The utility of napsin‐A in the identification of primary and metastatic lung adenocarcinoma among cytologically poorly differentiated carcinomas

Stoll, Lisa; Johnson, Michael W.; Gabrielson, Edward; Askin, Fredrick; Clark, Douglas P.; Li, Qing Kay

doi:10.1002/cncy.20108

Cited by 98 publications

(111 citation statements)

References 24 publications

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“…Naps-A was expressed in 4 TTF1À cases (that had CK7 expression only), supporting its role as an additional ADC marker. 25 In TTF1À tumors, coexpression of DSC-3 and p63 supported a diagnosis of SQCC (confirmed in 72.7% of cases at surgery), and proved highly specific for SQCC (SP ¼ 1), irrespective of p63/p40 reactivity. DSC-3 was never seen in association with TTF1, with the exception of the adenosquamous carcinoma having a composite differentiation.…”

Section: Discussionmentioning

confidence: 80%

Immunohistochemical subtyping of nonsmall cell lung cancer not otherwise specified in fine‐needle aspiration cytology

Righi

Graziano

Fornari

et al. 2011

Cancer

134

132

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BACKGROUND: Histopathological subtyping of nonsmall cell lung cancer (NSCLC) is currently relevant in treatment decision because of a differential activity of specific therapeutic agents. Immunohistochemistry highlights cell differentiation lineages and, in this study, it was applied to maximize the proportion of accurately subtyped NSCLC not otherwise specified (NOS) on fine-needle aspiration cytology (FNAC) samples. METHODS: Cell blocks from 103 FNAC samples with a morphological diagnosis of NSCLC-NOS were immunostained for cytokeratin (CK) 7, CK5, TTF1, and p63, whereas p40, napsin A (Naps-A), and desmocollin-3 (DSC-3) were only assessed in a subgroup of cases with discordant (CK7 and TTF1þ for nonsquamous, CK5 and p63þ for squamous) findings. Results were correlated with surgical specimens evaluated by morphology alone. RESULTS: Thirty-seven (36%) tumors with CK7/TTF1þ and CK5/p63À corresponded to 35 cases of adenocarcinoma (ADC) and 2 cases of large cell carcinoma, whereas 9 (9%) cases with the reverse immunoprofile were squamous cell carcinoma (SQCC) at surgery (P < .001). Although the remaining 57 cases had different marker combinations, a correlation was found with ADC histology for TTF1þ samples (independent of other markers) and with SQCC for p63þ/TTF1À immunophenotype (P < .001). p40 was never expressed in p63þ ADC, whereas Naps-A was restricted to ADC and DSC-3 to SQCC lineage. The percentage of unclassified NSCLC-NOS decreased from 36% to 14%. Combinations of 2 antibodies (TTF1/DSC-3 or p63/Naps-A) in the same section allowed diagnostic optimization in scant cytological samples. CONCULSIONS: This 4-antibody panel approach may contribute to refine lung cancer classification in FNAC cell blocks, remarkably reducing the NSCLC-NOS diagnostic category. Cancer 2011;117:3416-

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Section: Discussionmentioning

confidence: 80%

Immunohistochemical subtyping of nonsmall cell lung cancer not otherwise specified in fine‐needle aspiration cytology

Righi

Graziano

Fornari

et al. 2011

Cancer

134

132

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“…Studies using a monoclonal napsin A antibody to distinguish primary pulmonary from nonpulmonary tumors have reported high specificity. 5,11,12,14 We used a polyclonal napsin A antibody and observed decreased specificity, with napsin A expressed in 48% of extrapulmonary mucinous tumors. One other study has used the same polyclonal antibody used in our study, although with different results.…”

Section: 711-13mentioning

confidence: 99%

Polyclonal Napsin A Expression: A Potential Diagnostic Pitfall in Distinguishing Primary From Metastatic Mucinous Tumors in the Lung

Heymann

Hoda

Scognamiglio

2014

Archives of Pathology &Amp; Laboratory Medicine

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Context.-Napsin A is a useful marker for distinguishing primary from metastatic lung tumors. Mucinous lung tumors may be difficult to distinguish from metastatic mucinous tumors.Objectives.-To evaluate napsin A expression in lung and extrapulmonary mucinous tumors on both histology and cytology specimens and to determine napsin A's utility in differentiating primary from metastatic mucinous tumors.Design.-Napsin A immunohistochemistry was performed using a rabbit polyclonal antibody on formalinfixed, paraffin-embedded surgical and fine-needle aspiration biopsy-derived, paraffin-embedded cell block specimens. Positive expression was defined as coarse, granular, cytoplasmic staining in 10% or more of tumor cells.Results.-Sixteen of 32 mucinous lung tumors (50%) and 16 of 33 extrapulmonary mucinous tumors (48%), including 15 of 18 of gastrointestinal origin (83%), expressed napsin A. Positivity was concordant between surgical and cell block specimens in 5 of 9 cases (56%). In 3 of 4 discordant cases, napsin A expression was detected on the surgical specimen but not the cell block. The cell block material in these cases was paucicellular.Conclusions.-Napsin A shows decreased sensitivity and specificity for mucinous lung tumors and is unlikely to be reliable as a sole immunohistochemical marker of lung origin for such tumors (52% specificity in this study). The high frequency of napsin A expression in gastrointestinal mucinous tumors makes it particularly unreliable in distinguishing metastatic gastrointestinal from primary lung mucinous tumors. However, napsin A expression analysis may facilitate distinguishing mucinous tumors of pulmonary from those of nongastrointestinal origin. Interpretation of napsin A staining may be problematic in mucinous tumor specimens of low cellularity such as cell blocks.

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“…Studies have shown that thyroid transcription factor 1 (TTF-1) and napsin A are specific markers for primary lung adenocarcinoma (31,32), and that cytokeratin 20 (CK20) and caudal type homeobox 2 (CDX2) positivity supported the diagnose of primary pancreatic cancer (30); however, the positivity rate of TTF-1 and Napsin A is low. Krasinskas et al (30) reported that KRAS G12C mutations, TTF-1 and napsin A are associated with primary lung adenocarcinoma, whereas KRAS G12R mutations, CK20 and CDX2 are more common in pancreatic adenocarcinoma.…”

Section: Discussionmentioning

confidence: 99%

Clinical diagnosis and detection of genetic mutations of pancreatic metastases: A report of four cases and review of the literature

Zhang

et al. 2017

Oncology Letters

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Abstract. The present study aimed to report our clinical experience regarding the diagnosis and detection of genetic mutations of pancreatic metastases, and to review the relevant literature to expand knowledge of this disease. A total of 4 cases involving pancreatic metastases, which were treated at The First Affiliated Hospital of Soochow University between January 2013 and July 2016, were retrospectively analyzed. This retrospective study considered the clinicopathological variables of the 4 patients, and compared this data with those from the literature, which was searched using PubMed, EMBASE and the Cochrane Library. All 4 patients with pancreatic metastases were diagnosed by computed tomography (CT) scan and confirmed by pathological staining and immunohistochemistry. Mutation analysis was performed in 3 patients to obtain precise mutation information for guiding and evaluating the use of molecularly targeted drugs. In summary, pancreatic metastases are rare and the majority of pancreatic metastases develop from renal cell carcinoma. Diagnoses of pancreatic metastases predominantly rely on CT, pathology and immunohistochemistry. Detection of mutations has clinical value in auxiliary diagnosis and therapy of pancreatic metastases. Based on mutation information, molecularly targeted drugs may prolong the survival of patients with unresectable pancreatic metastases. IntroductionPancreatic metastases are rare. Metastases are reported to account for 2-5% of all malignant lesions occurring in the pancreas (1-5). Studies have reported that people of ~60 years old are at high risk of developing pancreatic metastases (1-3). Metastases to the pancreas may occur a significant amount of time subsequent to diagnosis and management of the primary tumor (3). Primary tumors that may give rise to pancreatic metastases include renal cell carcinoma (RCC), non-small cell lung carcinoma, melanoma, sarcoma and colorectal carcinoma. Previous studies have indicated that the kidney may be more common than the lung as a primary tumor site of metastases to the pancreas (1,4). Symptoms of pancreatic metastases are often not apparent, and these lesions are thus detected incidentally by physical examination in the majority of cases (6). Abdominal computed tomography (CT) scan and magnetic resonance imaging (MRI) examinations can be used in the differential diagnosis of pancreatic lesions (7). Pathological analysis is the gold standard in the diagnosis of pancreatic metastases (8). However, occasionally it is difficult to diagnose pancreatic metastasis based on pathology alone (9).In recent years, pancreatic metastases have been observed with increasing frequency, particularly at high-volume pancreatic surgery centers, due to increased utilization of advanced imaging methods, including ultrasonography, CT, MRI and endoscopic ultrasonography (EUS) (10). However, the treatment for pancreatic metastases remains controversial. The majority of patients with pancreatic metastases are in the advanced stages of primary disease (11); however, t...

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The utility of napsin‐A in the identification of primary and metastatic lung adenocarcinoma among cytologically poorly differentiated carcinomas

Cited by 98 publications

References 24 publications

Immunohistochemical subtyping of nonsmall cell lung cancer not otherwise specified in fine‐needle aspiration cytology

Immunohistochemical subtyping of nonsmall cell lung cancer not otherwise specified in fine‐needle aspiration cytology

Polyclonal Napsin A Expression: A Potential Diagnostic Pitfall in Distinguishing Primary From Metastatic Mucinous Tumors in the Lung

Clinical diagnosis and detection of genetic mutations of pancreatic metastases: A report of four cases and review of the literature

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