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Diagnostics
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Novel Biomarkers in Human Malignancies: Diagnostic, Prognostic and Predictive Values
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Novel Biomarkers in Human Malignancies: Diagnostic, Prognostic and Predictive Values

A special issue of Diagnostics (ISSN 2075-4418). This special issue belongs to the section "Pathology and Molecular Diagnostics".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 8860

Special Issue Editors

Dr. Ramziya Kiyamova

E-Mail Website
Guest Editor
“Biomarker” Research Laboratory, Institute of Fundamental Biology and Medicine, Kazan Federal University, Kazan, Russia
Interests: cancer biology; cancer biomarkers; molecular markers; ovarian cancer; pancreatic cancer; SEREX; CRISPR/Cas9; targeted-base therapy; chemoresistance; monoclonal antibodies; cancer-specific epitopes; NaPi2b; SLC34A2; structure and topology of membrane proteins; bioinformatics
Prof. Dr. Sergei Boichuk

E-Mail Website
Guest Editor
Department of Pathology, Kazan State Medical University, Kazan, Russia
Interests: cancer, gastrointestinal stromal tumors (GIST); soft tissue sarcomas (STS); targeted-based therapy; resistance; apoptosis; receptor tyrosine kinase inhibitors (RTKi); DNA damage repair (DDR); FGF-signaling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Tumor biomarkers are molecules produced by cancer cells and the tumor microenvironment, or might represent the general response of the host to the malignancy. These markers might be very informative in determining the risk of cancer; they can be also used in cancer diagnosis and classification, exhibit prognostic values and provide insights into prognosis, therefore offering a therapeutic advantage.

Thus, the molecular markers of cancer are receiving a great deal of attention from biologists and molecular oncologists aiming to identify the novel molecular mechanisms of carcinogenesis, achieve early and differential diagnosis of cancer, as well as predict response to therapy and disease prognosis.

Thanks to elegant studies of specific carcinogenic mechanisms and modern omics technologies, more and more molecular markers of cancer are being detected at the genome, transcriptome, and proteome levels, including mutations, circulating small RNAs, promoter methylations, and post-translational modifications of proteins. Biomarkers are found in the bloodstream as circulating tumor cells, free proteins or as new autoantibodies to such proteins, and can also be found in other body fluids and tissues. It is assumed that panels of analyzed biomarkers, but not single markers, will have sufficient sensitivity and specificity for the diagnosis or prognosis of cancer.

The aim of this Special Issue is to present the latest research on the identification and characterization of novel biomarkers of human malignancies. The discovery of new biomarkers will lead to the development of sensitive test systems for the early and differential diagnosis of cancer as well as personalized therapeutic approaches for the treatment of cancer patients.

Dr. Ramziya Kiyamova
Prof. Dr. Sergei Boichuk
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Diagnostics is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

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Published Papers (4 papers)

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Research

16 pages, 2055 KiB  
Article
Molecular Analysis of Biliary Tract Cancers with the Custom 3′ RACE-Based NGS Panel
by Natalia V. Mitiushkina, Vladislav I. Tiurin, Aleksandra A. Anuskina, Natalia A. Bordovskaya, Anna D. Shestakova, Aleksandr S. Martianov, Mikhail G. Bubnov, Anna S. Shishkina, Maria V. Semina, Aleksandr A. Romanko, Ekaterina S. Kuligina and Evgeny N. Imyanitov
Diagnostics 2023, 13(20), 3168; https://doi.org/10.3390/diagnostics13203168 - 10 Oct 2023
Cited by 3 | Viewed by 1833
Abstract
The technique 3’ rapid amplification of cDNA ends (3′ RACE) allows for detection of translocations with unknown gene partners located at the 3′ end of the chimeric transcript. We composed a 3′ RACE-based RNA sequencing panel for the analysis of FGFR1–4 gene rearrangements, [...] Read more.
The technique 3’ rapid amplification of cDNA ends (3′ RACE) allows for detection of translocations with unknown gene partners located at the 3′ end of the chimeric transcript. We composed a 3′ RACE-based RNA sequencing panel for the analysis of FGFR1–4 gene rearrangements, detection of activating mutations located within FGFR1–4, IDH1/2, ERBB2 (HER2), KRAS, NRAS, BRAF, and PIK3CA genes, and measurement of the expression of ERBB2, PD-L1, and FGFR1–4 transcripts. This NGS panel was utilized for the molecular profiling of 168 biliary tract carcinomas (BTCs), including 83 intrahepatic cholangiocarcinomas (iCCAs), 44 extrahepatic cholangiocarcinomas (eCCAs), and 41 gallbladder adenocarcinomas (GBAs). The NGS failure rate was 3/168 (1.8%). iCCAs, but not other categories of BTCs, were characterized by frequent FGFR2 alterations (17/82, 20.7%) and IDH1/2 mutations (23/82, 28%). Other potentially druggable events included ERBB2 amplifications or mutations (7/165, 4.2% of all successfully analyzed BTCs) and BRAF p.V600E mutations (3/165, 1.8%). In addition to NGS, we analyzed microsatellite instability (MSI) using the standard five markers and revealed this event in 3/158 (1.9%) BTCs. There were no instances of ALK, ROS1, RET, and NTRK1–3 gene rearrangements or MET exon 14 skipping mutations. Parallel analysis of 47 iCCA samples with the Illumina TruSight Tumor 170 kit confirmed good performance of our NGS panel. In conclusion, targeted RNA sequencing coupled with the 3′ RACE technology is an efficient tool for the molecular diagnostics of BTCs. Full article
(This article belongs to the Special Issue Novel Biomarkers in Human Malignancies: Diagnostic, Prognostic and Predictive Values)
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16 pages, 3902 KiB  
Article
Establishment and Characterization of Multi-Drug Resistant p53-Negative Osteosarcoma SaOS-2 Subline
by Sergei Boichuk, Firyuza Bikinieva, Elena Valeeva, Pavel Dunaev, Maria Vasileva, Pavel Kopnin, Ekaterina Mikheeva, Tatyana Ivoilova, Ilshat Mustafin and Aigul Galembikova
Diagnostics 2023, 13(16), 2646; https://doi.org/10.3390/diagnostics13162646 - 11 Aug 2023
Cited by 2 | Viewed by 2070
Abstract
Aim: To establish a p53-negative osteosarcoma (OS) SaOS-2 cellular subline exhibiting resistance to specific chemotherapeutic agents, including topoisomerase II inhibitors, taxanes, and vinca alkaloids. Methods: The OS subline exhibiting resistance to the chemotherapeutic agents indicated above was generated by the stepwise treatment of [...] Read more.
Aim: To establish a p53-negative osteosarcoma (OS) SaOS-2 cellular subline exhibiting resistance to specific chemotherapeutic agents, including topoisomerase II inhibitors, taxanes, and vinca alkaloids. Methods: The OS subline exhibiting resistance to the chemotherapeutic agents indicated above was generated by the stepwise treatment of the parental SaOS-2 cell line with increasing concentrations of doxorubicin (Dox) for 5 months. Half-inhibitory concentrations (IC50) for Dox, vinblastine (Vin), and paclitaxel (PTX) were calculated by a colorimetric MTS-based assay. Crystal violet staining was used to assess cellular viability, whereas the proliferation capacities of cancer cells were monitored in real-time by the i-Celligence system. Expression of apoptotic markers (e.g., cleaved PARP and caspase-3), DNA repair proteins (e.g., ATM, DNA-PK, Nbs1, Rad51, MSH2, etc.), and certain ABC transporters (P-glycoprotein, MRP1, ABCG2, etc.) was assessed by western blotting and real-time PCR. Flow cytometry was used to examine the fluorescence intensity of Dox and ABC-transporter substrates (e.g., Calcein AM and CMFDA) and to assess their excretion to define the activity of specific ABC-transporters. To confirm OS resistance to Dox in vivo, xenograft experiments were performed. Results: An OS subline generated by a stepwise treatment of the parental SaOS-2 cell line with increasing concentrations of Dox resulted in an increase in the IC50 for Dox, Vin, and PTX (~6-, 4-, and 30-fold, respectively). The acquisition of chemoresistance in vitro was also evidenced by the lack of apoptotic markers (e.g., cleaved PARP and caspase-3) in resistant OS cells treated with the chemotherapeutic agents indicated above. The development of the multidrug resistance (MDR) phenotype in this OS subline was due to the overexpression of ABCB1 (i.e., P-glycoprotein) and ABCC1 (i.e., multidrug resistance protein-1, MRP-1), which was evidenced on both mRNA and protein levels. Due to increased expression of MDR-related proteins, resistant OS exhibited an excessive efflux of Dox. Moreover, decreased accumulation of calcein AM, a well-known fluorescent substrate for both ABCB1 and ABCC1, was observed for resistant OS cells compared to their parental SaOS-2 cell line. Importantly, tariquidar and cyclosporin, well-known ABC inhibitors, retained the intensity of Dox-induced fluorescence in resistant SAOS-2 cells. Furthermore, in addition to the increased efflux of the chemotherapeutic agents from Dox-resistant OS cells, we found higher expression of several DNA repair proteins (e.g., Rad51 recombinase, Mre11, and Nbs1, activated forms of ATM, DNA-PK, Chk1, and Chk2, etc.), contributing to the chemoresistance due to the excessive DNA repair. Lastly, the in vivo study indicated that Dox has no impact on the SaOS-2 Dox-R xenograft tumor growth in a nude mouse model. Conclusions: An acquired resistance of OS to the chemotherapeutic agents might be due to the several mechanisms undergoing simultaneously on the single-cell level. This reveals the complexity of the mechanisms involved in the secondary resistance of OS to chemotherapies. Full article
(This article belongs to the Special Issue Novel Biomarkers in Human Malignancies: Diagnostic, Prognostic and Predictive Values)
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19 pages, 6651 KiB  
Article
Identification of m7G-Related LncRNA Signature for Predicting Prognosis and Evaluating Tumor Immune Infiltration in Pancreatic Adenocarcinoma
by Jiawei Lu, Pusheng Yang, Lanting Yu, Ni Xie, Ying Wu and Baiwen Li
Diagnostics 2023, 13(10), 1697; https://doi.org/10.3390/diagnostics13101697 - 11 May 2023
Cited by 1 | Viewed by 1954
Abstract
N7-Methylguanosine (m7G) modification holds significant importance in regulating posttranscriptional gene expression in epigenetics. Long non-coding RNAs (lncRNAs) have been demonstrated to play a crucial role in cancer progression. m7G-related lncRNA may be involved in the progression of pancreatic cancer (PC), although the underlying [...] Read more.
N7-Methylguanosine (m7G) modification holds significant importance in regulating posttranscriptional gene expression in epigenetics. Long non-coding RNAs (lncRNAs) have been demonstrated to play a crucial role in cancer progression. m7G-related lncRNA may be involved in the progression of pancreatic cancer (PC), although the underlying mechanism of regulation remains obscure. We obtained RNA sequence transcriptome data and relevant clinical information from the TCGA and GTEx databases. Univariate and multivariate Cox proportional risk analyses were performed to build a twelve-m7G-associated lncRNA risk model with prognostic value. The model was verified using receiver operating characteristic curve analysis and Kaplan–Meier analysis. The expression level of m7G-related lncRNAs in vitro was validated. Knockdown of SNHG8 increased the proliferation and migration of PC cells. Differentially expressed genes between high- and low-risk groups were identified for gene set enrichment analysis, immune infiltration, and potential drug exploration. We conducted an m7G-related lncRNA predictive risk model for PC patients. The model had independent prognostic significance and offered an exact survival prediction. The research provided us with better knowledge of the regulation of tumor-infiltrating lymphocytes in PC. The m7G-related lncRNA risk model may serve as a precise prognostic tool and indicate prospective therapeutic targets for PC patients. Full article
(This article belongs to the Special Issue Novel Biomarkers in Human Malignancies: Diagnostic, Prognostic and Predictive Values)
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18 pages, 4799 KiB  
Article
Comprehensive Analysis of Prognosis and Immune Landscapes Based on Lipid-Metabolism- and Ferroptosis-Associated Signature in Uterine Corpus Endometrial Carcinoma
by Pusheng Yang, Jiawei Lu, Panpan Zhang and Shu Zhang
Diagnostics 2023, 13(5), 870; https://doi.org/10.3390/diagnostics13050870 - 24 Feb 2023
Cited by 3 | Viewed by 2150
Abstract
(1) Background: The effect of tumor immunotherapy is influenced by the immune microenvironment, and it is unclear how lipid metabolism and ferroptosis regulate the immune microenvironment of uterine corpus endometrial carcinoma (UCEC). (2) Methods: Genes associated with lipid metabolism and ferroptosis (LMRGs-FARs) were [...] Read more.
(1) Background: The effect of tumor immunotherapy is influenced by the immune microenvironment, and it is unclear how lipid metabolism and ferroptosis regulate the immune microenvironment of uterine corpus endometrial carcinoma (UCEC). (2) Methods: Genes associated with lipid metabolism and ferroptosis (LMRGs-FARs) were extracted from the MSigDB and FerrDb databases, respectively. Five hundred and forty-four UCEC samples were obtained from the TCGA database. The risk prognostic signature was constructed by consensus clustering, univariate cox, and LASSO analyses. The accuracy of the risk modes was assessed through receiver operating characteristic (ROC) curve, nomogram, calibration,, and C-index analyses. The relationship between the risk signature and immune microenvironment was detected by the ESTIMATE, EPIC, TIMER, xCELL, quan-TIseq, and TCIA databases. The function of a potential gene, PSAT1, was measured by in vitro experiments. (3) Results: A six-gene (CDKN1A, ESR1, PGR, CDKN2A, PSAT1, and RSAD2) risk signature based on MRGs-FARs was constructed and evaluated with high accuracy in UCEC. The signature was identified as an independent prognostic parameter and it divided the samples into high- and low-risk groups. The low-risk group was positively associated with good prognosis, high mutational status, upregulated immune infiltration status, high expression of CTLA4, GZMA and PDCD1, anti-PD-1 treatment sensitivity, and chemoresistance. (4) Conclusions: We constructed a risk prognostic model based on both lipid metabolism and ferroptosis and evaluated the relationship between the risk score and tumor immune microenvironment in UCEC. Our study has provided new ideas and potential targets for UCEC individualized diagnosis and immunotherapy. Full article
(This article belongs to the Special Issue Novel Biomarkers in Human Malignancies: Diagnostic, Prognostic and Predictive Values)
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