Clinical and Translational Oncology

Publisher: Springer Verlag

Journal description

Clinical and Translational Oncology is an international journal devoted to fostering interaction between experimental and clinical oncology. It covers all aspects of research on cancer, from the more basic discoveries dealing with both cell and molecular biology of tumour cells, to the most advanced clinical assays of conventional and new drugs. In addition, the journal has a strong commitment to facilitating the transfer of knowledge from the basic laboratory to the clinical practice, with the publication of educational series devoted to closing the gap between molecular and clinical oncologists. Molecular biology of tumours, identification of new targets for cancer therapy, and new technologies for research and treatment of cancer are the major themes covered by the educational series. Full research articles on a broad spectrum of subjects, including the molecular and cellular bases of disease, aetiology, pathophysiology, pathology, epidemiology, clinical features, and the diagnosis, prognosis and treatment of cancer, will be considered for publication. Case reports describing unusual clinical cases or examples of unique reports dedicated to translational research will also be within the scope of the journal.

Current impact factor: 1.28

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2011 Impact Factor 1.327

Additional details

5-year impact 1.32
Cited half-life 3.80
Immediacy index 0.33
Eigenfactor 0.00
Article influence 0.36
Website Clinical and Translational Oncology website
ISSN 1699-3055
OCLC 198613137
Material type Series, Periodical
Document type Journal / Magazine / Newspaper

Publisher details

Springer Verlag

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
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  • Conditions
    • Author's pre-print on pre-print servers such as arXiv.org
    • Author's post-print on author's personal website immediately
    • Author's post-print on any open access repository after 12 months after publication
    • Publisher's version/PDF cannot be used
    • Published source must be acknowledged
    • Must link to publisher version
    • Set phrase to accompany link to published version (see policy)
    • Articles in some journals can be made Open Access on payment of additional charge
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Lung cancer in never smokers presents predominately as adenocarcinoma and in females. MicroRNA-183 (miR-183) has various expression patterns in types of human cancers. In the present study, we evaluated the expression of miR-183-3p in female lung adenocarcinoma and adjacent noncancerous tissues and explored its relationship with clinicopathological characteristics and prognosis. In the present study, a hundred female nonsmoking patients who were newly diagnosed and histologically confirmed as lung adenocarcinoma at Tianjin Medical University Cancer Hospital were included. miR-183-3p expression of surgically removed NSCLC tissues and their corresponding normal lung tissues was measured by qRT-PCR assay. Associations of miR-183-3p expression with clinicopathological features were determined using the Student's t test. Log-rank test, and Cox proportional hazards model were used for survival analysis. At first, miR-183-3p was up-regulated in lung cancer tissues when compared with the corresponding noncancerous lung tissues. Moreover, the expression of miR-183-3p in tumor tissue was found to be associated with lymph node metastasis (P = 0.043), clinical stage (P = 0.015), and EGFR mutation (P = 0.003). At last, high miR-183-3p expression was also associated with both poor overall survival and progression-free survival of women with lung adenocarcinoma (P = 0.005 and P = 0.010, respectively). This study suggested that miR-183-3p expression might be involved in lung cancer pathogenesis and progression, and could be used as a potential prognostic biomarker of female lung adenocarcinoma.
    Clinical and Translational Oncology 05/2014; 16(11).
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    ABSTRACT: ERG expression has been proposed to signify molecular subtype of PCA. However, its significance in early onset prostate cancer (PCA) is not characterized. ERG protein expression was investigated in a cohort of 121 men diagnosed with localized PCA at <50 years of age with a mean follow-up time of 65.7 months. ERG was correlated to patients' outcome and clinical-pathological parameters using univariate and multivariate analysis. ERG expression was detected in 76/118 (64.4 %) analyzable patients' samples and showed interfocal heterogeneity (differences between foci) in 17/118 (14.4 %) patients. There was significant association between ERG expression and Gleason score (p = 0.022), but not with any other clinical-pathologic parameter, including pre-surgical PSA levels, tumor volume, pathological stage, surgical margin or lymph-vascular invasion. ERG had significant effect on the rate of biochemical relapse following radical prostatectomy, with ERG positive patients showing higher relapse rates vs. ERG negative patients (p = 0.007). However, considering time till biochemical relapse post-radical prostatectomy, ERG expression showed positive insignificant trends (p = 0.071). Notably, and of great significance, in this cohort of early onset disease, none of the ERG negative PCA patients exhibited biochemical relapse. The study results suggest that ERG expression may be of added prognostic value in localized prostate cancer in patients with early onset PCA. However, the issue of ERG interfocal heterogeneity observed may require the evaluation of several tumor foci to assess ERG status per case. Incorporating ERG status into existing nomograms may be of added prognostic value in patients with early onset PCA.
    Clinical and Translational Oncology 05/2014;
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    ABSTRACT: An association between neuroendocrine tumors (NETs) and second primary malignancies (SPMs) has been reported. We have examined the incidence and etiology of SPMs in patients with NETs included in the Neuroendocrine Tumor Association of Andalusia (ATNEA) Registry. Data on 111 patients were collected. Sex, age, NET site, chromogranin A levels, neuropeptide secretion and disease stage were compared between NETs with and without SPMs. SPMs were present in 21 patients (18.9 %): five colorectal tumors, four non-small-cell lung cancers, three gastric cancers, two tumors in the small intestine, one hepatocarcinoma, two ovarian tumors, one breast adenocarcinoma, one hypernephroma, one bladder cancer, and one neuroblastoma. SPMs were present in 18 % of patients with a gastrointestinal NET and 22 % of those with a non-gastrointestinal NET. SPMs were found in 23 % of patients with elevated levels of serum chromogranin A, compared to 17 % of patients with normal levels, and in 22 % of patients with functional tumors, compared to 11 % of those with non-functional tumors. Finally, SPMs were observed in 24 % of patients with a local or locoregional tumor but in only 13 % of those with a metastatic tumor. No other differences between patients with and without SPMs were observed. The percentage of patients with SPMs in the ATNEA Registry is similar to those reported in other series. In our registry, patients with functional NETs and local/locoregional tumors have higher probability of SPMs. The low number of patients, selection bias and other etiologic factors of SPMs may have influenced our results.
    Clinical and Translational Oncology 05/2014;
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    ABSTRACT: HER2-positive breast cancer, accounting for 15 % of the total breast cancer patient population, carries in itself a bad prognosis, which has now become much better after the advent of anti-HER2 drugs. HER2-targeted therapy has significantly improved disease free- and overall survival in HER2-positive breast cancer, and has rendered better disease control both in the early and advanced disease setting. Trastuzumab treatment duration is often prolonged and poses significant time and resource challenges both on the treatment institutions and on the patient. The recent development of a subcutaneous formulation has meant a significant advance in this respect. We review the drug development of the compound and the current evidence on its use.
    Clinical and Translational Oncology 04/2014;
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    ABSTRACT: Carbonic anhydrase IX (CA IX), a transmembrane glycoprotein, is known as an endogenous marker for hypoxia. Overexpressed in cancer-associated fibroblasts, CA IX has been reported to be associated with a poor outcome for a number of malignant tumors. Aim of this study was to investigate the role of CA IX in the tumor surrounding stroma of esophageal cancer. Stromal expression of CA IX in 361 formalin-fixed, paraffin-embedded specimens of invasive esophageal cancers, 206 adenocarcinoma (AC) and 155 squamous cell carcinoma (SCC), was investigated. In 42 cases (11.6 %), CA IX expression in the tumor surrounding stroma (AC 23 and SCC 19) was observed. Expression of CA IX correlated with the factors tumor stage (p < 0.001) and lymph node status (p = 0.008). Patients with CA IX expressed in the tumor surrounding stroma had a significant shorter disease-free survival (p = 0.007) and overall survival (p = 0.013). In esophageal cancer, CA IX-expressing tumor stroma is associated with shorter survival. Inhibition of the tyrosine kinase CA IX might represent a new onset for therapies against esophageal cancer.
    Clinical and Translational Oncology 04/2014;
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    ABSTRACT: Exocrine pancreatic cancer (PC) is a very aggressive and heterogeneous tumor with several cellular signaling pathways implicated in its pathogenesis and maintenance. Several risk factors increase the risk of developing PC. Therapeutic strategies used are dictated by the extent of disease. Supportive treatment is critical because of the high frequency of symptoms. For localized disease, surgery followed by adjuvant gemcitabine is the standard. Neoadjuvant and new adjuvant chemotherapy regimens are being evaluated. Locally advanced disease should respond best guided by a multidisciplinary team. Various treatment options are appropriate such as chemotherapy alone or chemoradiotherapy with integration of rescue surgery if the tumor becomes resectable. In metastatic disease, chemotherapy should be reserved for patients with ECOG 0-1 using Folfirinox or gemcitabine plus nab-paclitaxel as the most recommended options. Several therapeutic strategies targeting unregulated pathways are under evaluation with an unmet need for biomarkers to guide management.
    Clinical and Translational Oncology 04/2014; 16(10).
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    ABSTRACT: Brain metastases of testicular germ cell tumor (TGCT) are a rare event. Prognostic is poor and there is not much evidence on optimal management of these patients. A review of case records of germ cell tumor patients within the Spanish Germ Cell Cancer Group data base from 1994 to 2012 was conducted. Thirty-three out of 6,200 cases (0.5 %). Nineteen patients (57 %) group 1: synchronous, 13 (40 %) group 2: metachronous and only one developed brain metastasis during cisplatin-based chemotherapy (excluded from the analysis). Median serum BHCG levels at initial diagnosis was higher in group 1, whereas elevated AFP serum levels were more common in group 2. Histology in the primary tumor: chorionic carcinoma for group 1 versus embryonal carcinoma for group 2. Mainly solitary brain metastasis in group 2 (54 versus 21 %, respectively). The median overall survival from the diagnosis of central nervous system involvement was 16 months for group 1 (CI 95 % 13.9-18) and 23 months (95 % CI 0-165) for group 2 (log rank p = 0.84). Long-term survivors were practically identical in the two groups (38.9 % group 1 versus 38.5 % group 2). Regardless of the timing of brain metastasis, those patients that achieved complete response to the treatment had better survival (log rank p 0.003). Although some distinctive clinical characteristics have been found between patients with synchronous versus metachronous brain metastasis from TGCT, the timing of brain metastasis did not seem to have prognostic influence, but due to the retrospective nature of the analysis and the results should be interpreted with caution.
    Clinical and Translational Oncology 04/2014; 16(11).
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    ABSTRACT: The present study aimed to investigate the expression level of MicroRNA-25 (miR-25) in epithelial ovarian cancer (EOC) tissue, and examine its relationship with clinicopathological factors and prognosis of patients with EOC. Expression levels of miR-25 in 86 pairs of EOC tissue and adjacent normal tissue were measured by quantitative real-time reverse-transcription polymerase chain reaction (qRT-PCR). The comparison of the expression level of miR-25 between EOC tissue and adjacent normal tissue was performed using the two-sample Student's t test. The correlation between the expression of miR-25 and clinicopathological characters was assessed with the two-sample Student's t test. The overall survival was analyzed by log-rank test, and survival curves were plotted according to Kaplan-Meier. The expression level of miR-25 in EOC tissue was significantly higher than in adjacent normal tissue. The miR-25 expression level was significantly positively correlated with tumor stage, histology, and regional lymph node involvement (P < 0.05). Kaplan-Meier analysis showed that patients with higher levels of miR-25 had significantly poorer survival than those with lower expression of this miRNA in patients, with a 6-year overall survival of 15.96 and 45.89 %, respectively, (P = 0.001). In the multivariate Cox proportional hazards analysis, high miR-25 expression was independently associated with poor survival (P = 0.002; HR = 2.119; 95 % CI = 1.568-3.221). The increased expression of miR-25 is closely related to poor prognosis of EOC, indicating that miR-25 may serve as a predictive biomarker for the prognosis of EOC.
    Clinical and Translational Oncology 04/2014; 16(11).
  • Clinical and Translational Oncology 04/2014; 16(6).
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    ABSTRACT: Our previous study showed the upregulation of inosine 5'-monophosphate dehydrogenase type II (IMPDH2) protein in human prostate cancer (PCa) tissues and sera compared to non-cancerous controls by proteomics and ELISA analyses. However, the clinical significance of IMPDH2 in PCa has not been fully elucidated. Thus, the aim of the current study was to investigate the associations of IMPDH2 upregulation with tumor progression in patients with PCa. IMPDH2 expression at mRNA and protein levels in human PCa and non-cancerous prostate tissues was respectively detected by qRT-PCR, Western blot and immunohistochemistry analyses, which was validated by microarray-based Taylor Data. Then, the association of IMPDH2 expression with clinicopathological features of PCa patients was statistically analyzed. Compared with non-cancerous prostate tissues, IMPDH2 mRNA and protein expression levels were both significantly upregulated (at mRNA level: 9.22 ± 2.49 vs 5.06 ± 1.45, P < 0.01; at protein level by Western blot: 0.674 ± 0.029 vs 0.418 ± 0.140, P < 0.001; at protein level by immunohistochemistry: 4.97 ± 0.760 vs 3.32 ± 1.66, P < 0.001) in PCa tissues, which were consistent with our previous data. In addition, the enhanced expression of IMPDH2 in PCa tissues was significantly correlated with the advanced clinical stage (for our cohort: P < 0.001; for Taylor data: P = 0.002), the presence of metastasis (for our cohort: P < 0.001; for Taylor data: P = 0.012) and the higher Gleason score (for our cohort: P = 0.002; for Taylor data: P = 0.028). These findings suggest for the first time that the enhanced expression of IMPDH2 may promote the tumor metastasis and the advanced tumor progression in patients with PCa.
    Clinical and Translational Oncology 03/2014;
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    ABSTRACT: Cancer is a leading cause of death worldwide accounting to 13 % of all deaths. One of the main causes behind the failure of treatment is the development of various therapy resistance mechanisms by the cancer cells leading to the recurrence of the disease. This review sheds a light on some of the mechanisms developed by cancer cells to resist therapy as well as some of the structures involved such as the ABC members' involvement in chemotherapy resistance and MET and survivin overexpression leading to radiotherapy resistance. Understanding those mechanisms will enable scientists to overcome resistance and possibly improve treatment and disease prognosis.
    Clinical and Translational Oncology 03/2014; 16(6).
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    ABSTRACT: Aldehyde dehydrogenase enzymes are a family of intracellular enzymes that participate in cellular detoxification, differentiation and drug resistance through the oxidation of cellular aldehydes. The isoform 1 (ALDH1) has been proved useful for the identification of cancer stem cells. The ALDH1 cytoplasmatic expression has been associated with poor prognostis in several tumours, such as non-small cell lung cancer. The role of the ALDH1 nuclear expression remains unknown. We conducted a historical cohort study in 89 patients diagnosed of stage I non-small cell lung cancer treated with surgery between 2009 and 2004 in the Thoracic Surgery Department in the Universitary Hospital Puerta de Hierro. We selected from this sample those cases with nuclear expression of the ALDH1. Three of the 89 (3.3 %) patients showed a nuclear expression of the ALDH1. The three of them are still alive with a median time of follow up of 73 months (more than 6 years). We have identified ALDH1 as a nuclear protein in early stage non-small cell lung cancer. It might have a function in cell cycle control, associating a better prognosis to these patients. More studies are necessary to clarify the role of nuclear expression of ALDH1.
    Clinical and Translational Oncology 03/2014;
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    ABSTRACT: This study evaluated the effect of estrogen (E2), progesterone (P4), and the combination of them (E2 + P4) on survival rate, apoptosis, and the expressions of Bcl-2, hsa-let-7a and has-miR-34b in primary ovarian cancer cells to provide new clues for the clinical treatments of ovarian cancer. The primary ovarian cancer cells from 60 cases of clinical ovarian cancer tissues were isolated and then cultured. The survival rate of ovarian cancer cells after the treatment of E2, P4 and E2 + P4 was analyzed by MTT assay. Cell apoptosis rate and cell cycle were measured by FACS analysis. Moreover, the relative abundance of Bcl-2 and microRNAs (let-7a, miR-34b) expressions were detected by quantitative real-time PCR (qRT-PCR) and Western blotting. Low concentrations of estrogen (10(-10), 10(-8), 10(-6 )mol/L) did not affect the proliferation of ovarian cancer cells. However, the high concentration of estrogen (10(-4 )mol/L) inhibited survival rate of ovarian cancer cells. Progesterone (10(-4 )mol/L) inhibited the proliferation of cancer cells. The combination of estrogen and progesterone significantly inhibited the survival rate of ovarian cancer cells with a time- and dose-dependent manner. High concentration of estrogen combined with progesterone (E2 + P4) induced apoptosis of ovarian cancer cells. E2 + P4 promoted the expression of let-7a and miR-34b and reduced the expression of Bcl-2 in ovarian cancer cells. When the expression of let-7a or/and miR-34b was inhibited using miRNA inhibitors, E2 + P4 treatment did not change the protein level of Bcl-2. E2 + P4 significantly inhibited the cell survival, promoted the cell apoptosis, induced the expression of let-7a and miR-34b, and reduced the expression of Bcl-2 in ovarian cancer cells.
    Clinical and Translational Oncology 03/2014; 16(10).
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    ABSTRACT: Colorectal cancer (CRC) is one of the most frequent cancer in first world. Two hereditary CCR syndrome have been described: familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer. A recently described biallelic mutation of MYH, is responsible for adenomatous polyposis with an increased risk of CRC and is responsible for 30-40 % of adenomatous polyposis cases in which an APC mutation cannot be found. However, there is no clear consensus in the literature as whether a monoallelic mutation increases the risk for colorectal cancer. In addition, some authors have indicated that the spectrum of extracolonic lesions in MYH associated polyposis (MAP) might be far different from that observed in FAP and could be more similar to Lynch syndrome spectrum. In this review we are going to describe some general and specific aspects of MAP, including genetic topics, clinical features, different phenotypes and strategies to reduce CCR risk.
    Clinical and Translational Oncology 03/2014;
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    ABSTRACT: To evaluate the incidence of venous thromboembolism (VTE) in ambulatory pancreas cancer patients receiving chemotherapy and analyze Khorana's predictive model of chemotherapy-associated thrombosis. We performed a retrospective review to determine the incidence of VTE in the gastrointestinal cancer unit of our center. Between 2008 and 2011, 84 consecutives patients diagnosed with pancreas adenocarcinoma were identified and included in the analysis. Pancreatic neuroendocrine tumors were excluded. Thirty patients experienced VTE (35.7 %) and 66 % of the events were diagnosed during the first 6 months after diagnosis. Khorana's score: 33.3 % of the intermediate category patients developed a venous thromboembolic event and 37.5 % in the high-risk category. The high incidence of VTE observed in this study is consistent with prior reports. Specific predictive model for chemotherapy-associated thrombosis in pancreatic cancer must be investigated.
    Clinical and Translational Oncology 03/2014; 16(10).
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    ABSTRACT: Medullary thyroid carcinoma (MTC) is observed in nearly 100 % of patients with multiple endocrine neoplasia type 2A (MEN2A). The gene responsible for MEN2A is the RET proto-oncogene and about 95 % of MEN2A patients have germline mutations in five specific cysteine codons (609, 611, 618, 620 and 634). A retrospective study of children from families with MEN2A in our geographic area was performed. Variables analyzed included demographic data, kinship relations, age at genetic screening, age at prophylactic thyroidectomy, genetic mutation subtype and histological findings. The genetic study consisted in direct molecular analysis by automatic sequencing of RET mutated exon in the studied family. We performed 13 prophylactic total thyroidectomies from 1997 to 2013, 8 females and 5 males. The mean age at genetic diagnosis was 3.8 years (range 2-5.9). All children belonged to four interconnected families living in the same geographic area and presenting C634Y mutation in all the cases. The mean age at prophylactic thyroidectomy was 5.6 years (range 4-8.5). Histopathological findings demonstrated seven cases of C-cells nodular hyperplasia, one lymphocytic thyroiditis, two without evidence of disease, two micro-carcinomas and one multicentric carcinoma. The mutation found in the RET proto-oncogene responsible for MEN2A in pediatric patients in the south of Spain is the C635Y. It is considered a high-risk mutation, associated with an earlier malignant transformation and development of MTC.
    Clinical and Translational Oncology 03/2014;
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    ABSTRACT: Multidrug resistance (MDR) is a major obstacle to successful cancer chemotherapy. One of the main underlying mechanisms of this resistance is the over-expression of P-glycoprotein (P-gp), an ATP-dependent transmembrane transporter protein encoded by the MDR1 gene. P-gp might transport anti-cancer drugs out of cancer cells and decrease effective intracellular drug concentrations. An effective approach to overcome MDR is to inhibit the function of P-gp or its expression on the surface of cancer cells. Thus, application of MDR reversal agents can be seen as a potentially important means by which to overcome the clinical drug resistance of tumour cells and improve the efficacy of chemotherapy. Recently, research efforts worldwide have focused on reversal mechanisms for MDR and on the identification of reversal agents. Chinese scholars have performed a great deal of exploratory work by screening for efficacy and low toxicity in drug resistance reversal compounds. These compounds may provide more lead compounds with greater activity, leading to the development of more effective therapies for MDR cancer cells. In this review, the function and efficiency of novel compounds derived from traditional Chinese medicines are described.
    Clinical and Translational Oncology 03/2014;
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    ABSTRACT: Radiotherapy (RT) is an essential part of the patient's treatment diagnosed with cancer. Determination of the most common RT secondary effect, the cutaneous toxicity, is usually based on visual rating scales, like Common Terminology Criteria for Adverse Events with an inherent subjectivity. The aim of this work is to perform an objective method to evaluate the radiodermatitis using a non-invasive imaging technique based on laser Doppler flowmetry (LDF). A prospective study was performed analysing 1,824 measurements. A LDF was used to measure the cutaneous microcirculation in real time. A basal measurement was taken prior to radiotherapy treatment. To be able to observe the microcirculation changes related to the delivered dose, several sets of measurements were taken in the irradiated area along the RT treatment and in the contralateral non-irradiated area. A relative increase in blood flow at all measured points was found in the irradiated area. This relative increase in blood flow increases with the dose administered. In the non-irradiated contralateral area, the relative increase in blood flow is not significant and is independent of the dose administered. After treatment, a decrease in blood flow was detected with a trend towards returning to the baseline measurements. LDF is an objective technique that assesses early radiodermatitis. This method is useful to develop strategies to prevent onset of radiation dermatitis in patients irradiated, such as the modification and individualization of fractionation parameters of the RT. This allows the reduction of radiation morbidities and maintains patient quality of life.
    Clinical and Translational Oncology 03/2014; 16(10).
  • Clinical and Translational Oncology 03/2014;