Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001418 (adenocarcinoma)
 68,496 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two cases of a distinctive variety of basaloid squamous carcinoma (BSC) of the anal canal are described. Both occurred in female patients who presented with bleeding per rectum. Histologic evaluation of the tumors showed lobules and aggregates of medium-sized basaloid cells with distinctive peripheral palisading and focal areas of central, comedo-necrosis. Accompanying dysplasia of the overlying squamous mucosa was absent. However, the microscopic pattern was dominated by the presence of eosinophilic, hyaline, paucicellular basement membrane-like material around and within tumor nests. This appearance together with microcystic spaces simulated that of an adenoid cystic carcinoma. Immunohistochemistry of the tumors revealed the following profile: CK7, CK5/CK6, 34betaE12 positive, CK14 focally positive but CK20 negative. The following were all negative: EMA, CEA, smooth muscle and muscle-specific actin, calponin, and S-100. The tumor cells exhibited diffuse nuclear positivity with p63. The eosinophilic basement membrane hyaline material was positive for collagen type IV and also for laminin. BSC of the anal canal with an adenoid cystic pattern is an infrequently encountered and reported variant, although it is seen more often in the aerodigestive tract. There may be an increased propensity for BSC with an adenoid cystic pattern to metastasize to the liver, but the number of cases encountered are too small to be definitive. The histologic differential diagnosis is true salivary gland-type adenoid cystic carcinoma and basal cell adenocarcinoma. Immunohistochemistry and awareness of this unusual pattern of BSC will facilitate the correct diagnosis being reached.
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PMID:Basaloid squamous carcinoma of the anal canal with an adenoid cystic pattern: histologic and immunohistochemical reappraisal of an unusual variant. 1632 41

Morules develop in several neoplasms and have been considered as a type of squamous metaplasia despite the absence of keratinization and intercellular bridges. The objective of this study was to clarify the pathological significance of morules and to distinguish morules from squamous metaplasia in colonic neoplasms. Ten cases of morule-associated colonic neoplasms (4 adenocarcinomas, 1 adenoma with carcinoma in situ, and 5 adenomas), and 3 cases of squamous metaplasia in colonic adenocarcinoma were examined morphologically and immunohistochemically. Morules were well-defined structures composed of small, oval to short-spindled cells with bland nuclei, and frequently associated with intranuclear inclusions that were positive for biotin and biotin-binding enzymes (pyruvic acid carboxylase and propionyl CoA carboxylase). On immunohistochemical examination, morules characteristically showed nuclear overexpression of beta-catenin, cyclin D1 and p63, low Ki-67 labeling index (<1%), cytoplasmic overexpression of CD10, and no expression of cytokeratin 20. These molecules were useful for the differentiation of morules. Furthermore, p63 and 34betaE12 positivities in morules suggested that they have a basal/stem cell phenotype. Thus, morules were morphologically and qualitatively different from squamous metaplasia. We consider that morules in colonic neoplasms are cell clusters with a basal/stem cell phenotype, and have less proliferative and less invasive potential than other cancer cells.
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PMID:Immunohistochemical analysis of morules in colonic neoplasms: morules are morphologically and qualitatively different from squamous metaplasia. 1637 71

Immunohistochemistry (IHC) can play an important role in diagnostic surgical pathology of the prostate. Basal cell markers, such as the 34betaE12 antibody and antibodies directed against cytokeratin 5 and 6 or p63, are very useful for demonstration of basal cells as their presence argues against a diagnosis of invasive prostatic carcinoma (PC). However, several benign mimickers of PC, including atrophy, atypical adenomatous hyperplasia (AAH), nephrogenic adenoma, and mesonephric hyperplasia, can stain negatively with these markers, and thus, a negative basal cell marker immunostain alone does not exclude a diagnosis of benignancy. Although there are examples in the literature of high grade PC that stain focally with some of the basal cell markers, these cases are usually readily diagnosed based on H&E appearances and are unlikely to be confused with these benign mimickers. Alpha-methylacyl-coenzyme-A racemase (AMACR) is a sensitive marker of PC (except for a few uncommon variants: atrophic, foamy gland, and pseudohyperplastic variants), and its detection by immunohistochemical staining in atypical prostatic lesions can be very useful in confirming an impression of adenocarcinoma. AMACR expression can also be identified in high grade prostatic intraepithelial neoplasia (PIN), prostatic atrophy, AAH, and benign prostatic glands, and accordingly, a diagnosis of PC should not be based solely on a positive AMACR immunostain, especially when the luminal staining is weak and/or noncircumferential. The use of AMACR/basal cell antibody cocktails has been found to greatly facilitate the distinction between PC and its benign mimickers, especially when only limited tissue is available for staining. Prostate specific antigen (PSA) and prostate specific acid phosphatase (PSAP) are both quite sensitive and fairly specific markers of PC (there are a few nonprostatic tumors that can express one or both), and are both very helpful in establishing or confirming the diagnosis of PC when the differential diagnosis includes other tumors that can involve the prostate such as urinary bladder urothelial carcinoma. 34betaE12, p63, thrombomodulin, and uroplakin III are additional urothelial associated markers useful in this differential diagnosis. CDX2 and villin are useful markers to diagnostically separate colonic adenocarcinoma from PC. AMACR positivity and negative basal cell marker reactions are useful to confirm the presence of residual PC after hormonal or radiation therapy. Pan-cytokeratin, PSA, and PSAP can also highlight subtle infiltrates of PC with hormonal or radiation therapy effect. PSA and PSAP immunohistochemical stains are valuable in confirming metastatic carcinoma as being of prostatic origin and should always be utilized in the diagnostic evaluation of metastatic adenocarcinoma of unknown primary origin in males.
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PMID:Immunohistochemistry in diagnostic surgical pathology of the prostate. 1651 1

Typically glands of prostatic adenocarcinoma have a single cell lining, although stratification can be seen in invasive carcinomas with a cribriform architecture, including ductal carcinoma. The presence and diagnostic significance of stratified cells within non-cribriform carcinomatous prostatic glands has not been well addressed. The histomorphological features and immunohistochemical profile of cases of non-cribriform prostatic adenocarcinoma with stratified malignant glandular epithelium were analyzed. These cases were identified from needle biopsy cases from the consultation files of one of the authors and from a review of 150 consecutive in-house needle biopsy cases of prostatic adenocarcinoma. Immunohistochemistry was performed utilizing antibodies reactive against high molecular weight cytokeratin (34betaE12), p63 and alpha-methylacyl-coenzyme-A racemase (AMACR). A total of 8 cases were identified, including 2 from the 150 consecutive in-house cases (1.3%). In 4 cases, the focus with glands having stratified epithelium was the sole carcinomatous component in the biopsy, while such a component represented 5-30% of the invasive carcinoma seen elsewhere in the remaining cases. The main attribute in all these foci was the presence of glandular profiles lined by several layers of epithelial cells with cytological and architectural features resembling flat or tufted high-grade prostatic intraepithelial neoplasia, but lacking basal cells as confirmed by negative 34betaE12 and/or p63 immunostains in all cases. The AMACR staining profile of the stratified foci was variable, with 4 foci showing positivity, and 3 foci being negative, including two cases that displayed AMACR positivity in adjacent non-stratified prostatic adenocarcinoma. Prostatic adenocarcinoma with stratified malignant glandular epithelium can be identified in prostate needle biopsy samples harboring non-cribriform prostatic adenocarcinoma and resembles glands with high-grade prostatic intraepithelial neoplasia. These 'PIN-like' carcinomas can present in pure form. Recognition of this pattern of prostatic adenocarcinoma is necessary to correctly diagnose such cases as invasive carcinoma.
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PMID:Stratified epithelium in prostatic adenocarcinoma: a mimic of high-grade prostatic intraepithelial neoplasia. 1660 76

Adenocarcinoma of the prostate comprises 95% of all prostate cancer. Commercially available primary cultures of "normal" prostate epithelial cells, PrECs, have been used as a convenient model to investigate neoplastic transformation. Here PrECs were characterized for the expression of lineage- and developmental-specific markers cytokeratin (CK) 8 and 18, p63, chromogranin A, TMEPAI, S100P, NKX 3.1, ANKH, and FN 1 as well as androgen receptor and prostate-specific antigen by Western blot and Northern blot analyses, immunohistochemistry, reverse transcriptase-polymerase chain reaction (RT-PCR), and quantitative real-time PCR. Immunohistochemical staining detected PrECs positive in varying degrees for p63, CK 8, and CK 18, with only the rare cell being positive for chromogranin A. The PrECs also tested positive for p63 protein by Western blot analysis. RT-PCR with PrEC cDNA showed products for FN 1 and S100P but not for ANKH and androgen receptor or prostate-specific antigen. This profile of markers in PrEC cells is consistent with that expected for pubertal prostate epithelial cells.
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PMID:Molecular analysis and characterization of PrEC, commercially available prostate epithelial cells. 1661 9

In this study, we sought to validate the importance of p63, CK5/CK6, CK7, and surfactant-A (SP-A) to classify 42 non-small cell lung cancers in autopsy and surgical resection specimens and to study the usefulness of these markers in distinguishing between squamous cell carcinomas and adenocarcinomas because of their different implications regarding treatment and prognosis. All adenocarcinoma cases were negative for p63; 9 (56.2%) of 16 were CK5/CK6 positive, 16 (94.1%) of 17 were CK7 positive, and 4 (26.6%) of 15 were SP-A positive. In squamous cell carcinoma, 1 case was CK7 and SP-A positive and 14 (77.8%) of 18 were p63 positive. The latter appears to be useful in differentiating squamous cell carcinoma from adenocarcinoma of the lung in small biopsies without keratinization or glandular differentiation; thus, for advanced-stage cases, where there is no possibility of surgical resection and the treatment of choice is radiotherapy plus chemotherapy, we would be able to differentiate between the two histological types, establishing then a different therapy.
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PMID:Expression of p63, keratin 5/6, keratin 7, and surfactant-A in non-small cell lung carcinomas. 1664 51

Lung cancer is the leading cause of cancer mortality worldwide. With the recent success of molecularly targeted therapies in this disease, a detailed knowledge of the spectrum of genetic lesions in lung cancer represents a critical step in the development of additional effective agents. An integrated high-resolution survey of regional amplifications and deletions and gene expression profiling of non-small-cell lung cancers (NSCLC) identified 93 focal high-confidence copy number alterations (CNAs), with 21 spanning less than 0.5 Mb with a median of five genes. Most CNAs were novel and included high-amplitude amplification and homozygous deletion events. Pathogenic relevance of these genomic alterations was further reinforced by their recurrence and overlap with focal alterations of other tumor types. Additionally, the comparison of the genomic profiles of the two major subtypes of NSCLC, adenocarcinoma (AC) and squamous cell carcinoma (SCC), showed an almost complete overlap with the exception of one amplified region on chromosome 3, specific for SCC. Among the few genes overexpressed within this amplicon was p63, a known regulator of squamous cell differentiation. These findings suggest that the AC and SCC subtypes may arise from a common cell of origin and they are driven to their distinct phenotypic end points by altered expression of a limited number of key genes such as p63.
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PMID:Common and contrasting genomic profiles among the major human lung cancer subtypes. 1686 34

The aim of this study was to investigate the role of TAp63 and DeltaNp63 isoforms in uterine cervical cancers. The messenger RNA (mRNA) and protein expressions of TA and DeltaN forms as well as alpha, beta, and gamma isoforms of p63 were studied in seven SiHa, ME-180, SNU17, SNU902, SNU1160, SNU703, and SNU1299 human papillomavirus (HPV)-positive uterine cervical squamous cell carcinoma (SCC) cell lines, one HT3 HPV-negative SCC cell line, and one HeLa adenocarcinoma cell line using reverse transcription-polymerase chain reaction (RT-PCR) and western blotting. Fresh nonneoplastic and neoplastic tissues of uterine cervical and endometrial cancers were also studied. RT-PCR for TA and DeltaN form and three isoforms of p63 showed positive bands for both TA and DeltaN forms and for all three isoforms in cervical cancer cell lines but weak band for alpha isoform in HPV-negative HT3 SCC cell line and no band for beta isoform in HeLa adenocarcinoma cell line. RT-PCR for TA and DeltaN and three isoforms of p63 mRNA in tissue samples showed positive bands in almost all samples, except for gamma isoform, the expression was weak or absent in nonneoplastic tissues compared with neoplastic tissues. In western blotting, cancer cell lines and both nonneoplastic and neoplastic tissue samples showed expression of TA and DeltaN, and gamma isoform but beta isoform expression with or without alpha isoform was only found in cancer cell lines and neoplastic tissues. beta isoform, possibly of DeltaNp63, may be considered as an important isoform in uterine cervical squamous cell carcinogenesis.
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PMID:Reverse transcription-polymerase chain reaction and western blotting analysis for detection of p63 isoforms in uterine cervical cancers. 1688 78

It was reported that 15 of 19 consultation cases of prostatic partial atrophy were a-methylacyl coenzyme A racemase (AMACR)-positive. We investigated partial atrophy cases from a single institution using a standard AMACR immunostaining method. Immunohistochemical analysis was performed using an antibody cocktail containing p63, high-molecular-weight keratin (34bE12), and AMACR antibodies on 122 foci of partial atrophy. AMACR staining was analyzed in partial atrophy (n = 122) and compared with adjacent benign glands (n = 122) and prostatic carcinomas (n = 28). Of 122 foci of partial atrophy, 38 (31.1%) showed AMACR immunoreactivity. Typically, AMACR staining was weak or moderate. In addition, 82 (67.2%) showed patchy to negative distribution of basal cells. Partial atrophy may show AMACR immunoreactivity when using a 34bE12, p63, and AMACR antibody cocktail staining method. Compounding this problem, focal lack of basal cells may be seen. However, the AMACR staining pattern of partial atrophy is usually comparable to that of adjacent benign glands and substantially different from adenocarcinoma.
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PMID:Alpha-methylacyl coenzyme A racemase immunoreactivity in partial atrophy of the prostate. 1707 84

Differentiating malignant mesothelioma (MM) from pulmonary carcinoma in pleural fluid cytology can be challenging. Recent studies have suggested that D2-40, a novel lymphatic marker, may be a useful marker for mesothelial differentiation in surgical specimens. However, there are no available data regarding its utility in effusion cytology specimens. We investigated the utility of D2-40 in pleural fluid cytology in differentiating MM from pulmonary carcinomas. Twenty cases of pleural effusion smears of surgically confirmed MM with their corresponding cell blocks were retrieved from the database of the hospital computer system. We also included 10 cases of metastatic pulmonary adenocarcinoma (PA) and 10 cases metastatic pulmonary squamous cell carcinoma (PSCC) involving the pleural fluid. Cell blocks were formalin-fixed, paraffin embedded, and immunostained for TTF1, p63, calretinin, CK5/6, WT-1, and D2-40. Cases were scored as negative (<5% positivity) or positive (>5% moderate/strong positivity). The positive rates for TTF1, p63, calretinin, CK5/6, WT-1, and D2-40 were as follows: MM (0/20), (0/20), (17/20), (18/20), (19/20), (17/20), for PA (8/10), (0/10), (3/10), (0/10), (0/10), (0/10), and for PSCC (1/10), (10/10), (6/10), (10/10), (0/15), (0/10). The staining pattern for D2-40 was characterized by thick membranous staining. Diffuse cytoplasmic staining by D2-40 was seen in 2 cases of pulmonary carcinoma, counted as negative. Our study showed that in differentiating MM from PA, CK5/6, WT-1, and D2-40 have high specificity and sensitivity for MM. Although calretinin is a sensitive IHC marker for MM, it is not specific since it stained 30% of PA. Conversely, to differentiate between MM and PSCC, p63 and WT-1 are the best available markers. We recommend a panel of CK5/6, p63, D2-40, and WT-1 to differentiate MM from pulmonary carcinomas in effusion cytology specimens.
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PMID:The diagnostic utility of D2-40 for malignant mesothelioma versus pulmonary carcinoma with pleural involvement. 1711 39


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