Molecular and clinical oncology最新文献

{"title":"New advances in circulating tumor cell‑mediated metastasis of breast cancer (Review).","authors":"Jiang-Shan Zhou,&nbsp;Zi-Ning Liu,&nbsp;Yuan-Yuan Chen,&nbsp;Yu-Xi Liu,&nbsp;Hua Shen,&nbsp;Li-Jun Hou,&nbsp;Yi Ding","doi":"10.3892/mco.2023.2667","DOIUrl":"https://doi.org/10.3892/mco.2023.2667","url":null,"abstract":"<p><p>Breast cancer stands as the most prevalent form of cancer affecting women, with metastasis serving as a leading cause of mortality among patients with breast cancer. Gaining a comprehensive understanding of the metastatic mechanism in breast cancer is essential for early detection and precision treatment of the disease. Circulating tumor cells (CTCs) play a vital role in this context, representing cancer cells that detach from tumor tissues and enter the bloodstream of cancer patients. These cells travel in the blood circulation as single cells or clusters. Recent research has shed light on the enhanced metastatic potential of CTC clusters compared to single CTCs, despite their limited occurrence. The aim of the present review was to explore recent findings on CTCs with a particular focus on the clustering phenomenon of CTCs observed in breast cancer. Additionally, the present review delved into the comparison between single CTCs and CTC clusters regarding their implications for the treatment and prognosis of patients diagnosed with metastatic breast cancer. By examining the role and mechanisms of CTCs in breast cancer metastasis, the present review provided an improved understanding of CTCs and their significance in early detection of breast cancer metastasis through peripheral blood analysis. Moreover, it contributed to the comprehension of cancer prognosis and prediction by highlighting the implications of CTCs in these aspects. Ultimately, the present study seeks to advance knowledge in the field and pave the way for improved approaches to breast cancer management.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"19 3","pages":"71"},"PeriodicalIF":1.2,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/41/67/mco-19-03-02667.PMC10442766.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10065855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sequential autologous and allogeneic stem cell transplantation for treatment of primary plasma cell leukemia: A case report.","authors":"Weijia Fu,&nbsp;Aijie Huang,&nbsp;Yanrong Luo,&nbsp;Miaomiao Liu,&nbsp;Gusheng Tang,&nbsp;Jianmin Yang,&nbsp;Xiong Ni","doi":"10.3892/mco.2023.2671","DOIUrl":"https://doi.org/10.3892/mco.2023.2671","url":null,"abstract":"<p><p>Primary plasma cell leukemia (pPCL) is a rare and aggressive form of plasma cell disorder, which accounts for ~70% of all PCL. Survival of pPCL remains poor, and is related with early mortality. There is no standard therapy for patients with pPCL. In the present study, a 26-year-old man who was diagnosed with pPCL was reported. The patient achieved stringent complete remission to the successful treatment of intensive chemotherapy combined with sequential autologous and allogeneic stem cell transplantation (SCT) followed by maintenance therapy with oral administration of ixazomib, thalidomide and dexamethasone (IRD regimen). Development of complex treatment algorithms that combine novel agents, SCT and post-transplantation remission strategies may translate into survival in patients with pPCL.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"19 3","pages":"75"},"PeriodicalIF":1.2,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ee/37/mco-19-03-02671.PMC10442742.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10065856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current status and prospects of GREM1 research in cancer (Review).","authors":"Dantong Zhu,&nbsp;Dong Zhao,&nbsp;Naixue Wang,&nbsp;Fei Cai,&nbsp;Mingzhe Jiang,&nbsp;Zhendong Zheng","doi":"10.3892/mco.2023.2665","DOIUrl":"https://doi.org/10.3892/mco.2023.2665","url":null,"abstract":"<p><p>GREM1 is a secreted protein that antagonizes bone morphogenetic proteins (BMPs) and participates in critical biological processes, including embryonic development, organogenesis and tissue differentiation. Gremlin 1 (GREM1) is also an inhibitor of TGF-β and a ligand for vascular endothelial growth factor receptor 2. In addition, GREM1 can induce cells, participate in the process of epithelial-mesenchymal transition, and then participate in tumor development. GREM1 has a variety of biological functions and can participate in the malignant progression of a variety of tumors through the BMP signaling pathway. GREM1 also can inhibit TGF-β in some tumors, thereby inhibiting tumors, and its involvement in tumor development varies in different types of cancer. The present review examines the role and function of GREM1 in tumors. GREM1 is expressed in a variety of tumor types. GREM1 expression can affect the epithelial-mesenchymal transformation of tumor cells. GREM1 has been studied in breast and colon cancer, and its potential role is to promote cancer. However, in pancreatic cancer, which was found to act differently from other cancer types, overexpression of GREM1 inhibits tumor metastasis. The present review suggests that GREM1 can be a diagnostic and prognostic indicator. In future studies, the study of GREM1 based on single-cell sequencing technology will further clarify its role and function in tumors.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"19 3","pages":"69"},"PeriodicalIF":1.2,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/50/5a/mco-19-03-02665.PMC10442762.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10065853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic analysis of fundic gland‑type gastric adenocarcinoma.","authors":"Lei Liu,&nbsp;Xuedong Zhang,&nbsp;Xue Fan,&nbsp;Xiaoyun Zhu","doi":"10.3892/mco.2023.2678","DOIUrl":"https://doi.org/10.3892/mco.2023.2678","url":null,"abstract":"<p><p>This study aimed to analyze the molecular characteristics of gastric adenocarcinoma of the fundic-gland type (GAFG) and explore the possible mechanism of tumor development. Samples from 10 Chinese patients with GAFG were collected at the Peking University International Hospital and Liaocheng People's Hospital between January 2015 and March 2022. The nucleic acid sequence of Epstein Barr virus-encoded RNA (EBV-EBER) was detected by <i>in situ</i> hybridization. Genetic mutation information for <i>GNAS</i>, <i>KRAS</i>, <i>NRAS</i>, <i>BRAF</i>, <i>PIK3CA</i>, <i>TP53</i>, <i>APC</i>, <i>CTNNB1</i>, <i>HER2</i>, <i>MLH1</i>, <i>MSH2</i>, <i>MSH6</i>, and <i>PMS2</i> was obtained by Next-Generation Sequencing, and the relevant literature was reviewed. A total of eight instances of missense mutations were detected, consisting of seven cases with <i>GNAS</i> mutations, two cases with <i>KRAS</i> mutations, and one case with a <i>TP53</i> mutation. Additionally, two patients had simultaneous missense mutations in <i>GNAS</i> and <i>KRAS</i>. Nonsynonymous mutations in <i>APC</i>, <i>CTNNB1</i>, <i>NRAS</i>, <i>BRAF</i>, <i>PIK3CA</i>, <i>HER2</i>, <i>MLH1</i>, <i>MSH2</i>, <i>MSH6</i>, or <i>PMS2</i> were not observed in any cases. In addition, all tumors were EBER-negative. GAFG exhibits diversity at the molecular level, and <i>GNAS</i> mutations are more common than <i>KRAS</i> mutations, <i>TP53</i> mutations, and microsatellite instability. To date, no association between EBV/<i>HER2</i> and GAFG has been found.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"19 4","pages":"82"},"PeriodicalIF":1.2,"publicationDate":"2023-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/81/2f/mco-19-04-02678.PMC10512195.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41133651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinicopathological significance of concurrent ErbB receptor expression in human meningioma.","authors":"Sverre Helge Torp,&nbsp;Magnus Bossum Arnli,&nbsp;David Scheie","doi":"10.3892/mco.2023.2675","DOIUrl":"10.3892/mco.2023.2675","url":null,"abstract":"<p><p>In general, human meningiomas grow slowly and have a favourable prognosis; however, some are prone to recur despite their benign histology. Therefore, knowledge of their tumour biology is essential to determine objective biomarkers that can identify cases with an increased risk for recurrence and to generate effective treatment options. Thus, studies on the epidermal growth factor receptor (EGFR) family, comprising ErbB1/EGFR, ErbB2/HER2, ErbB3/HER3 and ErbB4/HER4, are important. We have recently published papers on the expression of each of these receptor proteins in human meningiomas. The present study aimed to assess the clinicopathological significance of their concurrent expression. A total of 185 grade 1 and 2 meningiomas with robust clinical data underwent immunohistochemical analyses with antibodies against the aforementioned receptors. All meningiomas exhibited upregulation of these receptor proteins relative to normal meninges. In addition, the expression of phosphorylated/activated ErbB1/EGFR1 and phosphorylated/activated ErbB2/HER2 was significantly associated with histological malignancy grade and prognosis, respectively. The concurrent upregulation of ErbB receptors in human meningioma supports their fundamental role in the tumourigenesis of these tumours, and they could thus be exploited in diagnostics, prognosis, and ultimately, in targeted clinical interventions.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"19 4","pages":"79"},"PeriodicalIF":1.2,"publicationDate":"2023-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d3/bd/mco-19-04-02675.PMC10502797.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10307527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Secondary leiomyosarcoma of the nasal cavity in a treated patient with possible hereditary retinoblastoma with germline reciprocal translocation of RB1 and DMXL1 and somatic TP53 mutation: A case report.","authors":"Toshinari Yagi,&nbsp;Harumi Nakamura,&nbsp;Yoji Kukita,&nbsp;Toru Wakamatsu,&nbsp;Hironari Tamiya,&nbsp;Shou Nakai,&nbsp;Makiyo Watanabe,&nbsp;Shigeki Kakunaga,&nbsp;Haruna Takami,&nbsp;Rie Suzuki,&nbsp;Satoshi Takenaka,&nbsp;Yoshiko Hashii","doi":"10.3892/mco.2023.2661","DOIUrl":"https://doi.org/10.3892/mco.2023.2661","url":null,"abstract":"<p><p>Retinoblastoma is a common primary intraocular malignant tumor that affects infants and young children. Radiation therapy for hereditary retinoblastoma increases the risk of secondary malignancy. The present report discusses the case of a retinoblastoma survivor who developed secondary leiomyosarcoma 42 years after receiving radiation therapy. The retinoblastoma of the patient was unilateral, and the patient had no family history of the disease. RNA and DNA panel sequencing of the leiomyosarcoma tissue was performed to elucidate the molecular mechanism of this secondary malignancy. The RNA panel sequencing detected a germline reciprocal translocation of RB1 and DMXL1, leading to a diagnosis of possible hereditary retinoblastoma. Furthermore, it detected a somatic fusion gene (RAD51-KNL1). The DNA panel sequencing identified various germline or somatic variants, including a somatic splice acceptor site mutation of TP53. We hypothesized that the molecular mechanism of the secondary malignancy of this patient was the combination of a germline reciprocal translocation of RB1 and DMXL1 and the accumulation of various somatic mutations containing the splice acceptor site mutation of TP53, which ultimately led to the development of a secondary leiomyosarcoma. Further prospective investigations are necessary to fully understand the role of reciprocal translocation of RB1 and DMXL1 or other mutations in the tumorigenesis of second malignancies in patients with hereditary retinoblastoma.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"19 2","pages":"65"},"PeriodicalIF":1.2,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0d/0d/mco-19-02-02661.PMC10407467.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9970789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>KRAS</i> mutations and their associations with clinicopathological features and survival in Vietnamese non‑polyp colon cancer patients.","authors":"Hoang Minh Cuong,&nbsp;Vu Hong Thang,&nbsp;Bui-Thi Thu Huong,&nbsp;Nguyen Thuan Loi,&nbsp;Nguyen Minh Duc","doi":"10.3892/mco.2023.2659","DOIUrl":"https://doi.org/10.3892/mco.2023.2659","url":null,"abstract":"<p><p>The aim of the present study was to determine Kirsten Ras sarcoma virus (<i>KRAS</i>) mutations and the associations of <i>KRAS</i> mutations with clinicopathological features and treatment outcomes in Vietnamese non-polyp colon cancer (NPCC) patients. The data in the present study covered 194 patients with non-polyp colon cancers at stages II or III, according to the 8th edition of the American Joint Committee on Cancer staging system, in northern Vietnam from January 2016 to August 2020. All patients underwent radical surgery and adjuvant therapy with FOLFOX4 or XELOX. Subsequently, the recruited patients were followed-up with scheduled hospital exams for diagnosing recurrence. Genomic DNA samples were prepared from dissected tumors and specific sequences of the <i>KRAS</i> gene were amplified by polymerase chain reactions (PCR). The mutations at codons 12, 13, 59, 60, 61, 117 and 146 of the gene were determined. Possible associations of the <i>KRAS</i> mutations with clinicopathological properties and the survival of patients were analysed. The <i>KRAS</i> mutation rate was 47.9% in Vietnamese patients with NPCC, of those, mutations in exon 2 accounted for 91.4% of all detected mutations. The mutated-KRAS patients exhibited a significantly higher rate of anemia. Moreover, the <i>KRAS</i> mutation rate was higher in females (57.1%) than in males (39.8%). The <i>KRAS</i> mutation rate was also higher in patients with right colon cancers. Furthermore, <i>KRAS</i> mutations were an independent prognosis for poor disease-free survival (DFS) and overall survival (OS) in stage II patients. Among left-sided colon patients, mutated <i>KRAS</i> was a significant predictive factor for poor DFS but not for OS. The present study revealed a very high mutation rate of <i>KRAS</i> in Vietnamese patients with NPCC. The data of the present study indicated that the mutation status was associated with female patients and right-sided tumors. The <i>KRAS</i> mutations were a negative factor for the survival of patients with stage II NPCC and patients with left-sided colon cancer.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"19 2","pages":"63"},"PeriodicalIF":1.2,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7b/2b/mco-19-02-02659.PMC10345899.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9823087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Postoperative relative decrease in skeletal muscle mass as a predictor of quality of life in patients with gastric cancer.","authors":"Yoshinori Ueda,&nbsp;Akiyoshi Seshimo,&nbsp;Takahiro Okamoto","doi":"10.3892/mco.2023.2655","DOIUrl":"https://doi.org/10.3892/mco.2023.2655","url":null,"abstract":"<p><p>Low skeletal muscle mass reflects poor nutritional condition, which may impair the functional status and quality of life (QOL) of survivors of gastrectomy. The present cross-sectional study examined the association between a relative change in skeletal muscle mass and perceived postoperative health and QOL in patients with gastric cancer. The study comprised 74 patients (48 men and 26 women; median age, 68.5 years) who underwent surgery for stage I-III gastric cancer. Outcomes were measured using the Postgastrectomy Syndrome Assessment Scale-45, which was specifically developed to measure post-gastrectomy symptoms, living status, dissatisfaction with daily life and generic QOL. The skeletal muscle mass index (SMI) was estimated using computed tomography by tracing the area of the psoas major muscle to calculate the ΔSMI, defined as: (SMI before surgery-SMI at completion of the PGSAS-45 survey)/SMI before surgery x100. Associations between ΔSMI and health outcomes were assessed using univariate and multivariate analyses. The mean ΔSMI (SD) was 8.64% (10.6%). The effect size (Cohen's d) of ΔSMI <10% compared with ΔSMI ≥10% was 0.50 (95% CI: 0.02 to 0.97) for total symptom scores, -0.51 (-0.98 to -0.03) for general health, and -0.52 (-0.99 to -0.05) for the physical component summary (PCS). Multiple regression analysis showed that ΔSMI was significantly associated with PCS decline, and its standardized regression coefficient was -0.447 (-0.209 to -0.685). Determining ΔSMI may help clinicians to facilitate the objective evaluation of low skeletal mass, which reflects poor nutritional condition that can impair functional status and QOL of postoperative patients surviving gastrectomy.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"19 2","pages":"59"},"PeriodicalIF":1.2,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/6f/0f/mco-19-02-02655.PMC10326561.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9806661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toll‑like receptor 3 ligands for breast cancer therapies (Review).","authors":"Carly Butkowsky,&nbsp;Natalie Aldor,&nbsp;Sarah J Poynter","doi":"10.3892/mco.2023.2656","DOIUrl":"https://doi.org/10.3892/mco.2023.2656","url":null,"abstract":"<p><p>Breast cancer is the most common cause of cancer worldwide and is the leading cause of mortality for women across most of the world. Immunotherapy is a burgeoning area of cancer treatment, including for breast cancer; these are therapies that harness the power of the immune system to clear cancerous cells. Toll-like receptor 3 (TLR3) is an RNA receptor found in the endosome, and ligands that bind to TLR3 are currently being tested for their efficacy as breast cancer immunotherapeutics. The current review introduces TLR3 and the role of this receptor in breast cancer, and summarizes data on the potential use of TLR3 ligands, mainly polyinosinic:polycytidylic acid and its derivatives, as breast cancer monotherapies or, more commonly, as combination therapies with chemotherapies, other immunotherapies and cancer vaccines. The current state of TLR3 ligand breast cancer therapy research is summarized by reporting on past and current clinical trials, and notable preliminary <i>in vitro</i> studies are discussed. In conclusion, TLR3 ligands have robust potential in anticancer applications as innate immune stimulants, and further studies combined with innovative technologies, such as nanoparticles, may contribute to their success.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"19 2","pages":"60"},"PeriodicalIF":1.2,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f5/0e/mco-19-02-02656.PMC10326562.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9806662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An overview of the role of telomeres and telomerase in pre‑neoplastic lesions (Review).","authors":"Eleftheria Karaviti,&nbsp;Athanasios Kontogiannis,&nbsp;Aristotelis Anastopoulos,&nbsp;Elias Kotteas,&nbsp;Georgia Gomatou","doi":"10.3892/mco.2023.2657","DOIUrl":"https://doi.org/10.3892/mco.2023.2657","url":null,"abstract":"<p><p>Telomeres are tandem repeats of DNA sequences protecting the end of linear chromosomes. Replicative senescence due to telomere attrition is considered a tumor-preventing mechanism in differentiated somatic cells. However, telomere shortening is associated with genome instability and several disease entities. During carcinogenesis, the development of a telomere maintenance mechanism, predominately through the activation of the telomerase enzyme, represents a hallmark of cancer, since it enables cancer cells to avert senescence and divide indefinitely. Although research of the involvement of telomeres and telomerase in various malignant neoplasms has gained a large amount of interest, the timing and relevance of their role in pre-neoplastic lesions remain to be determined. The present narrative review aims to summarize the evidence regarding the role of telomeres and telomerase in pre-neoplasia across different types of tissues.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"19 2","pages":"61"},"PeriodicalIF":1.2,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0e/93/mco-19-02-02657.PMC10326563.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9799548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}