti-cancer drug for GC.

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<![CDATA[Dihydroartemisinin Prevents Progression and Metastasis of Head and Neck Squamous Cell Carcinoma by Inhibiting Polarization of Macrophages in Tumor Microenvironment]]> https://www.researchpad.co/product?articleinfo=N2711109f-0f80-479f-aff7-72b2658f3ed0

Background

Polarized M2 macrophages are an important type of tumor-associated macrophage (TAM), with roles in the growth, invasion, and migration of cancer cells in the tumor microenvironment. Dihydroartemisinin (DHA), a traditional Chinese medicine extract, has been shown to inhibit the progression and metastasis of head and neck squamous cell carcinoma (HNSCC); however, the effect of DHA on cancer prevention, and the associated mechanism, has not been investigated in the tumor microenvironment.

Materials and Methods

First, human Thp-1 monocytes were induced and differentiated into M2 macrophages using phorbol 12-myristate 13-acetate (PMA), interleukin-6 (IL-6), and interleukin-4 (IL-4). Induction success was confirmed by cell morphology evaluation, flow cytometry, and quantitative real-time polymerase chain reaction (qRT-PCR). Then, DHA was applied to interfere with M2 macrophage polarization, and conditioned medium (CM), including conditioned medium from M2 macrophages (M2-CM) and conditioned medium from M2 macrophages with DHA (M2-DHA-CM), was obtained. CM was applied to Fadu or Cal-27 cells, and its effects on cancer invasion, migration, and angiogenesis were evaluated using transwell, wound-healing, and tube formation assays, respectively. Finally, Western blotting was used to evaluate the relationship between signal transducer and activator of transcription 3 (STAT3) signaling pathway activation and M2 macrophage polarization.

Results

Human Thp-1 monocytes were successfully polarized into M2-like TAMs using PMA, IL-6, and IL-4. We found that M2-like TAMs promoted the invasion, migration, and angiogenesis of HNSCC cells; however, DHA significantly inhibited IL-4/IL-6-induced M2 macrophage polarization. Additionally, as DHA induced a decrease in the number of M2-like TAMs, M2-DHA-CM inhibited the induction of invasion, migration, and angiogenesis of Fadu and Cal-27 cells. Finally, DHA inhibited M2 macrophage polarization by blocking STAT3 pathway activation in macrophages.

Conclusion

DHA inhibits the invasion, migration, and angiogenesis of HNSCC by preventing M2 macrophage polarization via blocking STAT3 phosphorylation.

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<![CDATA[An Oncolytic Vaccinia Virus Armed with GM-CSF and IL-24 Double Genes for Cancer Targeted Therapy]]> https://www.researchpad.co/product?articleinfo=Nb48b35f5-1f83-4ab9-9c0f-23e96a7d6974

Purpose

Targeted oncolytic vaccinia virus is an attractive candidate for cancer therapy due to its replication causing lysis of infected tumor cells as well as a delivery vector to overexpress therapeutic transgenes. This study constructed a novel oncolytic vaccinia virus carrying granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-24 (IL-24) double genes to improve efficacy for cancer therapy.

Methods

Vaccinia virus co-expressing GM-CSF and IL-24 based on Chinese Guang9 strain (VG9-GMCSF-IL24) was constructed with disruption of the viral thymidine kinase (TK) gene. The cytotoxicity of VG9-GMCSF-IL24 in various cell lines was assessed by MTT. The synergistic antitumor effect of VG9-GMCSF-IL24 in vivo was assessed on multiple tumor models.

Results

In vitro cytotoxicity assay showed that VG9-GMCSF-IL24 exerted a strongly cytotoxic effect on cancer cells, but with no significant cytotoxicity to normal cells. Significant tumor growth inhibition and prolonged survival were observed in different tumor models treated with VG9-GMCSF-IL24. Additionally, systemic and specific antitumoral immunity was investigated in vivo, and enhanced antitumor immunity was observed in VG9-GMCSF-IL24-treated mice.

Conclusion

Our results indicated that VG9-mediated GM-CSF and IL-24 co-expression performed cooperative and overlapping antitumor effect. As a novel and effective therapeutic strategy for cancer, the combination of oncolysis and immunotherapy with vaccinia virus carrying one or more immunostimulatory genes may have a satisfactory clinical application prospect.

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<![CDATA[Biliverdin Reductase A (BLVRA) Promotes Colorectal Cancer Cell Progression by Activating the Wnt/β-Catenin Signaling Pathway]]> https://www.researchpad.co/product?articleinfo=N6e07a1dd-b61d-4a81-b427-1482aede88a1

Purpose

Biliverdin reductase A (BLVRA) is a pleiotropic enzyme that converts biliverdin-IX-alpha into the antioxidant and anti-nitrosative compound, bilirubin-IX-alpha. It is related to various diseases, including cancer. It is overexpressed in many types of cancers and promotes cancer development and metastasis, but the effects of BLVRA in colorectal cancer have not been researched at present. This study was aimed to investigate the effects of biliverdin reductase A (BLVRA) in vivo and vitro experiments and its possible mechanism.

Methods

The clinical samples of CRC patients and CRC cell lines HT-29 and SW620 were chosen to perform the experiments. ELISA and Immunohistochemistry (IHC) were applied to test the level of BLVRA in patients. HT-29 knockdown of BLVRA and SW620 overexpression of BLVRA was established by the lentiviral vector transfection. Reverse transcription-quantitative real-time polymerase chain reaction and Western blotting were performed to examine the expression of BLVRA. MTT was used to detect the proliferation of CRC cells. Flow cytometry was applied to assess the rate of apoptosis. Transwell assay was performed to examine the capacity of migration and invasion. Immunofluorescence staining was adopted to assess the expression of E-cadherin and vimentin. Western blotting was utilized to detect the expression of apoptosis-related proteins, EMT-related proteins and target proteins of Wnt/β-catenin signaling pathway.

Results

Analysis of the clinical samples revealed that BLVRA was overexpressed in CRC patients and implied poor prognosis. BLVRA overexpression in the in vitro studies revealed that it increased the potential of CRC cells for proliferation, migration and invasion; augmented EMT; and hindered apoptosis. In addition, BLVRA overexpression was found to upregulate positive target genes and downregulate negative target genes of the Wnt/β-catenin signaling pathway, which implied that the biological effects of BLVRA in CRC were mediated by this pathway. In contrast, knockdown of BLVRA manifested the opposite effects.

Conclusion

Our results suggested that BLVRA might be a promising prognostic marker and a potential therapeutic target in CRC.

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<![CDATA[The Synchronous Presence of Multiple Myelomas and Other Primary Malignant Tumors: Case Series with Literature Review]]> https://www.researchpad.co/product?articleinfo=N0854b78e-8482-4735-8d15-99e460aea262

Objective

The synchronous presence of multiple myeloma (MM) and other primary malignant tumors (PMTs) were rarely reported. This study aimed to analyze several cases of MM and other PMTs in order to improve clinicians’ understanding of multiple myeloma (MM) with sMPMTs.

Methods

This study was a retrospective trial. We retrospectively analyzed six cases of the synchronous presence of MM and other PMTs and reviewed the literature to summarize the clinical features and treatment.

Results

The results showed that five cases of immunoglobulin G (IgG) and one case of kappa light chain; D-S stage: six case of stage III; ISS stage: one case of stage I, two cases of stage II, and three cases of stage III; one case each of gastric cancer (pT2N0MO, stage I), breast cancer (pT1bN0M0, stage I), lung cancer (pT1N0M0, stage I), cervical cancer (stage IB2), thyroid cancer (pT1N0M0, stage I), and diffuse large B-cell lymphoma (Ann-Arbor stage II); three of five patients underwent surgery alone, one patient underwent surgery first and then received chemotherapy at the time of pleural metastasis and the other patient only received radiotherapy; two patients were still alive, three died of progression of MM, and one died of lung cancer. The median survival time was 33.5 months (95% CI, 14.17 to 59.5months).

Conclusion

The relationship between synchronous MM and other PMTs remains unknown. Clinicians should improve their understanding of MM with sMPMTs by carrying out multidisciplinary collaboration and a patient-oriented approach to optimize treatment and prolong the survival rates of patients.

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<![CDATA[ATF3 Demethylation Promotes the Transcription of ARL4C, Which Acts as a Tumor Suppressor in Human Breast Cancer]]> https://www.researchpad.co/product?articleinfo=Ncb66c365-b2c3-4781-a0c7-b342816abb03

Introduction

Breast cancer is a common malignancy in females worldwide. In this study, we investigated the role of activating transcription factor 3 (ATF3) and ADP-ribosylation factor like-4 (ARL4) in human breast cancer, and the associated mechanisms.

Materials and Methods

We measured ATF3 and ATL4C expressions in 15 paired breast cancer tissues using qRT-PCR, Western blotting and IHC. Cell growth, migration and invasion were tested in ATF3 or ARL4C overexpression breast cancer cells. TCGA database analysis was done to identify the correlation between ATF3 and ARL4C. We evaluated the binding of ATF3 to ARL4C promoter sequences and the effect of hypermethylation and demethylation of ATF3. A meta-analysis was done to investigate the relationship between the expression of ATF3 and/or ARL4C and the poor prognoses.

Results

Our results showed that ATF3 and ARL4C were decreased in breast cancer specimens at both mRNA and protein levels. Restoration of ATF3 or ARL4C reduced breast cancer tumorigenesis, evidenced by decreased cell growth, migration and invasion. The expression of ATF3 was positively correlated with ARL4C in breast cancer specimens, and ATF3 was shown to bind to the ARL4C promoter sequences. Furthermore, the expression of ATF3 was negatively regulated by hypermethylation, and demethylation of ATF3 stimulated ATF3 expression, which further promoted ARL4C transcription. Finally, a meta-analysis showed that patients with breast cancer with lower expression levels of ATF3 and/or ARL4C had worse prognoses.

Conclusion

Our results suggest that the ATF3/ARL4C axis may be a prospective biomarker for diagnosis and determination of prognosis, and a potential target for breast cancer treatment.

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<![CDATA[Comparative Diagnostic Evaluation with Contrast-Enhanced Ultrasound, Computed Tomography and Magnetic Resonance Imaging in Patients with Pancreatic Cystic Neoplasms]]> https://www.researchpad.co/product?articleinfo=Na8f5ebe5-5af5-44ce-8b39-b27d8c3e6c5f

Purpose

The purpose of our study was to evaluate the role of contrast-enhanced ultrasound (CEUS) with magnetic resonance imaging (MRI) and computed tomography (CT) in the pathological diagnosis of pancreatic cystic neoplasms (PCNs).

Methods

A total of 90 patients (66 women, 24 men) aged 18–71 years were studied prospectively. CEUS was performed in all patients, whereas MRI was performed in 85 patients and CT in 69 patients. We analyzed the sensitivity and accuracy of these three imaging modalities to diagnose the PCNs. Neoplasm size, location, shape, intralesional mural nodules, septa and duct dilatation were also assessed by different radiologists.

Results

There were no significant differences in sensitivity for discriminating PCNs from pancreatic cystic lesions between CEUS and MRI (p=0.614) or between CEUS and CT (p=0.479). The diagnostic accuracy of CEUS for classifying PCNs was 64.4% (58/90), which was higher than that of CT (53.6%, 37/69, P=0.017), and lower than that of MRI (70.6%, 60/85, p=0.791). Regarding tumor size for lesions larger than 3 cm, CEUS was superior to CT in differentiating the specific type of PCN (p=0.041), and CEUS had the same value as MRI (p=0.774). Furthermore, CEUS is valuable for precisely characterizing internal structures, for instance, septa (p=0.003, compared with CT; p=0.443, compared with MRI) and nodules (p= 0.018, compared with CT; p=0.033, compared with MRI). The number of septa (p=0.033) and cyst morphology (p=0.016) were meaningful indicators in differentiating serous and mucinous adenoma. There was no significant difference in evaluating size and detecting duct dilatation among the three imaging methods.

Conclusion

CEUS compares favorably with MRI in displaying the inner structure of PCNs and offers advantages over CT. CEUS can contribute in an important way to the diagnosis of pancreatic cystic neoplasms.

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<![CDATA[Long Non-Coding RNA UCA1 Modulates Paclitaxel Resistance in Breast Cancer via miR-613/CDK12 Axis]]> https://www.researchpad.co/product?articleinfo=N33862d24-803f-4348-90d4-0fa190abaed8

Background

Paclitaxel (PTX) occupies a considerable status in the chemotherapies of breast cancer (BC), but the drug resistance keeps an obstructive factor of PTX treatment. This study was designed to explore the molecular mechanism of long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) in PTX resistance of BC.

Methods

UCA1, microRNA-613 (miR-613) and cyclin-dependent kinase 12 (CDK12) expression was assayed through quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit-8 (CCK-8) assay was implemented for evaluating the half inhibitory concentrations (IC50) of PTX and cell viability. Cell apoptosis was examined by flow cytometry. The target relationship was explored using dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. CDK12 protein level was detected through Western blot. Xenograft tumor assay was applied for assessing the influence of UCA1 on PTX resistance of BC in vivo.

Results

UCA1 expressed highly in PTX-resistant BC tissues and cells and regulated PTX resistance in BC cells by affecting cell viability and apoptosis in part. UCA1 negatively interacted with miR-613 and modulated PTX resistance via sponging miR-613. CDK12 was a downstream gene of miR-613 and miR-613 exerted the modulation of PTX resistance via targeting CDK12. Furthermore, UCA1 regulated CDK12 level through interacting with miR-613. The regulatory role of UCA1 in PTX resistance of BC was achieved by miR-613/CDK12 axis in vivo.

Conclusion

UCA1 mediated PTX resistance in BC through the miR-613/CDK12 axis, manifesting that UCA1 might improve the PTX treatment of BC as a significant therapeutic biomarker.

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<![CDATA[Phosphoproteomics Reveals Key Regulatory Kinases and Modulated Pathways Associated with Ovarian Cancer Tumors]]> https://www.researchpad.co/product?articleinfo=N6e54be71-efea-4456-a8e5-42ce660ba5f7

Background

Ovarian cancer (OC) is the seventh most common cancer worldwide for women. However, there are no sufficient diagnostic methods and few treatment options available due to poor understanding of its pathogenic mechanisms.

Methods

To comprehensively analyze the phosphoproteomic characterization for OC, we took advantage of a quantitative global phosphoproteomics method, titanium(IV) immobilized metal affinity chromatography (Ti4+-IMAC) coupled to nanoscale liquid chromatography and quadrupole time-of-flight tandem mass spectrometry (nanoLC/Q-TOF-MS/MS) on ovarian tissue samples obtained from five OC patients and five matched controls.

Results

A total of 722 phosphorylated sites corresponding to 534 proteins were significantly different (fold change ≥ 2, p < 0.01) between OC patients and the controls. Among them, 83 transcription factors mainly consisted of transcription cofactors, zf-C2H2, and chromatin remodeling factors and 29 kinases were included. Further functional analysis suggested significantly biological processes were highly enriched and involved in the pathogenesis of OC, especially fructose and mannose metabolism. Moreover, the regulatory roles of modulated pathways, including MAPK, ErbB, and GnRH signaling pathways were also identified as critical processes involved in OC. The results here highlighted key phosphorylated proteins, particularly kinases, and the corresponding cancer-related metabolic and signal pathways that played important roles in the development of OC. Additionally, the expression levels of two kinases, phosphorylated CDK (T14) and phosphorylated PRKCQ (S695), were validated by Western blot analysis in the other group of ovarian tissue samples.

Conclusion

Altogether, our data not only provided novel insights into the potential biomarkers and therapy options for OC but also extended our knowledge on its pathophysiological mechanism.

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<![CDATA[BCL-2 Expression in Primary Cutaneous Follicle Center B-Cell Lymphoma and Its Prognostic Role]]> https://www.researchpad.co/product?articleinfo=N236ab245-63f1-4604-b065-07209ab42a09 ]]> <![CDATA[Emerging Role of Mucolipins TRPML Channels in Cancer]]> https://www.researchpad.co/product?articleinfo=Ncb5d899f-7097-4425-9744-a259b14060b2 ]]> <![CDATA[Corrigendum: Targeting JUN, CEBPB, and HDAC3: A Novel Strategy to Overcome Drug Resistance in Hypoxic Glioblastoma]]> https://www.researchpad.co/product?articleinfo=N18a7c102-5101-4616-9186-a6a4da47f835 ]]> <![CDATA[Unusual Chemotherapeutic Resistant Testicular Embryonal Germ Cell Tumor with Widespread Metastasis in a Case of Klinefelter Syndrome: A Case Report]]> https://www.researchpad.co/product?articleinfo=N6cacab52-b5eb-4c1d-9153-78b1d096414c

Cryptorchidism is an undeniable risk factor for testicular germ cell tumors (TGCTs) and is also commonly associated with Klinefelter syndrome (KS) patients. Embryonal cell carcinoma usually shows strong expression of CD30 and OCT3/4, with patchy staining of PLAP1. Most patients with nonseminomatous GCTs (NSGCTs) can achieve total remission with proactive chemotherapy, and most can be cured. We present an extremely rare case of a testicular embryonal germ cell tumor that is atypical in its gene expression and response to chemotherapy treatment.

A 71-year-old male patient presented in July 2019 with abdominal pain of unknown duration, weight loss for one year, and recent history of altered bowel habits. His past medical history is significant for KS and congenital unilateral cryptorchidism. Physical examination yielded mild abdominal distention and bilateral inguinal lymphadenopathy. Imaging revealed a posterior mediastinal mass and large retroperitoneal masses. The above features, in addition to the history of KS and unilateral cryptorchidism, were highly suggestive of a testicular retroperitoneal germ cell tumor. Serologic studies revealed elevated lactate dehydrogenase (LDH) while other tumor markers were normal. Excisional biopsy of inguinal lymph nodes revealed poorly differentiated embryonal cell carcinoma with strong expression of SALL4, a rare expression of OCT 3/4, and the absence of expression of CD30 and placental alkaline phosphatase (PLAP). The patient was given four cycles of bleomycin, etoposide and platinum (BEP) chemotherapy, as is the standard chemotherapy regimen for these tumors, without any significant change in the size of the masses or lymph nodes.

Unfortunately, there are no specific guidelines when it comes to the management of KS patients with testicular GCTs (embryonal cell carcinoma) with aberrant histological markers and normal serum tumor markers. These findings in combination with chemotherapeutic resistance indicate a need for more specific treatment modalities and follow-up for unusual testicular embryonal GCTs in KS patients.

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<![CDATA[LabBM Score and Extracranial Score As New Tools for Predicting Survival in Patients with Brain Metastases Treated with Focal Radiotherapy]]> https://www.researchpad.co/product?articleinfo=N4bb910af-261d-42ca-8a99-ebe0e7e39fff

Background

Two recently validated, untraditional prognostic scores include serum albumin and lactate dehydrogenase, among other parameters. The latter are hemoglobin, platelet counts, and C-reactive protein (three-tiered LabBM score), whereas the four-tiered extracranial score includes more than one extracranial site of metastatic involvement. Until now, head-to-head comparisons of these two scores in patients treated with focal radiotherapy for newly diagnosed brain metastases are not available.

Methods

This was a retrospective single-institution analysis of 51 patients, most of whom were managed with first-line stereotactic radiosurgery (SRS). Survival was stratified by the LabBM score and extracranial score.

Results

Both scores predicted survival, but the analyses were hampered by small subgroups. In particular, very few patients belonged to the unfavorable groups. Survival shorter than two months, which was recorded in 14%, was not well predicted by the LabBM score and extracranial score.

Conclusions

Very few patients treated with focal radiotherapy (largely SRS) had unfavorable prognostic features according to the two untraditional scores, which do not include the number of brain metastases and performance status. Additional research is needed to improve the tools that predict short survival because overtreatment during the terminal phase of metastatic disease continues to represent a relevant issue.

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