Pathology & Oncology Research (PATHOL ONCOL RES)

Publisher: Springer Verlag

Journal description

POR is devoted especially to basic problems of Pathology and Oncology, together with related clinical and clinicopathological aspects; is a forum for high quality papers from all over the world, including, naturally, our closer geographical area; entertains teaching material from internationally recognized experts. (The only restriction: manuscripts must be in English.)

Current impact factor: 1.86

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 1.855
2013 Impact Factor 1.806
2012 Impact Factor 1.555
2011 Impact Factor 1.366
2010 Impact Factor 1.483
2009 Impact Factor 1.152
2008 Impact Factor 1.26
2007 Impact Factor 1.272
2006 Impact Factor 1.241
2005 Impact Factor 1.162

Impact factor over time

Impact factor

Additional details

5-year impact 1.67
Cited half-life 4.20
Immediacy index 0.45
Eigenfactor 0.00
Article influence 0.41
Website Pathology and Oncology Research website
Other titles Pathology oncology research (Online), Pathology and oncology research, POR, Pathology & oncology research
ISSN 1219-4956
OCLC 41429364
Material type Periodical, Internet resource
Document type Internet Resource, Journal / Magazine / Newspaper

Publisher details

Springer Verlag

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    • 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
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Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Merkel cell carcinoma (MCC) is a rare, highly aggressive skin tumour. In 2008, a Merkel cell polyomavirus (MC) was identified in MCCs as a potential etiological factor of MCC. The aims of this retrospective study were to investigate the epidemiological, clinicopathological and virological features of MCCs. Between 2007 and 2012, 11 patients had been diagnosed with MCC by histological methods in University of Pécs, Hungary. In eight MCC cases MC was tested by PCR (in primary skin lesions, lymph nodes/cutan metastases, MCC neighboring carcinomas). Clinicopathological characteristics (age, histological pattern, lymphovascular invasion, co-morbidities) of MC-positive and MC-negative cases were compared. MC was detected in three (37.5 %) out of eight patients' primary tumour or metastasis. The average age was 73.8 (64.3 in MC-positive group). Except the youngest, 55 year-old patient (the primary tumour appeared on his leg), all tumours were found at the head and neck region. Immunosuppression (steroid therapy, chronic lymphoid leukaemia, chronic obstructive pulmonary disease) and/or old age were characteristic for all cases. Histological pattern was different in MC-positive and in MC-negative groups: MCCs with MC showed more homogeneous histological pattern, lack of lymphovascular invasion and were associated with better prognosis (mortality rate: 33 % versus 80 %). MCC associated with oncogenic virus is a newly recognized clinical entity. However, MC could not be detected in all histologically proven MCCs. The well-defined selection of patients/disease groups and better characterization of differences between MC-positive and negative cases is an important step towards the recognition of the etiology and pathogenesis of all MCCs.
    Pathology & Oncology Research 08/2015; DOI:10.1007/s12253-015-9974-z
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    ABSTRACT: Id (DNA binding and/or differentiation) proteins occur physiologically during ontogenesis and negatively regulate the activity of other helix-loop-helix (HLH) proteins. Id2 protein causes block of cells differentiation in the S phase of the cell cycle and regulates the activity of Rb protein. The role of Id2 protein in physiological cell cycle progression and in neuroblastoma (NBL) pathogenesis was proposed by Lasorella. The aim of the study was evaluation of Id2 expression and its prognostic significance in NBL cells coming from primary tumors and evaluation of its prognostic significance, and correlation of Id2 expression with known prognostic factors. Sixty patients with primary NBL treated from 1991 to 2005 were included in the analysis. We found 50 patients with high and 10 patients with low intensity of Id2 expression. The median percentage of NBL cells with Id2 expression was 88 %. We found no correlation between the number of NBL cells or the intensity of Id2 expression and OS and DFS. In patients with stage 4 NBL, almost all patients had high expression of Id2 and it was significantly more common than in other disease stages (p = 0,03). We found no correlation between Id2 expression and other known prognostic factor in NBL patients. We assume that Id2 is not prognostic factor. However, due to its abundant expression in most of NBL cells and its role in cell cycle, it may be potential therapeutic target. Exact knowledge of expression time may be helpful in explaining mechanisms of oncogenesis.
    Pathology & Oncology Research 03/2015; 21(4). DOI:10.1007/s12253-015-9908-9
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    ABSTRACT: To identify patients who actually need a re - biopsy, based on alterations in PSA readings after 6-month treatment with Dutasteride. We also sought to bring out the most beneficial re-biopsy scheme. We have reviewed the records of patients with persistently elevated PSA and at least one set of TRUS biopsies. Patients who were treated with alpha -blockers/Dutasteride combination were considered as the study group, while patients in control received alpha-blockers alone. Patients in both groups underwent re-biopsy 6 months later. The two protocols of re-biopsies were used at that time: 20-24 cores saturation transrectal (ST)) and ≥40 cores saturation transperineal template-guided (STT) biopsies. One hundred thirty-three patients were included in this study. In 86.7 % of the patients in the study group mean PSA decreased from 7.4 ± 2.69 to 4.037 ± 1.53 (p-0.001). The overall cancer detection rate was 29 % (n-39: 19 v/s 20, control and study groups, respectively). In the study group PSA decreased to 26.73 ± 11.26 % in patients with cancer, compared with 40.54 ± 13.3 % in patients without. It must be emphasized that STT-biopsies detected significantly more cancers (38.46 v/s 20.59 %, p- 0.005). Mean cores number got to 21 ± 2.45 and 45 ± 5.65 in ST and STT biopsies, respectively. Six-month treatment with Dutasteride decreases PSA readings in 86.7 % of the patients. A PSA decline of less than 40% (cutoff) should be considered as an indicator for re-biopsy. Transperineal template-guided biopsies had a higher cancer detection rate.
    Pathology & Oncology Research 03/2015; 21(4). DOI:10.1007/s12253-015-9910-2
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    ABSTRACT: To correlate the molecular data to the clinicopathological parameters in Bulgarian prostate cancer patients. PCA3 overexpression, TMPRSS2-ERG gene fusion, GSTP1 promoter hypermethylation, somatic mutations in the AR gene and the IVS1-27G > A polymorphism in the KLF6 gene were studied. A total of 148 patients were analyzed: 16 aggressive PCa, 83 non-aggressive PCa, 25 BPH and 24 chronic inflammatory diseases. Real-time RT-PCR, DNA sequencing, and bisulfite conversion of DNA, were applied. All cases with aggressive PCa before treatment were tested positive for PCA3 overexpression, expression of a T2-ERG gene fusion product and GSTP1 promoter hypermethylation. No somatic mutations were detected in the AR gene and all patients showed normal KLF6-IVS1-27G > A genotype. The TMPRSS2-ERG positive status correlates with moderate to poorly differentiated prostate tumors and it is considered as unfavorable disease predictor. Positive GSTP1 promoter hypermethylation seems to be highly specific and the earliest epigenetic change in the prostate gland, which indicates the beginning of the pathological process. The appearance of positive molecular markers in blood was considered as a predictor of PCa dissemination. GSTP1 promoter hypermethylation was found as the earliest and a long-lasting epigenetic marker in blood samples of PCa patients, which makes it suitable as a marker for treatment follow-up. The molecular profile of prostate cancer needs to be strictly monitored during the course of disease treatment, which is of a great help in determining the patient's individual therapy response.
    Pathology & Oncology Research 03/2015; 21(4). DOI:10.1007/s12253-015-9915-x
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    ABSTRACT: The evaluation of the effects of 1-year endocrine therapy (NET) was aimed at. A retrospective analysis of 42 cases with 46 stage II-III invasive, hormone receptor-positive, HER2-negative breast cancers was performed. One-year NET was planned with letrozole (n = 33, postmenopausal group), or with goserelin plus letrozole (n = 7) or with goserelin plus tamoxifen (n = 2) (premenopausal group). Surgery was performed in accordance with the initial stage and the response to therapy. With regard to the tumor remaining in the surgical specimen, risk groups were constructed: Group 1: stage 0, pathological complete regression (pCR); Group 2: stages IA-IIA; Group 3: stages ≥IIB + cases with clinical progression. Due to local progression, NET was replaced by neoadjuvant chemotherapy in three patients (four tumors). In two postmenopausal patients, letrozole was replaced by tamoxifen because of the insufficient treatment effect. In 19/42 cases, breast-conserving surgery was performed. Within Group 1, there was no cancer in four cases, while only DCIS remained in 2 (pCR: 13 %); Groups 2 and 3 comprised 25 and 15 cases, respectively. The likeliness of a good response (Groups 1 and 2 vs. Group 3) to NET was increased by 7 % for every 1 % increase of the expression of ER (OR = 1.070; 95 % CI: 1.007-1.138, p = 0.029). Progression-free survival differed according to treatment response (p = 0.001). The post-therapy Ki67 value of ≤15 % had only a marginal effect on survival. No other associations were detected between the tumor characteristics and the therapeutic response or survival. Long-duration NET is effective and safe in cases of hormone-sensitive breast cancer.
    Pathology & Oncology Research 03/2015; 21(4). DOI:10.1007/s12253-015-9911-1
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    ABSTRACT: The aim of the study was to investigate trastuzumab anti-tumor efficacy and its correlation with HER-2 status in primary xenograft models derived from Chinese patients with gastric adenocarcinoma. Patient-derived gastric adenocarcinoma xenograft (PDGAX) mouse models were firstly generated by implanting gastric adenocarcinoma tissues from patients into immune deficient mice. A high degree of histological and molecular similarity between the PDGAX mouse models and their corresponding patients' gastric adenocarcinoma tissues was shown by pathological observation, HER-2 expression, HER-2 gene copy number, and mutation detection. Based on Hoffmann's criteria in gastric cancer, three models (PDGAX001, PDGAX003 and PDGAX005) were defined as HER-2 positive with fluorescence in situ hybridization (FISH) amplification or immunohistochemistry (IHC) 2+/ 3+, while two models (PDGAX002, PDGAX004) were defined as HER-2 negative. Upon trastuzumab treatment, significant tumor regression (105 % TGI) was observed in model PDGAX005 (TP53 wt), while moderate sensitivity (26 % TGI) was observed in PDGAX003, and resistance was observed in PDGAX001, 002 and 004. A significant increase in HER-2 gene copy number was only observed in PDGAX005 (TP53 wt). Interestingly, trastuzumab showed no efficacy in PDGAX001 (HER2 IHC 3+ and FISH amplification, but with mutant TP53). Consistent with this finding, phosphor-HER2 modulation by trastuzumab was observed in model PDGAX005, but not in PDGAX001.
    Pathology & Oncology Research 03/2015; 21(4). DOI:10.1007/s12253-015-9909-8
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    ABSTRACT: BRAF and NRAS are the two most frequent oncogenic driver mutations in melanoma and are pivotal components of both the EGF and FGF signaling network. Accordingly, we investigated the effect of BRAF and NRAS oncogenic mutation on the response to the stimulation and inhibition of epidermal and fibroblast growth factor receptors in melanoma cells. In the three BRAF mutant, two NRAS mutant and two double wild-type cell lines growth factor receptor expression had been verified by qRT-PCR. Cell proliferation and migration were determined by the analysis of 3-days-long time-lapse videomicroscopic recordings. Of note, a more profound response was found in motility as compared to proliferation and double wild-type cells displayed a higher sensitivity to EGF and FGF2 treatment when compared to mutant cells. Both baseline and induced activation of the growth factor signaling was assessed by immunoblot analysis of the phosphorylation of the downstream effectors Erk1/2. Low baseline and higher inducibility of the signaling pathway was characteristic in double wild-type cells. In contrast, oncogenic BRAF or NRAS mutation did not influence the response to EGF or FGF receptor inhibitors in vitro. Our findings demonstrate that the oncogenic mutations in melanoma have a profound impact on the motogenic effect of the activation of growth factor receptor signaling. Since emerging molecularly targeted therapies aim at the growth factor receptor signaling, the appropriate mutational analysis of individual melanoma cases is essential in both preclinical studies and in the clinical trials and practice.
    Pathology & Oncology Research 03/2015; 21(4). DOI:10.1007/s12253-015-9916-9
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    ABSTRACT: Double strand DNA breaks are the most dangerous DNA damage which, if non-repaired or misrepaired, may result in genomic instability, cancer transformation or cell death. RAD51 and XRCC2 encode proteins that are important for the repair of double-strand DNA breaks by homologous recombination. Therefore, genetic variability in these genes may contribute to the occurrence and progression of triple-negative breast cancer. The polymorphisms of the XRCC2 gene -41657C/T (rs718282) and of the RAD51 gene, -172G/T (rs1801321), were investigated by PCR-RFLP in 70 patients with triple-negative breast cancer and 70 age- and sex matched non-cancer controls. The obtained results demonstrated a significant positive association between the RAD51 T/T genotype and TNBC, with an adjusted odds ratio (OR) of 4.94 (p = 0.001). The homozygous T/T genotype was found in 60 % of TNBC cases and in 14 % of the used controls. Variant 172 T allele of RAD51 increased cancer risk (OR = 2.81 (1.72-4.58), p < .0001). No significant associations were observed between -41657C/T genotype of XRCC2 and the incidence of TNBC. There were no significant differences between the distribution of XRCC2 -41657C/T genotypes in the subgroups assigned to histological grades. The obtained results indicate that the polymorphism of RAD51, but not of XRCC2 gene, may be positively associated with the incidence of triple-negative breast carcinoma in the population of Polish women.
    Pathology & Oncology Research 03/2015; 21(4). DOI:10.1007/s12253-015-9922-y
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    ABSTRACT: Endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD) is an effective alternative treatment for early gastric cancer. However, a major concern is the likelihood of lymph node metastasis. From December 1987 to December 2006, 391 patients who underwent curative surgery for gastric cancer with mucosal (T1a, n = 265) or submucosal (T1b, n = 126) invasion and a retrieved lymph node number≧15 were enrolled. The frequency and risk factors of lymph node metastasis were analyzed. The frequency of lymph node metastasis was 4.9 % in T1a lesions and 21.4 % in T1b lesions. Although the depth of submucosal tumor invasion was < 2 mm, there was a 28.6 % chance of lymph node metastasis. A T1b lesion, i.e., the width of the submucosal tumor invasion was < 5 mm, resulted in fewer lymph node metastases than lesions > 5 mm in width. Multivariate analysis demonstrated that Lauren's diffuse type and lymphatic invasion were independent risk factors for lymph node metastasis in T1a lesions, while lymphatic invasion was the strongest risk factor for lymph node metastasis in T1b lesions. EMR/ESD is a good alternative for T1a intestinal type adenocarcinoma without lymphatic invasion. Surgical resection is necessary for patients with T1b gastric cancer with lymphatic invasion.
    Pathology & Oncology Research 03/2015; 21(4). DOI:10.1007/s12253-015-9920-0
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    ABSTRACT: In multiple myeloma the angiogenic process is enhanced by various mediators. Among them interleukin-10 (IL-10), secreted mainly by myeloma-associated macrophages seems to participate in myeloma progression with variable manners. The aim of the study was to measure serum levels of IL-10 in various stages of MM patients and to correlate them with various angiogenic cytokines, such as vascular endothelial growth factor and angiopoietin-2 and with known proliferation parameters, such as serum levels of B-cell activating factor and bone marrow infiltration by myeloma plasma cells, in order to explore their clinical significance. We measured serum levels of the above parameters by ELISA in 54 newly diagnosed MM patients. All of them were higher in MM patients and were increasing in parallel with disease progression. Furthermore, IL-10 correlated positively with both angiogenic cytokines and proliferation markers. This correlation of IL-10 with both angiogenic cytokines and markers of disease activity implicates that they all have an important role in MM pathogenesis and progression.
    Pathology & Oncology Research 03/2015; 21(4). DOI:10.1007/s12253-015-9921-z
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    ABSTRACT: Protein therapeutics, particularly of heterologous origin are shown to elicit immunogenic responses which result in adverse allergic reactions in spite of their promising clinical benefit. L-Asparaginase is one such well known chemotherapeutic agent that has enhanced the survival rates to 90 % in the treatment of acute lymphoblastic leukaemia for past 30 years. But the use of this enzyme is accompanied by hypersensitive reactions ranging from allergy to anaphylactic shock which have a drastic influence in treatment outcomes. Numerous attempts have been made to minimize the problems of immunogenicity, which remained as a major bottleneck in the treatment protocols. Conjugating the enzyme L- Asparaginase with PEG was successful as it has reduced the complications in therapy and frequency of injections (dosages), and thus became prominent in reducing the immunogenicity up to a certain extent. Keeping the bottlenecks in consideration during the development of therapeutics, the present study concentrates on engineering of protein as an alternative to the PEGylated enzyme, having reduced immunogenicity as an inbuilt character of protein by using in silico approaches. L-Asparaginase from Escherichia coli and Pectobacterium carotovorum were selected for the present study. The methodology consists of (i) locating the B and CD4+ T cell epitopes of enzyme by in silico tools (ii) generating point mutations of these epitopes to alter or reduce the immunogenicity of protein (iii) generating enzyme models by molecular modelling (iv) assessing the binding affinity of the substrate with L-Asparaginase variants by in silico docking methods using Autodock 4.2 and (v) validating the mutated model for stability by molecular dynamics simulation studies using Gromacs.
    Pathology & Oncology Research 03/2015; 21(4). DOI:10.1007/s12253-015-9912-0
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    ABSTRACT: Prostate cancer is the second most common malignancy in men worldwide. Abnormal epigenetic alterations such as DNA methylation and histone modification play an important role in tumor initiation, progression and regulation of cancer-related genes such as integrin α4 and E-cadherin. Expression of these genes was determined by semi-quantitative reverse transcriptase-PCR in prostate cancer cell lines, DU145 and PC3, before and after treatment with 5-aza-2-deoxycytidine and trichostatin A. Laser capture microdissection microscopy was used to obtain exclusively affected epithelial cells from prostate gland biopsies of 30 patients with prostate cancer and 40 with benign prostate hyperplasia. DNA bisulfite modifications followed by methylation-specific PCR were used to evaluate the promoter methylation status of E-cadherin and α4 integrin genes in extracted DNA from patients and aforementioned cell lines. The integrin α4 promoter in DU145 was fully methylated, whereas in PC3 cells, partial methylation was detected. E-cadherin was expressed in both cell lines; trichostatin A and 5-aza-2-deoxycytidine treatment had no effect on E-cadherin expression, however the combined treatment of both drugs or 5-aza-2-deoxycytidine alone increased integrin α4 expression. Integrin α4 and E-cadherin were hypermethylated in 66.6 % and 6.6 % of prostate cancer cases, respectively; no hypermethylation was observed in patients with benign prostate hyperplasia. These results together suggest that aberrant DNA methylation is one of the mechanisms involved in integrin α4 expression and may play an important role in human prostate carcinogenesis. In addition, the higher rate of integrin α4 gene methylation in prostate cancer patients elects it as a potential molecular tumor marker.
    Pathology & Oncology Research 03/2015; 21(4). DOI:10.1007/s12253-015-9917-8
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    ABSTRACT: Protein expression changes in relation to cell cycles provide important information, and it may represent a new method for an early diagnosis of metaplasia - dysplasia - adenocarcinoma sequence. We investigated potential changes in cell cycle genes such as protooncogenes (PCNA, EGFR), tumour suppressor gene (p53), apoptotic TUNNEL (Tdt mediated dUTP nick and labelling) gene, as well as small intestinal mucus antigen (SIMA) and large intestinal mucus antigen (LIMA), which accumulates in metaplastic epithelium due to the inflammatory process in routine oesophageal biopsies using immunohistochemistry. Oesophageal biopsies were taken from patients with Barrett's oesophagus (n = 30), reflux oesophagitis (n = 30), healthy oesophagus (n = 30) and healthy cardia (n = 10). Immunohistochemical signalling was carried out by Streptavidin-Biotin-AEC (aminoetil-carbazol). Expression of PCNA was statistically significantly lower in healthy oesophagus (p < 0.05) versus reflux oesophagitis and Barrett's oesophagus. However, no significant change was detected in the expression of SIMA and LIMA in intestinal metaplasia. Further, EGFR, p53 and TUNNEL levels were significantly different in healthy versus Barrett's oesophagus. Manual counting using virtual microscopy was comparable with the result using conventional light microscopy, but the former is significantly quicker. There was no difference between manual and automated cell counting (p > 0.05).
    Pathology & Oncology Research 03/2015; 21(3). DOI:10.1007/s12253-014-9873-8
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    ABSTRACT: To the Editors:Guanine Nucleotide-binding protein, Alpha-Stimulating activity polypeptide 1 (GNAS) is a subunit of the stimulatory G protein that transmits signals to generate cAMP [1]. Mutations in GNAS gene result in several inherited diseases, including pseudohypoparathyroidism, pseudopseudohypoparathyroidism, progressive osseous heteroplasia, McCune-Albright syndrome, polyostotic fibrous dysplasia and several endocrine tumors [2]. Also, somatic mutations of GNAS have been reported in many tumors, including pituitary adenoma, colorectal carcinoma/adenoma, thyroid adenoma, juvenile ovarian granulosa cell tumor, low-grade appendix mucinous neoplasm, hepatocellular carcinomas, pancreatic mucinous neoplasm, fluke-associated cholangiocarcinoma and myelodysplasia [2-9]. Of note, most of the somatic GNAS mutations affected codon 201 [3-9]. Functionally, tumor-derived GNAS mutant constitutively activates cAMP signaling [3]. These data indicate that somatic mutations of GNAS are detected not ...
    Pathology & Oncology Research 03/2015; 21(3). DOI:10.1007/s12253-015-9919-6
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    ABSTRACT: Mycosis fungoides (MF) is a common, indolent primary cutaneous T-cell lymphoma (CTCL), with rare, more aggressive variants, such as folliculotropic MF (FMF). A minority of the MF cases may undergo large cell transformation (T-MF) associated with poor prognosis. A selection of microRNAs (miRs) contribute to the pathogenesis and progression of classic MF, and may also be useful in differential diagnostics. However, the molecular background of FMF and the mechanisms involved in large cell transformation are obscure. We analyzed the expression of 11 miRs in 9 FMF and 7 T-MF cases. Three miRs, including miR-93-5p, miR-181a and miR-34a were significantly upregulated in both FMF and T-MF. FMF also showed overexpression of miR-155 and miR-223, while miR-181b and miR-326 were overexpressed in T-MF cases compared to controls. These results by identifying a number of differentially expressed microRNAs add further insight into the molecular pathogenesis of folliculotropic MF and large cell transformation of MF.
    Pathology & Oncology Research 02/2015; 21(3). DOI:10.1007/s12253-015-9897-8