Cancers最新文献

{"title":"Prevention and Treatment of Venous Thromboembolism Associated with Amivantamab-Based Therapies in Patients with Lung Cancer-Provisional Clinical Opinion Based on Existing Clinical Practice Guidelines.","authors":"Florian Moik, Gudrun Absenger, Robert Wurm, Maximilian J Hochmair, Cihan Ay","doi":"10.3390/cancers17020259","DOIUrl":"10.3390/cancers17020259","url":null,"abstract":"<p><p>Improved efficacy has been shown for amivantamab and amivantamab-based combination therapies in patients with epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC) compared to established treatment options in clinical trials. However, a high risk of venous thromboembolism (VTE) was observed in patients treated with amivantamab-based therapies, with considerable differences in VTE risk according to the line of systemic treatment, concomitant treatment with lazertinib, and intravenous vs. subcutaneous amivantamab administration. Based on early reports of high VTE rates, prophylactic anticoagulation has been implemented in ongoing clinical trials for the first 4 months of amivantamab-lazertinib therapy. However, open questions remain concerning the type, dosing, and duration of primary pharmacological thromboprophylaxis in patients treated with amivantamab-based therapies. Therefore, the aim of this clinical opinion piece is to provide provisional guidance on how to mitigate VTE risk in patients treated with amivantamab-based therapies following existing clinical practice guidelines on primary thromboprophylaxis and treatment of VTE in ambulatory patients with cancer.</p>","PeriodicalId":9681,"journal":{"name":"Cancers","volume":"17 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763553/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatial Distribution of Tumor Cells in Clear Cell Renal Cell Carcinoma Is Associated with Metastasis and a Matrisome Gene Expression Signature.","authors":"Prahlad Bhat, Pheroze Tamboli, Kanishka Sircar, Kasthuri Kannan","doi":"10.3390/cancers17020249","DOIUrl":"10.3390/cancers17020249","url":null,"abstract":"<p><p><b>Background/Objectives:</b> Predicting the behavior of clear cell renal cell carcinoma (ccRCC) is challenging using standard-of-care histopathologic examination. Indeed, pathologic RCC tumor grading, based on nuclear morphology, performs poorly in predicting outcomes of patients with International Society of Urological Pathology/World Health Organization grade 2 and 3 tumors, which account for most ccRCCs. <b>Methods:</b> We applied spatial point process modeling of H&E-stained images of patients with grade 2 and grade 3 ccRCCs (<i>n</i> = 72) to find optimum separation into two groups. <b>Results:</b> One group was associated with greater spatial randomness and clinical metastasis (<i>p</i> < 0.01). Notably, spatial analysis outperformed standard pathologic grading in predicting clinical metastasis. Moreover, cell-to-cell interaction distances in the metastasis-associated group were significantly greater than those in the other patient group and were also greater than expected by the random distribution of cells. Differential gene expression between the two spatially defined groups of patients revealed a matrisome signature, consistent with the extracellular matrix's crucial role in tumor invasion. The top differentially expressed genes (with a fold change > 3) stratified a larger, multi-institutional cohort of 352 ccRCC patients from The Cancer Genome Atlas into groups with significant differences in survival and TNM disease stage. <b>Conclusions:</b> Our results suggest that the spatial distribution of ccRCC tumor cells can be extracted from H&E-stained images and that it is associated with metastasis and with extracellular matrix genes that are presumably driving these tumors' aggressive behavior.</p>","PeriodicalId":9681,"journal":{"name":"Cancers","volume":"17 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"γδ T Are Significantly Impacted by CLL Burden but Only Mildly Influenced by M-MDSCs.","authors":"Michał Zarobkiewicz, Wioleta Kowalska, Agata Szymańska, Natalia Lehman, Bożena Kowalczyk, Waldemar Tomczak, Agnieszka Bojarska-Junak","doi":"10.3390/cancers17020254","DOIUrl":"10.3390/cancers17020254","url":null,"abstract":"<p><strong>Background/objectives: </strong>The current study explores the impact of CLL on γδ T cells and, in an attempt to better understand the sources of immunosuppression, assesses the impact of M-MDSCs on γδ T cells in vitro.</p><p><strong>Methods: </strong>The study included 163 CLL patients and 34 healthy volunteers. γδ T cells were screened with flow cytometry, including NKG2D, Fas, FasL, and TRAIL staining. Additionally, to deepen understanding of the immunosuppressive impact of CLL on γδ T, a set of in vitro co-cultures of γδ T and M-MDSCs was performed.</p><p><strong>Results: </strong>RNAseq revealed significant, though relatively minor, changes in the transcriptome. Functional analyses showed a minor drop in cytotoxic potential against CLL cells. Finally, depletion of M-MDSCs from CLL-derived peripheral blood mononuclear cells did not restore γδ T cells' proliferative response.</p><p><strong>Conclusions: </strong>Altogether, this suggests a minor impact of M-MDSCs on activated γδ T. Thus, it seems probable that other mechanisms than M-MDSCs mediate the negative impact of CLL on circulating γδ T cells.</p>","PeriodicalId":9681,"journal":{"name":"Cancers","volume":"17 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763719/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of TERT mRNA Levels and Clinicopathological Features in Patients with Peritoneal Mesothelioma.","authors":"Antonio d'Amati, Gabriella Serio, Andrea Quaranta, Luigi Vimercati, Michelina De Giorgis, Loredana Lorusso, Mariella Errede, Vito Longo, Andrea Marzullo, Domenico Ribatti, Tiziana Annese","doi":"10.3390/cancers17020252","DOIUrl":"10.3390/cancers17020252","url":null,"abstract":"<p><strong>Background/objectives: </strong>Telomerase reverse transcriptase (TERT) is the catalytic subunit of the telomerase enzyme responsible for telomere length maintenance and is an important cancer hallmark. Our study aimed to clarify the mRNA expression of TERT in peritoneal mesothelioma (PeM), and to explore the relationship between its expression and the clinicopathological parameters and prognosis of patients with PeM.</p><p><strong>Methods: </strong>In a cohort of 13 MpeM patients, we evaluated histotype, nuclear grade, mitotic count, necrosis, inflammation, Ki67, BAP1, MTAP and p16 expression by immunohistochemistry, <i>p16</i>/<i>CDKN2A</i> status by FISH and TERT mRNA expression by RNAscope.</p><p><strong>Results: </strong>Our results showed several statistical correlations between TERT mRNA-score and other investigated features: (i) a poor positive correlation with BAP1 score (<i>r</i> = 0.06340; <i>p</i> ≤ 0.0001); (ii) a moderate positive correlation with <i>p16</i> FISH del homo (<i>r</i> = 0.6340; <i>p</i> ≤ 0.0001); (iii) a fair negative correlation with <i>p16</i> FISH del hetero (<i>r</i> = -0.3965; <i>p</i> ≤ 0.0001); a negative poor correlation with MTAP (<i>r</i> = -0.2443; <i>p</i> ≤ 0.0001); and (iv) a negative fair correlation with inflammatory infiltrate (r = -0.5407; <i>p</i> = 0.0233). Moreover, patients survive for a significantly longer time if they have a low mitotic index adjusted (2-4 mitotic figures per 2 mm²) (<i>p</i> ≤ 0.0001), are male (<i>p</i> = 0.0152), lose BAP1 (<i>p</i> = 0.0152), are p16 positive and present no deletion or heterozygous for <i>p16</i> (<i>p</i> ≤ 0.01).</p><p><strong>Conclusions: </strong>TERT is highly expressed in PeM, but it is not one of the crucial factors in evaluating the prognosis of patients. Nevertheless, the results validate the prognostic significance of the mitotic index, BAP1 loss and <i>p16</i>/CDKN2A status.</p>","PeriodicalId":9681,"journal":{"name":"Cancers","volume":"17 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11764446/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Review of Telomere Attrition in Cancer and Aging: Current Molecular Insights and Future Therapeutic Approaches.","authors":"Mina Iskandar, Miguel Xiao Barbero, Muhamed Jaber, Roy Chen, Romulo Gomez-Guevara, Edwin Cruz, Sandy Westerheide","doi":"10.3390/cancers17020257","DOIUrl":"10.3390/cancers17020257","url":null,"abstract":"<p><strong>Background/objectives: </strong>As cells divide, telomeres shorten through a phenomenon known as telomere attrition, which leads to unavoidable senescence of cells. Unprotected DNA exponentially increases the odds of mutations, which can evolve into premature aging disorders and tumorigenesis. There has been growing academic and clinical interest in exploring this duality and developing optimal therapeutic strategies to combat telomere attrition in aging and cellular immortality in cancer. The purpose of this review is to provide an updated overview of telomere biology and therapeutic tactics to address aging and cancer.</p><p><strong>Methods: </strong>We used the Rayyan platform to review the PubMed database and examined the ClinicalTrial.gov registry to gain insight into clinical trials and their results.</p><p><strong>Results: </strong>Cancer cells activate telomerase or utilize alternative lengthening of telomeres to escape telomere shortening, leading to near immortality. Contrarily, normal cells experience telomeric erosion, contributing to premature aging disorders, such as Werner syndrome and Hutchinson-Gilford Progeria, and (2) aging-related diseases, such as neurodegenerative and cardiovascular diseases.</p><p><strong>Conclusions: </strong>The literature presents several promising therapeutic approaches to potentially balance telomere maintenance in aging and shortening in cancer. This review highlights gaps in knowledge and points to the potential of these optimal interventions in preclinical and clinical studies to inform future research in cancer and aging.</p>","PeriodicalId":9681,"journal":{"name":"Cancers","volume":"17 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11764024/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143036543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamic Multilevel Regulation of EGFR, KRAS, and MYC Oncogenes: Driving Cancer Cell Proliferation Through (Epi)Genetic and Post-Transcriptional/Translational Pathways.","authors":"Mario Seres, Katarina Spacayova, Zdena Sulova, Jana Spaldova, Albert Breier, Lucia Pavlikova","doi":"10.3390/cancers17020248","DOIUrl":"10.3390/cancers17020248","url":null,"abstract":"<p><p>The epidermal growth factor receptor (EGFR) regulates gene expression through two primary mechanisms: as a growth factor in the nucleus, where it translocates upon binding its ligand, or via its intrinsic tyrosine kinase activity in the cytosol, where it modulates key signaling pathways such as RAS/MYC, PI3K, PLCγ, and STAT3. During tumorigenesis, these pathways become deregulated, leading to uncontrolled proliferation, enhanced migratory and metastatic capabilities, evasion of programmed cell death, and resistance to chemotherapy or radiotherapy. The <i>RAS</i> and <i>MYC</i> oncogenes are pivotal in tumorigenesis, driving processes such as resistance to apoptosis, replicative immortality, cellular invasion and metastasis, and metabolic reprogramming. These oncogenes are subject to regulation by a range of epigenetic and post-transcriptional modifications. This review focuses on the deregulation of EGFR, RAS, and MYC expression caused by (epi)genetic alterations and post-translational modifications. It also explores the therapeutic potential of targeting these regulatory proteins, emphasizing the importance of phenotyping neoplastic tissues to inform the treatment of cancer.</p>","PeriodicalId":9681,"journal":{"name":"Cancers","volume":"17 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143036809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Outcomes of Brain Metastasis from Lung Cancer.","authors":"James M Mobley, Kerry I Phillips, Quan Chen, Ellen Reusch, Niharika Reddy, Julia B Magsam, Laurie E McLouth, Bin Huang, John L Villano","doi":"10.3390/cancers17020256","DOIUrl":"10.3390/cancers17020256","url":null,"abstract":"<p><p><b>Background/Objectives</b>: Little information has been published on patients diagnosed with brain metastasis secondary to lung cancer. Correlating outcome patterns (hospice care, lost to follow-up, death before hospice care or treatment) and specific characteristics of treated and untreated patients may identify subsets of patients who may benefit from treatment. <b>Methods</b>: We evaluated data from the Kentucky Cancer Registry and identified 284 cases who were diagnosed with brain metastasis secondary to non-small cell lung cancer (NSCLC) between 1 August 2016, and 31 December 2019. We evaluated type and timing of treatment received, as well as focused on those patients who did not receive treatment. For those patients who did not receive treatment, various characteristics that may have impacted their decision or ability to undergo follow-up were also evaluated. This included social history, disease burden, as well as oncology treatment timelines. Lastly, due to the high smoking rate in Kentucky, we conducted an analysis of patient tobacco use. <b>Results</b>: Our results show that 61 cases (21.8%) never received treatment for lung cancer with brain metastasis. Further analysis of the non-treated cases demonstrated that 19 cases (31.1%) never met with an oncology team while in the hospital or after discharge; 14 of the 61 cases (23.0%) were too sick to receive treatment and died prior to having the option of treatment; and 47 of the 61 cases (77.0%) may have had the option of treatment but declined. <b>Conclusions</b>: Historically, patients with brain metastases have faced poor prognoses and limited treatment options. However, advancements in systemic chemoimmunotherapy and targeted therapies have introduced new treatment possibilities, offering improved symptom control and the potential for prolonged survival. This analysis is crucial for identifying potential barriers to care, optimizing resource allocation, and guiding future research.</p>","PeriodicalId":9681,"journal":{"name":"Cancers","volume":"17 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11764313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diagnosis and Management of Skin Toxicities in Systemic Treatment of Genitourinary Cancers.","authors":"Deepro Chowdhury, Laura Chin, Roupen Odabashian, Ali Fawaz, Christina Canil, Michael Ong, Mark G Kirchhof, Martin Neil Reaume, Ana-Alicia Beltran-Bless, Marie-France Savard, David J Tsoulis, Dominick Bossé","doi":"10.3390/cancers17020251","DOIUrl":"10.3390/cancers17020251","url":null,"abstract":"<p><p>The landscape of available therapeutic options for treatment of genitourinary (GU) cancers is expanding dramatically. Many of these treatments have distinct, sometimes severe, skin toxicities including morbilliform, bullous, pustular, lichenoid, eczematous, psoriasiform, and palmoplantar eruptions. Pruritus and skin pigmentation changes have also been noted. This review aims to synthesize dermatologic events observed with antibody drug conjugates, poly (ADP-ribose) polymerase (PARP) inhibitors, androgen receptor pathway inhibitors, tyrosine kinase inhibitors, immune checkpoint inhibitors, and the combination of these agents used for the treatment of GU cancers. It provides a guide on diagnosis and initial management of these rashes for medical oncologists.</p>","PeriodicalId":9681,"journal":{"name":"Cancers","volume":"17 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent Advances in the Clinical Translation of Small-Cell Lung Cancer Therapeutics.","authors":"Subhadeep Das, Shayak Samaddar","doi":"10.3390/cancers17020255","DOIUrl":"10.3390/cancers17020255","url":null,"abstract":"<p><p>Small-cell lung cancer (SCLC) is a recalcitrant form of cancer, representing 15% of lung cancer cases globally. SCLC is classified within the range of neuroendocrine pulmonary neoplasms, exhibiting shared morphologic, ultrastructural, immunohistochemical, and molecular genomic features. It is marked by rapid proliferation, a propensity for early metastasis, and an overall poor prognosis. The current conventional therapies involve platinum-etoposide-based chemotherapy in combination with immunotherapy. Nonetheless, the rapid emergence of therapeutic resistance continues to pose substantial difficulties. The genomic profiling of SCLC uncovers significant chromosomal rearrangements along with a considerable mutation burden, typically involving the functional inactivation of the tumor suppressor genes TP53 and RB1. Identifying biomarkers and evaluating new treatments is crucial for enhancing outcomes in patients with SCLC. Targeted therapies such as topoisomerase inhibitors, DLL3 inhibitors, HDAC inhibitors, PARP inhibitors, Chk1 inhibitors, etc., have introduced new therapeutic options for future applications. In this current review, we will attempt to outline the key molecular pathways that play a role in the development and progression of SCLC, together with a comprehensive overview of the most recent advancements in the development of novel targeted treatment strategies, as well as some ongoing clinical trials against SCLC, with the goal of improving patient outcomes.</p>","PeriodicalId":9681,"journal":{"name":"Cancers","volume":"17 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11764476/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characteristics, Treatment and Outcomes of Stage I to III Colorectal Cancer in Patients Aged over 80 Years Old.","authors":"Melissa R Yeo, Ioannis A Voutsadakis","doi":"10.3390/cancers17020247","DOIUrl":"10.3390/cancers17020247","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer primarily affects older adults and poses treatment challenges due to age-related comorbidities and frailty, which hinder surgical and chemotherapy options for many elderly patients. This study aims to analyze treatment and disease patterns in elderly colorectal cancer patients, aged over 80 years old, to inform personalized therapies that accommodate their unique clinical needs and improve their outcomes.</p><p><strong>Patients and methods: </strong>The medical records of all patients aged 80 years old and above, and those aged 65 to 75 years old, who were diagnosed with colorectal cancer at a cancer center in Canada over a seven year period, were retrospectively reviewed.</p><p><strong>Results: </strong>No significant differences in the initial presentation, location, grade or stage at colorectal cancer diagnosis were observed between age groups. Patients aged 80 years old and above were less likely to receive neoadjuvant and adjuvant chemotherapy treatments for stage II disease (19.2% versus. 58.6%, <i>p</i> = 0.002; 7.9% versus. 40.0%, <i>p</i> = 0.002). There were also differences in the intensity of chemotherapy received and the frequency of dose reductions (76.0% vs. 10.0%, <i>p</i> = 0.0001), neoadjuvant and adjuvant radiation therapy (34.6% vs. 65.5%, <i>p</i> = 0.02) and surgical management (83.7% vs. 95.3%, <i>p</i> = 0.006). Despite these differences in treatments, recurrence rates were not statistically significant between the two groups. However, overall survival was reduced in the older age group.</p><p><strong>Conclusions: </strong>Treatment plans for patients aged 80 years old and above should be tailored to the patient's colorectal cancer presentation, comorbidity status and life expectancy, weighing the impact of cancer treatments on the patient's short- and long-term outcomes.</p>","PeriodicalId":9681,"journal":{"name":"Cancers","volume":"17 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763545/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037167","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}