Pathology Journal Impact Factor & Information

Publisher: Royal College of Pathologists of Australasia, Lippincott, Williams & Wilkins

Journal description

Pathology is committed to publishing peer-reviewed, original articles related to the science of pathology in its broadest sense, including chemical pathology, experimental pathology, genetics, haematology, histopathology, immunology, microbiology, molecuar pathology and morbid anatomy. Call for Papers Manuscripts to be considered for publication should be submitted to the Editor: Professor C. S. Lee, Editorial Office, Royal College of Pathologists of Australasia, Durham Hall, 207 Albion Street, Surry Hills, NSW 2010, Australia. Tel: +61 2 8356 5858; Fax: +61 2 8356 5828. All submissions will be independently judged by at least two referees. Authors should consult the ' Notes for Contributors ' before sending a manuscript.

Current impact factor: 2.19

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.188
2013 Impact Factor 2.62
2012 Impact Factor 2.657
2011 Impact Factor 2.378
2010 Impact Factor 2.168
2009 Impact Factor 2.673
2008 Impact Factor 2.324
2007 Impact Factor 1.772
2006 Impact Factor 1.643
2005 Impact Factor 1.471
2004 Impact Factor 1.26
2003 Impact Factor 1.112
2002 Impact Factor 0.88
2001 Impact Factor 0.851
2000 Impact Factor 0.994
1999 Impact Factor 0.943
1998 Impact Factor 0.494
1997 Impact Factor 0.395

Impact factor over time

Impact factor

Additional details

5-year impact 2.29
Cited half-life 6.70
Immediacy index 0.66
Eigenfactor 0.00
Article influence 0.70
Website Pathology website
Other titles Pathology (Online)
ISSN 0031-3025
OCLC 41386267
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Lippincott, Williams & Wilkins

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Some journals have separate policies, please check with each journal directly
    • Pre-print must be removed upon acceptance for publication
    • Post-print may be deposited in personal website or institutional repository
    • Publisher's version/PDF cannot be used
    • Must include statement that it is not the final published version
    • Published source must be acknowledged with full citation
    • Set statement to accompany deposit
    • Must link to publisher version
    • NIH authors will have their accepted manuscripts transmitted to PubMed Central on their behalf after a 12 months embargo (see policy for details)
    • Wellcome Trust and HHMI authors will have their accepted manuscripts transmitted to PubMed Central on their behalf after a 6 months embargo (see policy for details)
    • Publisher last reviewed on 19/03/2015
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Few studies have comprehensively analysed histopathological findings of bone marrow clots for diagnosis of haematopoietic cell dysplasia. In particular, a limited number of studies have assessed the use of haematoxylin and eosin (H&E) staining, which is generally considered less informative than May-Giemsa staining. In the current study, the utility of bone marrow clot specimens for diagnosis was examined using H&E staining and immunohistochemistry. Patients with myelodysplastic syndromes (MDS) and myelodysplastic/myeloproliferative neoplasm (MDS/MPN), including chronic myelomonocytic leukaemia (CMML), atypical chronic myeloid leukaemia (aCML) lacking Philadelphia chromosome, and juvenile myelomonocytic leukaemia (JMML), were selected for histological evaluation. H&E stained specimens were advantageous for observation of atypical basophilic staining of the cytoplasm and nucleus related to dysplasia. This finding was significantly supported for both MDS and MDS/MPN (p < 0.05 versus May-Giemsa staining); therefore, we concluded that H&E staining could be used for identification of dysplastic cells. In addition, despite the loss of tissue structure, phosphorylated Stat5 immunostaining was sufficiently useful for the observation of myelodysplastic blasts. Thus, clot specimens are useful for diagnosis of haematopoietic dysplasia by pathologists.
    Pathology 10/2015; 47(7). DOI:10.1097/PAT.0000000000000328

  • Pathology 12/2014; 46(7):579-80. DOI:10.1097/PAT.0000000000000183

  • Pathology 12/2014; 46(7):655-7. DOI:10.1097/PAT.0000000000000171
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    ABSTRACT: Large cell transformation of mycosis fungoides (MF-LCT) occurs in 20-50% of advanced MF, and is generally associated with poor prognosis, although some patients have indolent disease. We sought to identify clinicopathological prognostic factors in a large number of patients with MF-LCT.We identified patients with MF-LCT treated between 1991 and 2012 at a referral centre for cutaneous lymphoma. Clinical and pathological records, and histopathological slides were reviewed. Associations of clinicopathological variables with disease-specific survival were analysed.In 51 patients with MF-LCT, factors significantly associated with shorter survival were: age >60 years (25 versus 61 months, p = 0.01), stage III/IV (25 versus 44 months, p = 0.049), high serum lactate dehydrogenase (LDH; 24 versus 53 months, p = 0.007), absent papillary dermal involvement (8 versus 30 months, p = 0.008); follicular mucin at transformation (24 versus 42 months, p = 0.007); and the absence of fibrosis at transformation (21 versus 42 months, p = 0.03). Patients presenting with transformation at diagnosis had better survival than those who started with a small cell phenotype (p = 0.02). Age >60 years was independently associated with poorer survival (HR 5.61, 95%CI 1.17-26.8, p = 0.03), and the presence of fibrosis at transformation was independently associated with improved survival (HR 0.30, 95%CI 0.09-0.97, p = 0.045).In patients with MF-LCT, clinical features (age, stage, serum LDH) are important in assessing prognosis. Additional clinical and pathological features identified in this study may also assist in prognostic stratification. Studies of larger cohorts should be performed to validate the prognostic significance of these features.
    Pathology 12/2014; 46(7):610-6. DOI:10.1097/PAT.0000000000000166

  • Pathology 12/2014; 46(7):660-2. DOI:10.1097/PAT.0000000000000170
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    ABSTRACT: We report two compound heterozygous mutants that caused severe type I protein C (PC) deficiency in two independent Chinese families.PC antigen was determined by enzyme-linked immunosorbent assay (ELISA), and PC activity was measured by chromogenic assay. Genetic mutations were screened with polymerase chain reaction (PCR) followed by direct sequencing. PC mutants were transiently expressed in COS-7 cells for the evaluation of PC secretory activity and function. The subcellular location was visualised by immunofluorescence assay. The structural analysis of mutation was performed as well.Compound heterozygous mutations of Arg178Trp and Asp255His with reduced PC activity and antigen levels were identified in Proband 1, a 28-year-old male with deep vein thrombosis (DVT) and pulmonary embolism. The other mutations of Leu-34Pro and Thr295Ile with reduced PC activity and antigen levels were identified in Proband 2, a 19-year-old male with DVT. The PC activities with Arg178Trp, Asp255His, Leu-34Pro and Thr295Ile mutations decreased significantly. Immunofluorescence assay demonstrated that only trace amount of PC with novel Thr295Ile mutation was transported to the Golgi apparatus. Subsequent structural analysis indicated severe impairments of intracellular folding and secretion.The two rare compound heterozygous mutations could cause type I PC deficiency via impairment of secretory activity of PC.
    Pathology 12/2014; 46(7):630-5. DOI:10.1097/PAT.0000000000000165
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    ABSTRACT: It is important to identify the sites of aldosterone biosynthesis in the adrenal glands, especially those involved in primary aldosteronism (PA). CYP11B2 catalyzes the last step of aldosterone biosynthesis but its close similarity to CYP11B1 has made it difficult to generate specific antibodies that distinguish between these two highly homologous cytochromes. We have recently produced specific monoclonal antibodies against CYP11B2. In addition, we have also produced the specific antibodies against 3BHSD 1/2, which is also the pivotal step in aldosterone biosynthesis. In 3BHSD, type 1 is the predominant form in idiopathic hyperaldosteronism (IHA) with diffuse glomerulosa hyperplasia but type 2 dominant in aldosterone producing adenoma (APA). Many of micro APA expressed 3BHSD2 and CYP11B2 with the absence of c17 and CYP11B1, which could explain the cause of hyperaldosteronism despite the small size of the lesions. In addition, many of the adrenals manifesting PA without discernible lesions demonstrated multiple clusters or nodules of cortical cells demonstrating the similar enzyme expression patterns as in micro APA. These results indicated that UMN or unilateral multiple nodules cases resulting in APA are much higher than previously considered.
    Pathology 10/2014; 46 Suppl 2:S14. DOI:10.1097/01.PAT.0000454095.30256.11
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    ABSTRACT: The experience of a 12-year long cooperation between the Pathology Department of the NICR in Dhaka/Bangladesh via the iPath Internet platform and consultants from Basle/Switzerland and Dresden/Germany confirmed that telecytology is a valuable learning tool in more than one direction. It offered the chance to this institution to improve the technical skills in cytology and opened the opportunity to get second opinions from experts. So very good FNA, fixation and staining techniques were achieved. The consultants had the opportunity to see many unusual nosological entities rarely seen in European centers. One example is hepatocellular carcinoma, which occurs much more frequently in an Asian country than in Europe. A cooperative study of our group on space occupying lesions of the liver showed an accuracy of the telemedical diagnoses of about 80%, which is in the range of other studies on various cytological materials. The study also showed that the accuracy of the telemedical diagnosis depends mainly on the number of the typical cytological HCC indicators expressed by a tumor. It could be shown by another study on images from optimally elaborated specimens from various organic sites, that the accuracy of telemedical diagnoses depends less on the grade of experience of the consulting pathologist than on the variety of tumors to be expected in a topographical region and on the intricate and overlapping morphology of tumors, what can only be overcome with immunochemical and other supportive tests. Finally, the collection of images from a large number of even rare nosological entities in such iPath folders as that of the Bangladesh discussing group makes telecytology a great learning tool for all pathologists, not only for those from underserved countries.
    Pathology 10/2014; 46 Suppl 2:S7. DOI:10.1097/01.PAT.0000454067.38772.22
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    ABSTRACT: Giant cell fibroblastoma is a rare fibroblastic tumor occurring mainly in young patients. Back of thigh, inguinal region and chest wall are the most common sites of involvement. The tumor is characterized by a locally aggressive behavior with no reported metastatic potential. Microscopically, it is composed of spindle cells with a moderate degree of nuclear pleomorphism that infiltrate deep dermis and subcutis. A distinctive feature of this tumor is the presence of peculiar pseudovascular spaces lined by a discontinuous row of multinucleated cells. Features very similar to dermatofibrosarcoma protuberans can be seen. Immunohistochemically, it shows positive staining for CD34, while being negative for S-100 protein and vascular markers. The molecular changes are overlapping with dermatofibrosarcoma protuberans. A case of giant cell fibroblastoma will be presented illustrating the clinicopathological and molecular features of this tumor.
    Pathology 10/2014; 46 Suppl 2:S11. DOI:10.1097/01.PAT.0000454081.24418.b4
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    ABSTRACT: Digital technology marked the first decade of the 21st century with the advent of whole slide imaging (WSI). Thanks to the invention of digital scanners, WSI technology enables the creation and permanent storage of high resolution images from traditional glass slides. The application of digital pathology has recently been explored within the subspecialty of renal pathology for teaching, pathology-based clinical trials, development of new classification systems, and in support to systems biology-based research in a setting of large consortia. Although an initial investment is required, several general advantages can be listed in support of its application, ultimately resulting in a more neutral budget: 1) enables the anywhere-anytime remote access model; 2) permanent storage of glass slides images, which otherwise with time may fade, get lost or broken; 3) allows annotation of specific structures for teaching, consultation, histology-based research or reproducibility studies; 4) archiving; 5) provide full transparency for regulatory agencies during clinical trials or for research protocols; 6) facilitate training of multiple students looking at the same annotated structures, whether in the classroom, during webinar sections or independent review. This presentation will highlight the current status of digital nephropathology applications in training, clinical and molecular research, and industry-sponsored clinical trials.
    Pathology 10/2014; 46 Suppl 2:S15. DOI:10.1097/
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    ABSTRACT: Primary mesenchymal tumors represent a rare subset of hepatic lesions with overlapping spindle cell morphology. These lesions pose unique diagnostic challenges for pathologists as they are infrequently seen in general practice and can be easily mistaken for their benign counterparts or mimickers. In the current era of personalized medicine, precise pathologic diagnosis of these lesions is critically important to guide targeted therapy. This expectation is difficult to meet when pathologists face uncommon lesions outside their scope of experience. This challenge is further exacerbated when interpreting small biopsy samples.In this lecture, we first present the clinicopathological features of 6 typical cases: inflammatory pseudotumor, angiomyolipoma, epitheleioid hemagioendothelioma, malignant fibrous histiocytoma, leiomyosarcoma, and follicular dendritic cell sarcoma. On each case, the focus of discussion is on the morphology characteristics and how to differentiate them from metastatic tumors, non-neoplastic lesions and other types of primary spindle cell neoplasms. We then outline a practical diagnostic approach based on the unique features of each entity. This lecture provides a comprehensive guidance to general pathologists and pathology trainees on how to navigate through this group of seemingly complex entities and to arrive at a specific diagnosis.
    Pathology 10/2014; 46 Suppl 2:S23. DOI:10.1097/01.PAT.0000454128.81835.fd
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    ABSTRACT: NGS is a new approach used to identify genetic mutations that may underline kidney disease. The advantages of NGS compared to Sanger sequencing are the ability to run multiple samples simultaneously, shorter turn-around time and lower cost. For example, compared to older methods that took weeks to complete, NGS can shorten the turn-around time for Alport syndrome diagnosis to just 6 days and the cost to 40%. In addition custom NGS can be designed to identify mutations in a selected group of genes associated with proteinuria and FSGS on renal biopsy. FSGS can be a histologic manifestation of a variety of glomerular diseases including specific podocyte gene mutations (NPHS2, PLC1E, CD2AP, TRPC6) but also glomerular basement membrane abnormalities due to COL4A3-5 mutations. Using custom designed NGS on 14 patients and 19 selected genes, we have identified novel and rare mutations in COLA3, COLA4 AND COLA5, but also mutations in LAMA5 in patients phenotyped as FSGS. Other patients with FSGS were found to have a 6p deletion in APOL1 that is known to be associated with the development of FSGS in African Americans. In this cohort, some patients had congenital hydronephrosis and VUR induced proteinuria. There was no history of familial disease. One of these patients unexpectedly was found to have a novel COLA3 mutation in addition to an expected SALL2 mutation known to be associated with urinary tract developmental anomalies. NGS results were verified using Sanger sequencing. The findings in this study suggest that NGS is a powerful method to identify specific structural changes in the genome that could not have been predicted by the histopathological phenotype. A high throughput approach for mutation analysis is more advantageous compared to single gene approaches and promises to become a clinically useful diagnostic tool.
    Pathology 10/2014; 46 Suppl 2:S39-S40. DOI:10.1097/01.PAT.0000454222.14383.98
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    ABSTRACT: Hypocomplementemic urticarial vasculitis syndrome (HUVS) is a rare immune-complex small vessel systemic vasculitis involving kidney in about 50% of patients. Characteristic clinical features are recurrent urticaria, decreased serum complement, skin vasculitis, arthritis, eye inflammation, abdominal pain, glomerulonephritis and positive anti-C1q antibodies. We report a 36-year-old woman with a 12-year history of recurrent urticaria and 2 years of urticarial vasculitis. On admission, she also had arthritis, pleuritis and pericarditis, abdominal pain, pathologic urinalysis, low serum values of C3, C4 and CH50. All immunoserology was negative except for ANA 1:80 and anti-C1q 620 IU. 'Full-house' immune complex vasculitis was demonstrated in skin and lung biopsies. A kidney biopsy showed diffuse proliferative segmental active and sclerosing glomerulonephritis with mesangial and endocapillary proliferation, neutrophil exudation, necrosis, extracapillary crescents and segmental and global glomerulosclerosis. 'Full-house' glomerular and extensive extraglomerular vascular and tubulointerstitial immune deposits with dominant IgG, C3 and C1q were noted by immunofluorescence. Electron microscopy revealed electron dense deposits with an ultrastructural 'fingerprint' pattern in the glomerular mesangium, transmembranous in capillary walls and in the arteriolar wall. Our patient fulfilled the criteria for HUVS and SLE, in accordance with the not infrequent clinical and immunoserological overlapping of the two diseases.
    Pathology 10/2014; 46 Suppl 2:S41-S42. DOI:10.1097/01.PAT.0000454230.52501.d8
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    ABSTRACT: Ameloblastic fibrosarcoma (AFS) of odontogenic origin involving mandible is very rare, which is the malignant counterpart of ameloblastic fibroma with fibrosarcomatous differentiation in mesenchymal stroma admixed with benign ameloblastic epithelium. A 27-year-old white male presented with a rapidly expanding radiolucent mandibular body mass. Extraoral examination revealed a large firm swelling in the region of the left mandibular body. No associated lymphadenopathy or sensory/motor neurological impairment. Mandibular function and range of motion were normal. Intraoral examination revealed buccal expansion in the body of the left mandible with normal overlying mucosa. There was no abnormal mobility or displacement of the associated dentition. Radiograph demonstrated a radiolucent, multi-locular lesion with ill defined borders. CT scan displayed a bulky, erosive and enhancing lesion of the body and ramus of the mandible. Biopsy was performed and was diagnosed as AFS. The patient was successfully treated with a composite resection of the affected mandible and immediate fibular free flap reconstruction.This case review provides detailed pathological diagnostic features and differentials. Aggressive treatment of AFS, including resection with negative margins is the treatment of choice.
    Pathology 10/2014; 46 Suppl 2:S18. DOI:10.1097/01.PAT.0000454111.11437.36
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    ABSTRACT: Tuberculosis (TB), a multi-systemic disease with myriad presentations and variable manifestations, is endemic in almost every part of the world and continues to remain the most common cause of infectious diseaserelated mortality and morbidity. The infection occurs most often via the pulmonary route through aerosols, producing pulmonary and/or extra-pulmonary disease. A remarkable feature of the organism M. tuberculosis is its ability to lie dormant within alveolar macrophages/granulomas that leads to active disease in 5-10% of immune-competent individuals; the endogenous reactivation usually causes abnormalities in the upper lobes of one or both lungs. Now, there has been a rise of progressive disease due to overt immune-suppression and emergence of drug-resistant strains. In the recent years, at autopsy, we have noted a definite affinity of the organisms for the intra-parenchymal bronchial tree with prominent or sole broncho-centric inflammation. The bronchial spread is often associated with consolidations (often in the lower lobes) and vasculitis. Many of the cases of miliary lesions are associated with diffuse alveolar damage and organizing pneumonia.
    Pathology 10/2014; 46 Suppl 2:S37. DOI:10.1097/01.PAT.0000454211.20221.d7
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    ABSTRACT: A wide variety of histologic prognostic parameters have been proposed for renal cell carcinoma and of these tumor morphotype, tumor grade, sarcomatoid and rhabdoid differentiation, and tumor necrosis were accepted as having utility in clinical practice by the Consensus Conference on Renal Neoplasia assembled by the International Society of Urological Pathology in Vancouver in 2012. With respect to morphotype it was determined that both papillary and chromophobe RCC have a more favourable prognosis than clear cell RCC, while collecting duct RCC was recognised as having a poor prognosis. At the conference it was agreed that for clear cell and papillary RCC grading should based on nucleolar prominence alone for grade 1 to 3 tumours, and that grade 4 tumors should be defined by the presence of extreme nuclear pleomorphism, tumor giant cells and/or rhabdoid/sarcomatoid differentiation. It was further agreed that chromophobe RCC should not be graded. For necrosis there was consensus that the presence or absence of tumour necrosis should be routinely included in the histological report and that this should be based upon both macroscopic and histological examination. There was also consensus that the area of necrosis should be recorded as a percentage of the total tumour area.
    Pathology 10/2014; 46 Suppl 2:S44. DOI:10.1097/
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    ABSTRACT: Bone-forming lesions and cartilage-forming lesions are the most common primary tumors of the bone. They are classified according to their biological potential as benign (chondroblastoma, chondromyxoid fibroma, enchondroma, osteochondroma, periosteal chondroma) and malignant (chondrosarcoma, clear cell chondorsarcoma, mesenchymal chondrosarcoma, dedifferentiated chondrosarcoma) and as to their anatomic location (central/intramedullary, or peripheral and periosteal). Radiographic and histologic features are the cornerstone reaching a diagnosis. Problems: poor inter-observer reproducibility in: 1) Transformation and distinction between benign (enchondroma) and malignant (low grade chondrosarcoma). 2) Different results in the treatment of low grade chondrosarcoma according to the anatomic locations (axial vs appendicular skeleton). Genetic findings: molecular markers increasingly used in the diagnosis of cartilaginous neoplasms: 1) IDH 1-2 mutations are frequent events in cartilaginous neoplasms (negative in osteosarcomas). 2) Mutation of COL2A1 in chondrosarcomas.
    Pathology 10/2014; 46 Suppl 2:S5. DOI:10.1097/01.PAT.0000454060.23525.07