BMC Cancer (BMC CANCER)

Publisher: BioMed Central

Journal description

BMC Cancer publishes original research articles in all aspects of research relating to cancer, including molecular biology, genetics, pathophysiology, epidemiology, clinical reports, and controlled trials.

Current impact factor: 3.32

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 3.319
2012 Impact Factor 3.333
2011 Impact Factor 3.011
2010 Impact Factor 3.153
2009 Impact Factor 2.736
2008 Impact Factor 3.087
2007 Impact Factor 2.709
2006 Impact Factor 2.359
2005 Impact Factor 1.992
2004 Impact Factor 2.29
2003 Impact Factor 1.702
2002 Impact Factor 1.05

Impact factor over time

Impact factor
Year

Additional details

5-year impact 3.59
Cited half-life 3.50
Immediacy index 0.33
Eigenfactor 0.04
Article influence 1.07
Website BMC Cancer website
Other titles BioMed Central cancer, Cancer
ISSN 1471-2407
OCLC 45893944
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

BioMed Central

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Publisher's version/PDF may be used
    • Eligible UK authors may deposit in OpenDepot
    • Creative Commons Attribution License
    • Copy of License must accompany any deposit.
    • All titles are open access journals
    • 'BioMed Central' is an imprint of 'Springer Verlag (Germany)'
  • Classification
    ​ green

Publications in this journal

  • BMC Cancer 12/2015; 15(1). DOI:10.1186/s12885-015-1236-7
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    ABSTRACT: Exactly assessing tumor response to different dose of chemotherapy would help to tailor therapy for individual patients. This study was to determine the feasibility of dynamic contrast-enhanced ultrasound (CEUS) in the evaluation of tumor vascular response to different dose cisplatin. MCF-7 breast cancer bearing mice were treated with different dose of cisplatin in group B (1 mg/kg) and group C (3 mg/kg). A control group A was given with saline. Sequential CEUS was performed on days 0, 3 and 7 of the treatment, in which time-signal intensity curves were obtained from the intratumoral and depth-matched liver parenchyma. Peak enhancement (PE), area under the curve of wash-in (WiAUC), wash-in rate (WiR) and wash-in perfusion index (WiPI) were calculated from perfusion time-intensity curves and normalized with respect to the adjacent liver parenchyma. Histopathological analysis was conducted to evaluate tumor cell density and microvascular density (MVD). Significant decreases in tumor normalized perfusion parameters were observed on day 3 in the high dose group and on day 7 in the low dose group. On day 7, nPE, nWiAUC, and nWiPI significantly decreased in group C and group B as compared with group A (P < 0.05), and further decreased in group C as compared with group B (P < 0.05). Significant decreases of tumor cell density and MVD were seen in treated group (group B and C) compared to control group (P < 0.05) and further decrease in group C compared to group B (P < 0.05). Dynamic CEUS for quantification of tumor perfusion could be used to evaluate tumor vascular response to different dose of chemotherapy.
    BMC Cancer 12/2015; 15(1):1170. DOI:10.1186/s12885-015-1170-8
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    ABSTRACT: Background: Breast cancer outcomes are influenced by multiple factors including access to care, and payer status is a recognized barrier to treatment access. To further define the influence of payer status on outcome, the National Cancer Data Base data from 1998-2006 was analyzed. Method: Data was analyzed from 976,178 female patients diagnosed with breast cancer registered in the National Cancer Data Base. Overall survival was the primary outcome variable while payer status was the primary predictor variable. Secondary predictor variables included stage, age, race, Charlson Comorbidity index, income, education, distance travelled, cancer program, diagnosing/treating facility, and treatment delay. Multivariate Cox regression was used to investigate the effect of payer status on overall survival while adjusting for secondary predictive factors. Results: Uninsured (28.68%) and Medicaid (28.0%) patients had a higher percentage of patients presenting with stage III and stage IV cancer at diagnosis. In multivariate analysis, after adjusting for secondary predictor variables, payer status was a statistically significant predictor of survival. Patients with private, unknown, or Medicare status showed a decreased risk of dying compared to uninsured, with a decrease of 36%, 22%, and 15% respectively. However, Medicaid patients had an increased risk of 11% compared to uninsured. The direct adjusted median overall survival was 14.92, 14.76, 14.56, 13.64, and 12.84 years for payer status of private, unknown, Medicare, uninsured, and Medicaid respectively. Conclusion: We observed that patients with no insurance or Medicaid were most likely to be diagnosed at stage III and IV. Payer status showed a statistically significant relationship with overall survival. This remained true after adjusting for other predictive factors. Patients with no insurance or Medicaid had higher mortality.
    BMC Cancer 12/2015; 15(1). DOI:10.1186/s12885-015-1228-7
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    ABSTRACT: Transformation of B-cell chronic lymphocytic leukaemia (B-CLL) to diffuse large B cell lymphoma (DLBCL) (Richter's syndrome (RS)) is a rare (2-15% of patients) but catastrophic complication of B-CLL. Dose-intense chemotherapy regimens investigated in small single institution trials, but with the exception of bone marrow transplantation for a minority of patients, little has improved the median overall survival of patients with RS beyond eight months. Patients are often elderly, immunosuppressed, possess co-morbidities and have a deteriorating performance status. TP53 disruption is a common molecular abnormality noted in RS and contributes to the tumour's chemotherapy resistance. Ofatumumab is a fully human anti-CD20 monoclonal IgG1κ antibody that targets a unique epitope on B lymphocytes. It has displayed increased binding affinity and a longer dissociation time when compared to rituximab resulting in improved complement dependent cellular cytotoxicity (CDCC); a mechanism with the potential to overcome apoptosis-resistance in TP53 disruption. Given the prevalence of TP53 disruption in RS, Ofatumumab was considered a relatively non-toxic agent with a sound rationale to test in a prospective multicentre trial as an adjunct to CHOP induction and subsequent ofatumumab maintenance therapy in responding patients. The CHOP-OR study is a prospective phase II study to evaluate the safety, feasibility and activity of a CHOP chemotherapy in combination with ofatumumab in induction and subsequent maintenance for patients with newly diagnosed RS. The primary objective will be the overall response rate (ORR) in patients with RS after six cycles of CHOP-O. The secondary objectives include feasibility of recruitment, progression free survival (PFS), overall survival (OS) and toxicity. The study will be accompanied by exploratory analysis of the genomic landscape of RS in newly diagnosed patients. The CHOP-OR trial evaluates the safety, feasibility and activity of CHOP plus Ofatumumab induction and Ofatumumab maintenance in new RS patients. The study is currently recruiting and has met the interim analysis criteria, with more than 7 of the first 25 participants achieving a CR or PR after six cycles of CHOP-O. The study has the potential to identify predictive biomarkers for this treatment modality. NCT01171378.
    BMC Cancer 12/2015; 15(1):52. DOI:10.1186/s12885-015-1048-9
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    ABSTRACT: Tumor suppression of Transforming Growth Factor (TGF-β) signaling pathway requires an adaptor protein, Embryonic Liver Fodrin (ELF). Disruption of ELF expression resulted in miscolocalization of Smad3 and Smad4, then disruption of TGF-β signaling. However, the prognostic significance of ELF for hepatocellular carcinoma (HCC) hasn't been clarified. This study aimed to investigate whether measuring both TGF-β1 and ELF provides a more powerful predictor for HCC prognosis than either marker alone. TGF-β1 and ELF protein were detected by immunohistochemistry. The relationship between TGF-β1/ELF expression and patients' clinicopathologic factors was analyzed. The association between TGF-β1/ELF expression and disease-free survival and overall survival was analyzed by Kaplan-Meier curves, the log-rank test, and Multivariate Cox regression analyses. The expression of TGF-β1 in HCC tissues was significantly higher than that in normal liver tissues. Conversely, the expression of ELF in HCC tissues declined markedly. ELF protein was correlated with HBsAg, tumor size, tumor number, TNM and recurrence. Data also indicated a significant negative correlation between ELF and TGF-β1. Patients with high TGF-β1 expression or/and low ELF expression appeared to have a poor postoperative disease-free survival and overall survival compared with those with low TGF-β1 expression or/and high ELF expression. Furthermore, the predictive range of ELF combined with TGF-β1 was more sensitive than that of either one alone. TGF-β1 and ELF protein are potential and reliable biomarkers for predicting prognosis in HCC patients after hepatic resection. Our current study has demonstrated that the prognostic accuracy of testing can be enhanced by their combination.
    BMC Cancer 12/2015; 15(1):1127. DOI:10.1186/s12885-015-1127-y
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    ABSTRACT: Preoperative radiochemotherapy improves outcomes in patients with locally advanced rectal carcinoma, and has been used increasingly in patient management. However, there is a strong clinical need to assess tumor response to neoadjuvant treatment, and a non-invasive technique that allows the precise identification of morphologic changes in tumors would be of considerable clinical interest. In this study, we used multiphoton microscopy (MPM) to detect morphologic alterations in rectal adenocarcinomas in patients treated with preoperative radiochemotherapy. MPM was able to identify histopathologic alterations in rectal cancer following preoperative radiochemotherapy, and allowed the qualitative assessment of treatment efficacy and feasibility in relation to dose or strategy. These findings may provide the groundwork for evaluating tumor response to neoadjuvant treatment, thus allowing the tailoring of effective treatment doses and strategies.
    BMC Cancer 12/2015; 15(1):1157. DOI:10.1186/s12885-015-1157-5
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    ABSTRACT: Background: The role of urine markers in the surveillance of patients with non-muscle invasive bladder cancer (NMIBC) is discussed extensively. In case of negative cystoscopy the additional prognostic value of these markers has not been clearly defined yet. The present study is the first systematic approach to directly compare the ability of a urine marker panel to predict the risk of recurrence and progression in bladder cancer (BC) patients with no evidence of relapse during surveillance for NMIBC. Methods: One hundred fourteen patients who underwent urine marker testing during surveillance for NMIBC and who had no evidence of BC recurrence were included. For all patients cytology, Fluorescence-in-situ-hybridization (FISH), immunocytology (uCyt+) and Nuclear matrix protein 22 enzyme-linked immunosorbent assay (NMP22) were performed. All patients completed at least 24 months of endoscopic and clinical follow-up of after inclusion. Results: Within 24 months of follow-up, 38 (33.0%) patients experienced disease recurrence and 11 (9.8%) progression. Recurrence rates in patients with positive vs. negative cytology, FISH, uCyt+ and NMP22 were 52.6% vs. 21.9% (HR = 3.9; 95% CI 1.75-9.2; p < 0.001), 47.6% vs. 25.0% (HR 2.7; 1.2-6.2; p = 0.01), 43.8% vs. 22.4% (HR 3.3; 1.5-7.6; p = 0.003) and 43.8% vs. 16.7% (HR 4.2; 1.7-10.8; p = 0.001). In patients with negative cytology, a positive NMP22 test was associated with a shorter time to recurrence (p = 0.01), whereas FISH or uCyt+ were not predictive of recurrence in these patients. In the group of patients with negative cytology and negative NMP22, only 13.5% and 5.4% developed recurrence and progression after 24 months. Conclusions: Patients with positive urine markers at time of negative cystoscopy are at increased risk of recurrence and progression. In patients with negative cytology, only NMP22 is predictive for recurrence. Patients with negative marker combinations including NMP22 harbour a low risk of recurrence. Therefore, the endoscopic follow-up regimen may be attenuated in this group of patients.
    BMC Cancer 12/2015; 15(1). DOI:10.1186/s12885-015-1089-0
  • BMC Cancer 12/2015; 15(1). DOI:10.1186/s12885-015-1207-z
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    ABSTRACT: Background: There are currently three ongoing studies on less radical surgery in cervical cancer: ConCerv, GOG-278, and SHAPE. The aim of this study was to evaluate the performance of the criteria used in ongoing studies retrospectively and suggest a new, simplified criterion in microscopic Stage IB1 cervical cancer. Methods: A retrospective analysis was performed in 125 Stage IB1 cervical cancer patients who had no clinically visible lesions and were allotted based on microscopic findings after conization. All patients had magnetic resonance imaging (MRI) after conization and underwent type C2 radical hysterectomy. We suggested an MRI criterion for less radical surgery candidates as patients who had no demonstrable lesions on MRI. The rates of parametrial involvement (PMI) were estimated for patients that satisfied the inclusion criteria for ongoing studies and the MRI criterion. Results: The rate of pathologic PMI was 5.6% (7/125) in the study population. ConCerv and GOG-278 identified 11 (8.8%) and 14 (11.2%) patients, respectively, as less radical surgery candidates, and there were no false negative cases. SHAPE and MRI criteria identified 78 (62.4%) and 74 (59.2%) patients, respectively, as less radical surgery candidates; 67 patients were identified as less radical surgery candidates by both sets of criteria. Of these 67 patients, only one had pathologic PMI with tumor emboli. Conclusions: This study suggests that the criteria used in three ongoing studies and a new, simplified criterion using MRI can identify candidates for less radical surgery with acceptable false negativity in microscopic Stage IB1 disease.
    BMC Cancer 12/2015; 15(1). DOI:10.1186/s12885-015-1184-2
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    ABSTRACT: Osteopontin (OPN) can recruit macrophages to the site of inflammation and promote tumorigenesis. M2 tumor-associated macrophages (M2-TAMs) also play an important role in cancer progression. This study aimed to clarify the role of OPN and M2-TAMs co-existence in gastric cancer. The levels of OPN and M2-TAMs were evaluated by immunohistochemical staining in 170 resected gastric cancer specimens that were collected from 1998 to 2012. M2-TAMs were identified by staining for an M2 marker, CD204. The prognostic significance and correlation between OPN and CD204 expression were analyzed. A co-culture system of OPN(+)-AGS and U937 cells was designed to study the effect of OPN on the skewing of macrophages toward M2-TAMs for gastric cancer progression in vitro and in vivo. Patients with high expression (>50%) of OPN or CD204 exhibited poor 5-year overall survival rates (48.61%, p = 0.0055, and 52.14%, p = 0.0498, respectively). A positive correlation was observed between OPN and CD204 expression and high co-expression of OPN and CD204 demonstrated poor 5-year overall survival rates (48.90%, p = 0.0131). In the co-culture study, OPN was able to attract U937 cells and skew them toward M2-TAMs through paracrine action. The M2-TAMs could increase the invasiveness of OPN(+)-AGS cells and the growth rate of xenograft of a mixture of co-cultured OPN(+)-AGS and U937 cells. OPN can skew macrophages toward M2-TAMs during gastric cancer progression. The co-existence of OPN and infiltrating M2-TAMs correlates with disease progression and poor survival and thus can serve as a prognostic marker in gastric cancer.
    BMC Cancer 12/2015; 15(1):1114. DOI:10.1186/s12885-015-1114-3
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    ABSTRACT: ADAM12-L and ADAM12-S represent two major splice variants of human metalloproteinase-disintegrin 12 mRNA, which differ in their 3'-untranslated regions (3'UTRs). ADAM12-L, but not ADAM12-S, has prognostic and chemopredictive values in breast cancer. Expression levels of the two ADAM12 splice variants in clinical samples are highly discordant, suggesting post-transcriptional regulation of the ADAM12 gene. The miR-29, miR-30, and miR-200 families have potential target sites in the ADAM12-L 3'UTR and they may negatively regulate ADAM12-L expression. miR-29b/c, miR-30b/d, miR-200b/c, or control miRNA mimics were transfected into SUM159PT, BT549, SUM1315MO2, or Hs578T breast cancer cells. ADAM12-L and ADAM12-S mRNA levels were measured by qRT-PCR, and ADAM12-L protein was detected by Western blotting. Direct targeting of the ADAM12-L 3'UTR by miRNAs was tested using an ADAM12-L 3'UTR luciferase reporter. The rate of ADAM12-L translation was evaluated by metabolic labeling of cells with (35)S cysteine/methionine. The roles of endogenous miR-29b and miR-200c were tested by transfecting cells with miRNA hairpin inhibitors. Transfection of miR-29b/c mimics strongly decreased ADAM12-L mRNA levels in SUM159PT and BT549 cells, whereas ADAM12-S levels were not changed. ADAM12-L, but not ADAM12-S, levels were also significantly diminished by miR-200b/c in SUM1315MO2 cells. In Hs578T cells, miR-200b/c mimics impeded translation of ADAM12-L mRNA. Importantly, both miR-29b/c and miR-200b/c strongly decreased steady state levels of ADAM12-L protein in all breast cancer cell lines tested. miR-29b/c and miR-200b/c also significantly decreased the activity of an ADAM12-L 3'UTR reporter, and this effect was abolished when miR-29b/c and miR-200b/c target sequences were mutated. In contrast, miR-30b/d did not elicit consistent and significant effects on ADAM12-L expression. Analysis of a publicly available gene expression dataset for 100 breast tumors revealed a statistically significant negative correlation between ADAM12-L and both miR-29b and miR-200c. Inhibition of endogenous miR-29b and miR-200c in SUM149PT and SUM102PT cells led to increased ADAM12-L expression. The ADAM12-L 3'UTR is a direct target of miR-29 and miR-200 family members. Since the miR-29 and miR-200 families play important roles in breast cancer progression, these results may help explain the different prognostic and chemopredictive values of ADAM12-L and ADAM12-S in breast cancer.
    BMC Cancer 12/2015; 15(1):1108. DOI:10.1186/s12885-015-1108-1
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    ABSTRACT: Background: Kif18A, the kinesin-8 motor protein, plays an essential role in regulating alignment of bi-oriented chromosomes at the midzone during mitosis. Kinesin proteins, including Kif18A, are often deregulated in many types of cancers and are thought to play a critical role in cancer progression. However, little is known about the post-translational modifications of Kif18A and their effects on its biological activity. Methods: Kif18A was identified to be a SUMO2 acceptor by using Ni-IDA resin to precipitate proteins from cells stably expressing His(6)-SUMO2. To identify the potential lysine residues, multi-site directed mutagenesis together with transient transfection and Ni-IDA pull-down assay were carried out. The confocal time-lapse imaging and immunofluorescent staining were used to study the roles of SUMO2 modification on Kif18A's activity during the cell cycle. Results: Kif18A is covalently modified by SUMO2 during the cell cycle, and its sumoylation peaks at metaphase and then rapidly decreases upon anaphase onset. Mutational analysis identifies multiple lysine residues (K148, K442, K533, K660 and K683) as potential SUMO acceptors. The functional studies reveal that sumoylation of Kif18A has little effect on protein stability and subcellular localization. However, compared with the wild-type control, ectopic expression of SUMO-resistant mutants of Kif18A results in a significant delay of mitotic exit. Confocal microscopy shows that cells expressing SUMO-resistant Kif18A display a compromised dissociation of BubR1 from kinetochores after anaphase onset. Conclusions: Our studies reveal that sumoylation functions as an unidentified form of post-translational modification that regulates Kif18A activity during mitotic progression.
    BMC Cancer 12/2015; 15(1). DOI:10.1186/s12885-015-1226-9
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    ABSTRACT: Background: Neurofibromatosis 1 is one of the most common genetic diseases in humans, presenting with multiple neurofibromas and an increased risk of various benign and malignant tumors, including breast cancer. Case presentation: In this paper we report a case of a woman with neurofibromatosis 1 and the challenge associated with detecting an advanced breast cancer because of numerous skin neurofibromas, which were responsible for a substantial delay in cancer diagnosis. Literature concerning the association of neurofibromatosis 1 and breast cancer is reviewed and discussed. Conclusions: Best practice guidelines for breast cancer detection are not sufficient for the screening of neurofibromatosis 1 carriers. A more intensive clinical and imaging approach should be used if the same early detection rate as in non-neurofibromatosis 1 women is to be achieved.
    BMC Cancer 12/2015; 15(1). DOI:10.1186/s12885-015-1215-z
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    ABSTRACT: Background: Our previous study suggested that the recurrent CHEK2 H371Y mutation is a novel pathogenic mutation that confers an increased risk of breast cancer. The purpose of this study was to investigate whether breast cancer patients with CHEK2 H371Y mutation were more likely to respond to neoadjuvant chemotherapy. Methods: We screened a cohort of 2334 Chinese women with operable primary breast cancer who received a neoadjuvant chemotherapy regimen for CHEK2 H371Y germline mutations. Pathologic complete response ( pCR) was defined as the absence of tumor cells in the breast after the completion of neoadjuvant chemotherapy. Results: Thirty- nine patients ( 1.7%) with CHEK2 H371Y germline mutation were identified in this cohort of 2334 patients. CHEK2 H371Y mutation carriers had a significantly higher pCR rate than non- carriers ( 33.3% versus 19.5%, P = 0.031) in the entire study population, and CHEK2 H371Y mutation- positive status remained an independent favorable predictor of pCR in a multivariate analysis ( odds ratio [ OR] = 3.01; 95% confidence interval [ CI]: 1.34- 6.78, P = 0.008). CHEK2 H371Y carriers had a slightly worse distant recurrence- free survival than non- carriers ( adjusted hazard ratio [ HR] = 1.24, 95% CI: 0.59- 2.63). Conclusions: CHEK2 H371Y mutation carriers are more likely to respond to neoadjuvant chemotherapy than are non- carriers.
    BMC Cancer 12/2015; 15(1). DOI:10.1186/s12885-015-1203-3