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: 1.81

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 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
Year

Additional details

5-year impact 1.64
Cited half-life 4.10
Immediacy index 0.45
Eigenfactor 0.00
Article influence 0.46
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

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • 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: 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; DOI:10.1007/s12253-015-9908-9
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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; DOI:10.1007/s12253-015-9911-1
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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; DOI:10.1007/s12253-015-9910-2
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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; DOI:10.1007/s12253-015-9897-8
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    ABSTRACT: The mammalian target of rapamycin (mTOR) has recently emerged as a promising target for therapeutic anti-cancer interventions in several human tumors. In present study, we investigated the expression of mTOR, and subsequently examined its relationship with clinicopathological factors and the anti-tumor effect of everolimus (also known as RAD001) in oral squamous cell carcinoma (OSCC). The expression of phosphorylated mTOR (p-mTOR) was immunohistochemically evaluated in specimens obtained from 70 OSCC patients who underwent radical surgery. The relationships between the expression of p-mTOR and clinicopathological factors and survival were determined. We also investigated the effect of everolimus on the OSCC cell lines, SAS, HSC-2, HSC-3, HSC-4, OSC-20, SCC25 and Ca9-22 by the MTT assay. We further evaluated whether mTOR contributed to cell functions by blocking its activity with everolimus, and confirmed the direct target by the Matrigel invasion assay, wound healing assay and Western blotting. p-mTOR was overexpressed in 37 tumors (52.8 %), and correlated with the T classification, N classification, and survival rate (P < 0.05). The treatment with everolimus significantly inhibited cell growth, and significantly reduced the expression of p-mTOR, downstream signaling proteins, and hypoxic related proteins as well as invasion and migration potentials (P < 0.05). The results of the present study suggest that everolimus may represent an attractive approach for the future treatment of OSCC.
    Pathology & Oncology Research 02/2015; DOI:10.1007/s12253-014-9888-1
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    ABSTRACT: To investigate the relationship between apoptosis and histologic types in invasive squamous cell carcinoma and adenocarcinoma of the uterine cervix. The present study involved the assessment of surgical specimens from 74 women with cervical carcinomas FIGO stage IB1 (54 squamous cell carcinomas and 20 adenocarcinomas). The study samples were obtained from selected paraffin blocks containing specimens from patients submitted to surgical procedures. The respective medical charts of patients were reviewed and epidemiologic, clinical and disease-related data were collected. Cervical specimens were assessed by the immunohistochemistry technique using the Bcl-2 protein as a marker. The reactions were considered positive when the cells became stained in brown color. Bcl-2 positive cells were counted in 10 fields under a high magnification (400x) using light microscopy, in the slides area containing squamous carcinoma and adenocarcinoma of the cervix. The total cell count was expressed as the number of positive Bcl-2 cells per mm(2). No significant difference in the number of cells marked by the Bcl-2 protein was found for the variables age, tumor diameter, angiolymphatic invasion or number of lymph nodes affected. Comparison of the number of cells marked by the Bcl-2 protein in the two histological groups revealed a statistically significant difference, with squamous tumors presenting a greater number of marked cells. Squamous cervical tumors present a greater number of positive Bcl-2 cells per mm(2), suggesting that that the rate of cell death in squamous cell carcinomas of the cervix is lower than in adenocarcinomas.
    Pathology & Oncology Research 02/2015; DOI:10.1007/s12253-015-9906-y
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    ABSTRACT: The X-ray complementing group 4 (XRCC4, OMIM: 194363) plays a key role in non-homologous end-joining DNA repair pathway in mammalian cells. This pathway is believed to help maintain genomic stability. In the present study, it is hypothesized that genetic polymorphisms in the NHEJ repair XRCC4 gene may be associated with an increased risk in developing colorectal cancer (CRC). We genotyped two polymorphisms of XRCC4, G-1394T (rs6869366) and intron 3 insertion/deletion (I/D; rs28360071) in 200 colorectal cancer patients as well as 256 healthy individuals, and evaluated their association with CRC. We found that in G-1394T polymorphism, neither the TG nor the GG genotypes (versus the TT genotype) were associated with the risk of developing CRC. The results of our study indicate that in comparison with the II genotype, ID and DD genotypes had no significant association with the risk of developing CRC. Subjects with TT genotype and positive family history in colorectal cancer were found to be at a much lower risk of developing CRC in comparison with the reference group (OR = 0.31, 95%CI: 0.11-0.85, P = 0.023). It should be noted that participants having at least one G allele (TG+GG genotypes) were at a significantly higher risk to develop the disease compared with the reference group (OR = 9.10, 95%CI: 2.00-41.3, P = 0.004). In relation to I/D polymorphism, among participants, those with positive family history, either with ID (OR = 4.78, 95%CI: 2.26-10.0, P < 0.001) or DD genotypes (OR = 5.73, 95%CI: 1.99-16.4, P = 0.001) had a significantly association with the disease. Among participants with a positive family history in CRC, the haplotype GD dramatically increased the risk of developing CRC (OR = 10.2, 95%CI: 2.28-46, P = 0.002). The results of this study indicate that G-1394T and I/D polymorphisms of XRCC4 among individuals with positive family history for colorectal cancer substantially increase the risk factor for developing colorectal cancers.
    Pathology & Oncology Research 02/2015; DOI:10.1007/s12253-015-9905-z
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    ABSTRACT: Whether an axillary lymph node dissection (ALND) is needed for breast cancer patients with minimal sentinel lymph node (SLN) involvement is arguable despite recent data supporting the omission of axillary clearance in these patients. Data on disease recurrence of 111 patients with SLN involvement and no ALND were analysed. Patients with minimal SLN involvement were assessed for their risk of non-SLN metastasis by means of several nomograms. The series included patients with isolated tumour cells (n = 76), micrmetastasis (n = 33) and macrometastasis (n = 2) who were followed for a median of 37 months (range 12-148 months). Six patients died, 3 of disease and 3 of unrelated causes. Eight further patients had breast cancer related events: 1 local breast recurrence and seven distant metastases. No axillary regional recurrence was detected. Disease related events were not associated with the risk of non-SLN metastasis. The presented data suggest that omitting ALND in patients with low volume SLN metastasis may be a safe procedure, and support the observation that systemic disease recurrence may not be associated with axillary recurrence or the risk of NSLN involvement predicted by nomograms.
    Pathology & Oncology Research 02/2015; DOI:10.1007/s12253-015-9899-6
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    ABSTRACT: This study is a retrospective analysis evaluating the efficacy and toxicity of combination chemotherapy with S-1 and oxaliplatin (SOX) as first-line treatment in elderly patients with advanced gastric cancer. One hundred and twenty-nine patients with recurrent or metastatic gastric adenocarcinoma were treated with SOX; S-1 (40-60 mg depending on patient's body surface area) was given orally, twice daily on days 1 to 14 followed by a 7-day rest period, 130 mg/m(2) oxaliplatin was given as an intravenous infusion over 2-hours on day one. The cycle was repeated every three weeks. All of the patients were older than 65 years. Among 129 patients enrolled, nine patients could not be evaluated for responses because of the absence of any measurable lesions or early discontinuation of therapy. Assessment of the response of 120 patients was made. The overall objective response rate was 54.2 % (95 %CI, 45.3-63.1 %), with three complete responses and 62 partial responses. The disease control rate was 80.8 % (95 %CI, 73.8-87.8 %). The median follow-up period was 23 months (range, 5-42 months). The median time to progression was 6.9 months (95 %CI, 5.5-8.3 months) and the median overall survival was 12.8 months (95 %CI, 11.4-14.2 months). The one-year survival rate was 57.5 % (95 %CI, 48.7-66.3 %). In 129 patients assessed safety, grade 3 and 4 toxicities included leucopenia (20.9 %), neutropenia (24.0 %), anemia (10.9 %), thrombocytopenia (10.1 %), anorexia (3.1 %), peripheral neurotoxicity (15.5 %), and fatigue (12.4 %). No treatment-related deaths occurred. Combination chemotherapy with SOX offers an effective, safe and well-tolerated regimen for elderly patients with advanced gastric cancer.
    Pathology & Oncology Research 02/2015; DOI:10.1007/s12253-015-9903-1
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    ABSTRACT: This study aimed to identify target genes regulated by KSHV miRNAs in KSHV-infected lymphoma cells. Original Ago HITS-CLIP data of BC-3 and BCBL-1 cell lines were downloaded from SRA database in NCBI, including mRNA and miRNA samples. The raw mRNA reads were mapped into human reference genome hg19 via TopHat for read alignment. PCR duplicates were removed via the SAM tool and the peaks of reads were analyzed via Cufflinks. For miRNA data, the raw data were mapped to the mature miRNA sequences based on miRBase via Bowtie. Peak intersection was computed by using intersectBed in BEDtools. Then, the mature miRNA seeds were identified and then were aligned with 3’ UTR merged peaks. The regulationships of miRNAs and their corresponding genes were analyzed based on the signal of RNA-induced silencing complex. Totally, 7 KSHV-related genes regulated by KSHV miRNAs were identified, including IPO5, EDA, NT5C3, WSB1, KCNS1, PRAM1 and MTRNR2L6. Among them, EDA, MTRNR2L6 and IPO5 were regulated by multiple KSHV miRNAs, such as kshv-miR-K12-1-5p, kshv-miR-K12-4-3p and kshv-miR-K12-3-5p, respectively. Furthermore, expression of kshv-miR-K12-1-5p and kshv-miR-K12-3-5p in BCBL-1 cell line were lower than that in BC-3 cell line, conversely, expression of kshv-miR-K12-4-3p in BCBL-1 cell line were higher than that in BC-3 cell line. In conclusion, potential target genes regulated by KSHV miRNAs in KSHV-infected lymphoma cells might play key roles in the nosogenesis of this disease. These findings might provide the basis for deep understanding of KSHV-infected tumors and further molecular experiments.
    Pathology & Oncology Research 02/2015; DOI:10.1007/s12253-015-9902-2
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    ABSTRACT: Gallbladder carcinoma is a rare and highly lethal malignancy. It stands out from amongst the other GI tract malignancies for its unique epidemiological profile, proclivity for female gender, definitional ambiguities, ability to escape early diagnosis, and absence of effective treatment. Pathobiology of gallbladder carcinoma continues to remain poorly understood. Recently, better characterization of the precursor lesions and elucidation of underlying molecular pathways has enhanced our understanding of gallbladder tumorigenesis. Proposal of a unified terminology and evolving consensus in classifying gallbladder pre-invasive neoplasia offers hope of better assimilation of rare data from diverse parts of the world. Identifying biomarkers and cancer specific cellular targets that will pave the way for novel therapeutic approaches for gallbladder carcinoma is urgently needed. In this review we delve into the epidemiologic, genetic and pathologic characteristics of this enigmatic disease with a special focus on the recent advancements in the field of gallbladder pathology.
    Pathology & Oncology Research 01/2015; DOI:10.1007/s12253-014-9886-3
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    ABSTRACT: Colorectal cancer (CRC) is among the most lethal human cancers, but the mechanism of the cancer is still unclear enough. We aimed to explore the key genes in CRC progression. The gene expression profile (GSE4183) of CRC was obtained from Gene Expression Omnibus database which included 8 normal samples, 15 adenoma samples, 15 CRC samples and 15 inflammatory bowel disease (IBD) samples. Thereinto, 8 normal, 15 adenoma, and 15 CRC samples were chosen for our research. The differentially expressed genes (DEGs) in normal vs. adenoma, normal vs. CRC, and adenoma vs. CRC, were identified using the Wilcoxon test method in R respectively. The interactive network of DEGs was constructed to select the significant modules using the Pearson's correlation. Meanwhile, transcriptional network of DEGs was also constructed using the g: Profiler. Totally, 2,741 DEGs in normal vs. adenoma, 1,484 DEGs in normal vs. CRC, and 396 DEGs in adenoma vs. CRC were identified. Moreover, function analysis of DEGs in each group showed FcR-mediated phagocytosis pathway in module 1, cardiac muscle contraction pathway in module 6, and Jak-STAT signaling pathway in module 19 were also enriched. Furthermore, MZF1 and AP2 were the transcription factor in module 6, with the target SP1, while SP1 was also a transcription in module 20. DEGs like NCF1, AKT, SP1, AP2, MZF1, and TPM might be used as specific biomarkers in CRC development. Therapy targeting on the functions of these key genes might provide novel perspective for CRC treatment.
    Pathology & Oncology Research 01/2015; DOI:10.1007/s12253-014-9880-9
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    ABSTRACT: Data discussed in recent reviews demonstrated that dysregulation of microRNA (miRNA) expression profiles occurs during cervical carcinogenesis and characteristic up- or downregulation of certain miRNAs might be used as biomarkers. The majority of altered miRNAs, however were found to be inconsistent upon comparison with cancerous and normal cervical epithelia in the discussed studies due to several reasons. The results obtained in this present review suggest the need for further investigations on miRNAs on larger sample sizes in order to indicate sensitivity and specificity by means of well defined, "unified" methods. In addition, obtaining further data on the clinical course and outcome of patients in comparison to the dysregulation of miRNA expression profile could turn miRNAs into prognostic and/or progression markers. Inhibition of overexpressed miRNAs, as suggested by some authors, might even serve as target for cancer therapy.
    Pathology & Oncology Research 01/2015; DOI:10.1007/s12253-014-9871-x
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    ABSTRACT: Anaplastic thyroid cancer (ATC) is a rare but aggressive malignancy of the thyroid. No effective treatment modalities are currently available. Targeted therapy against protein kinases showed promising results in preclinical studies. Our goal was to assess the mutational status of potential therapeutic targets, as well as the biomarker for immunotherapy in the clinical context. Using allele specific PCR, Sanger sequencing, fragment analysis and immunohistochemistry, we assessed BRAF, KRAS, EGFR mutations and protein overexpression of C-KIT and PDL1 in anaplastic thyroid cancer specimens. Results were compared to clinical information and patient outcome to assess the utility of these biomarkers. There were 13 patients in our study with a median overall survival of 19 weeks. Of the 13 ATC patients, 3 (23 %) had BRAF V600E mutation. C-KIT overexpression was found in 1 (8 %) patient who responded well to a tyrosine kinase inhibitor. PDL1 expression was seen in 3 (23 %) patients, none of them were surgical candidates due to unresectability and poor performance status. KRAS codon 12/13 and EGFR exon 18, 19, 20 and 21 were all wild type in our patients. Protein kinase inhibitors and immunotherapy may be useful adjuvant therapies for ATC.
    Pathology & Oncology Research 01/2015; DOI:10.1007/s12253-014-9876-5
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    ABSTRACT: Preterm preeclampsia is associated with the failure of trophoblast invasion, placental hypoxic/ischemic injury and the release of toxic substances, which promote the terminal pathway of preeclampsia. In term preeclampsia, factors yet unknown trigger the placenta to induce the terminal pathway. The contribution of the villous trophoblast to these pathologic events has not been fully elucidated. Here we aimed to study how stress and signaling pathways influence trophoblastic functions in various subforms of preeclampsia. Tissue microarrays (TMAs) were constructed from placentas obtained from pregnant women in the following groups: 1-2) preterm preeclampsia with (n = 8) or without (n = 7) HELLP syndrome; 3) late-onset preeclampsia (n = 8); 4-5) preterm (n = 5) and term (n = 9) controls. TMA slides were stained for phosphorylated Akt-1, ERK1/2, JNK, and p38 kinases, and trophoblastic immunostainings were semi-quantitatively evaluated. BeWo cells were kept in various stress conditions, and the expression of FLT1, GCM1, LEP, and PGF was profiled by qRT-PCR, while Akt-1, ERK1/2, JNK, and p38 kinase activities were measured with phospho-kinase immunoassays. We found that: 1) Placental LEP and FLT1 expression was up-regulated in preterm preeclampsia with or without HELLP syndrome compared to controls; 2) Mean pp38 immunoscore was higher in preterm preeclampsia, especially in cases with HELLP syndrome, than in controls. 3) Mean pERK1/2 immunoscore was higher in preterm preeclampsia with HELLP syndrome than in controls. 4) In BeWo cells, ischemia up-regulated LEP expression, and it increased JNK and decreased ERK1/2 activity. 5) Hypoxia up-regulated FLT1 and down-regulated PGF expression, and it increased ERK1/2, JNK and p38 activity. 6) IL-1β treatment down-regulated PGF expression, and it increased JNK and p38 activity. 7) The p38 signaling pathway had the most impact on LEP, FLT1 and PGF expression. In conclusion, hypoxic and ischemic stress, along with unknown factors, activates trophoblastic p38 signaling, which has a key role in villous trophoblastic functional changes in preterm preeclampsia. The activation of ERK1/2 signaling may induce additional trophoblastic functional changes in HELLP syndrome, while distinct mechanisms may promote late-onset preeclampsia.
    Pathology & Oncology Research 01/2015; DOI:10.1007/s12253-014-9872-9
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    ABSTRACT: Thyroid cancer comprises a heterogeneous group of lesions with great diversity of biological behaviour. Markers which could help clinicians to identify high-risk patients for tailored optimization of clinical management are of crucial importance. HBME-1 protein level was analysed immunohistochemically using routinely prepared archival tissue sections of a broad range of papillary thyroid carcinoma (PTC) variants and in corresponding lymph node metastases (LNM). The results were evaluated in comparison with clinicopathological features of PTC. Positive immunoreaction was noticed in most classical (83/92; 90.2 %), follicular (60/71; 84.5 %) and trabecular (4/5; 80.0 %) variants of PTC. All cases of macrofollicular, Warthin-like and diffuse sclerosing PTC variants were HBME-1 positive (4/4, 3/3, 2/2; 100 % respectively). Tall cell and solid PTC variants showed diversity of staining (2/3; 66.67 % and 13/23; 56.52 % respectively), while PTCs with mixed histological pattern containing insular areas were mainly weakly positive (2/5; 40.0 %). A single case of clear cell PTC variant showed no reaction. Moreover, all matched metastatic PTC into lymph nodes (LNM) were HBME-1 positive (17/17; 100 %) and expressed HBME-1 in a similar pattern to the matched primary tumour. We also found a statistically significant association between high HBME-1 expression and the presence of lymph node metastasis, advanced pT status and pTNM stage (P < 0.05), but only a tendency for association with extrathyroidal invasion of the tumour (P = 0.058). Therefore, we recommend using immunoexpression of HBME-1 as useful mean to increase the likelihood of detecting most PTC variants and to predict some unfavourable clinical parameters in these patients.
    Pathology & Oncology Research 01/2015; DOI:10.1007/s12253-014-9883-6
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    ABSTRACT: One-hundred-fourteen consecutive cases of breast ultrasound-guided 14-gauge needle core biopsy (14G NCB) performed from January 2001 to June 2013 and diagnosed as non-malignant papillary lesion (PL)-B3, were reviewed and compared with definitive histological diagnosis on surgical excision (SE) to evaluate the diagnostic accuracy of ultrasound-guided 14G NCB. PL with epithelial atypia on 14G NCB were associated to malignancy on definitive histological diagnosis on SE in 22 (7 DCIS and 15 invasive carcinomas) of 46 cases with an underestimation rate of 47.8 %, while 9 (4 DCIS and 5 invasive carcinomas) cases out of 68 cases of PL without epithelial atypia were upgraded to carcinoma with an underestimation rate of 13.2 %. In cases of PL with epithelial atypia on ultrasound-guided 14G NCB, SE appears mandatory due to the high risk of associated malignancy. The diagnosis of PL without epithelial atypia on ultrasound-guided 14G NCB does not exclude malignancy at subsequent SE, consequently further assessment (by surgical or vacuum-assisted excision) is recommended to avoid the risk of delaying a diagnosis of malignancy, although this tends to be lower (1 in 8 patients).
    Pathology & Oncology Research 01/2015; DOI:10.1007/s12253-014-9882-7
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    ABSTRACT: Thyroid cancer represents approximately 1% of new cancer and oestrogen may play a role in the pathogenesis of thyroid neoplasm. We aimed to study the clinicopathological criteria and ER expression of thyroid cancer in Mansoura University (Egypt), and to correlate the survival to these clinicopathological data and ER expression. This retrospective study reviewed 644 patients with histologically proven thyroid carcinoma during the period from 2003 to 2011. 152 cases during the period between 2008 and 2011 were retrieved from the archive and examined by immunohistochemistry for oestrogen receptor-α (ER) expression. ER-α expression is significantly associated with the female sex, lymph node metastasis, TNM stage, extrathyroid extension, multifocality disease and recurrence and in the whole series (p 0.5). The same was noticed in papillary carcinoma (PTC) except the gender of the patient. Tumour type, extrathyroid extension and ER expression were the independent prognostic factors of DFS, while in PTC, only ER expression was the independent one. The histological type was the only independent prognostic factor for OAS in the series were studied for ER expression, while extrathyroid extension was the only one that affected OAS of PTC. There was significant positive correlation with lymph node metastasis and ER expression in whole patient and PTC cases. No difference in survival between the low and high ranges of positive oestrogen expression. The prognosis of thyroid carcinoma in Egypt is similar to that occurs worldwide. ER-α expression was a significant prognostic marker for DFS in thyroid cancer and can be used as a predictive factor of lymph node metastasis.
    Pathology & Oncology Research 01/2015; DOI:10.1007/s12253-014-9892-5