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)

PURPOSE: In non-small cell lung cancer, higher thymidylate synthase (TS) levels have been reported in squamous cell carcinoma (SCC) compared with adenocarcinoma (ADC). Data on TS expression in large-cell carcinoma (LCC) are scanty. EXPERIMENTAL DESIGN: TS mRNA and protein levels were analyzed in 42 surgical cases of pulmonary LCC, including 8 large-cell neuroendocrine carcinomas, and were compared with controls represented by ADC (n = 41), SCC (n = 30), and small-cell lung carcinoma (SCLC; n = 33). TS levels were also correlated with the expression of Ki67 and E2F1. Moreover, the reliability of TS expression analysis was assessed in 22 matched cytologic and surgical specimens of non-small cell lung cancer. RESULTS: TS mRNA levels of LCC were comparable with those of control SCC, but significantly higher than those of ADC (P < 0.001) and lower than SCLC (P < 0.001). A correlation between TS mRNA and protein levels was observed in control ADC and SCC, but not in LCC. Large-cell neuroendocrine carcinomas had the highest TS expression, whereas in non-neuroendocrine LCCs, TS protein levels were significantly higher (P = 0.02) in LCC immunoreactive for p63 and desmocollin3 (markers of squamous differentiation) than those expressing TTF-1 (a marker of ADC). Both E2F1 and Ki67 levels were not correlated with TS in LCCs. Finally, a linear correlation in TS protein levels was observed between matched cytologic and surgical specimens. CONCLUSION: The pulmonary LCC immunoprofile may resemble that of SCCs or ADCs. This immunoprofile is associated with differential TS expression levels, which may support a more appropriate therapeutic strategy decision. (Clin Cancer Res 2009;15(24):7547-52).
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PMID:Differential Thymidylate Synthase Expression in Different Variants of Large-Cell Carcinoma of the Lung. 1999 14

Although clear cell adenocarcinoma have been described focally mimicking nephrogenic adenoma, we have identified a subset of clear cell adenocarcinoma that diffusely resembles nephrogenic adenoma (nephrogenic adenoma-like clear cell adenocarcinoma). Twelve classic clear cell adenocarcinomas of the bladder and urethra and 7 nephrogenic adenoma-like clear cell adenocarcinomas were compared to 10 nephrogenic adenomas. Classic clear cell adenocarcinomas and nephrogenic adenoma-like clear cell adenocarcinomas comprised 4 men and 15 women. The following features were seen in classic clear cell adenocarcinomas: nephrogenic adenoma-like clear cell adenocarcinomas: predominantly solid pattern (7/12:0/7), marked nuclear pleomorphism (7/12:1/7), prominent nucleoli (5/12:1/7), clear cytoplasm in 50% or greater of tumor (7/12:0/7), and necrosis (8/12:3/7), although the necrosis in nephrogenic adenoma-like clear cell adenocarcinomas was often focal and intraluminal. Both patterns of clear cell adenocarcinomas showed prominent hobnail features, although more pronounced in nephrogenic adenoma-like clear cell adenocarcinomas. Muscularis propria invasion was seen in 5 of 9 classic clear cell adenocarcinomas and 6 of 6 nephrogenic adenoma-like clear cell adenocarcinomas, where evaluable. Classic clear cell adenocarcinoma was associated with urothelial carcinoma (n = 2) and endometriosis (n = 1). The Ki-67 rate in clear cell adenocarcinomas ranged from 10% to 80% compared with 0% to 5% in nephrogenic adenoma. The following antibodies were not helpful in distinguishing nephrogenic adenoma-like clear cell adenocarcinoma from nephrogenic adenoma: CD10, estrogen receptor, p63, high-molecular-weight cytokeratin, and alpha-methylacyl coenzyme-A racemase. PAX2 expression was more frequent in nephrogenic adenoma (89%) compared to both patterns of clear cell adenocarcinoma (29%-32%). The key features discriminating between nephrogenic adenoma-like clear cell adenocarcinoma and nephrogenic adenoma include occasional clear cells, more prominent pleomorphism especially hyperchromatic enlarged nuclei, and extensive muscular invasion. Presence of mitoses and a high rate of Ki-67 expression in lesions resembling nephrogenic adenoma require clinical correlation, close follow-up, and repeat biopsy with more extensive sampling.
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PMID:Clear cell adenocarcinoma of the bladder and urethra: cases diffusely mimicking nephrogenic adenoma. 2006 Jan 52

We investigated the staining pattern of commonly used basal cell/myoepithelial markers, such as p63 (a p53-homologous nuclear protein), basal cell-specific cytokeratin antibody (34betaE12, K903), and smooth muscle myosin heavy chain (SMMHC) in benign and malignant bronchioloalveolar proliferations of the lung. We studied 85 lung lesions consisting of 35 bronchioloalveolar carcinoma, 30 well-differentiated adenocarcinoma, and 20 cases of benign lung lesions. In normal lung, p63, K903, and SMMHC decorated the basal cells of large and small airways and occasional cells of terminal bronchioles. In reactive processes, a distinctive staining pattern was present in 19/20 (95%) of the cases characterized by staining of basal cells of the airways and bronchiolar epithelium and squamous metaplastic epithelium for p63 and K903, whereas 12/20 (60%) stained with SMMHC. Respiratory ciliated cells, alveolar epithelial cells, and nonepithelial cells were negative. In bronchioloalveolar carcinoma, a discontinuous peripheral rim of p63-immunoreactive cells was retained surrounding and intermingled with the malignant bronchioloalveolar proliferation in 31/35 (88.5%) cases, SMMHC in 28/35 (80%) cases, and K903 in 20/35 (57%) cases. For adenocarcinoma, a majority of the cases (28/30, 93%) were negative for p63 and K903; however, SMMHC showed artifactual staining in the desmoplastic stroma in 6/30 (20%) cases. Our results highlighted the differential expression of basal cell markers across various bronchioloalveolar lesions. The staining pattern of basal cells in bronchioloalveolar carcinoma supports that these neoplasms may actually be carcinoma in-situ.
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PMID:Distribution of basal/myoepithelial markers in benign and malignant bronchioloalveolar proliferations of the lung. 2006 53

Cervical small cell neuroendocrine carcinoma (SCNEC) and large cell neuroendocrine carcinoma (LCNEC) are uncommon but highly aggressive neoplasms. From a diagnostic point of view, there may be problems both in distinguishing these from other neoplasms and in confirming a cervical origin. This is important as management is critically dependent on the correct histologic diagnosis. We undertook a detailed immunohistochemical analysis of a relatively large series of primary cervical SCNEC (n=13) and LCNEC (n=8). Cases were stained with AE1/3, chromogranin, CD56, synaptophysin, PGP9.5, TTF1, p16, p63, CK7, CK20, neurofilament, and CD99. CK20 and neurofilament staining was undertaken to investigate whether some of these neoplasms might exhibit a Merkel cell immunophenotype and CD99 staining to assess whether there is immunohistochemical overlap with neoplasms in the Ewing family of tumors (EFT). For all markers, staining was classified as negative, 1+ (<10% cells immunoreactive), 2+ (10 to 50% cells immunoreactive), or 3+ (>50% cells immunoreactive). Eleven and 6 SCNEC and LCNEC, respectively were positive with AE1/3. Chromogranin, CD56, synaptophysin, and PGP9.5 were positive in 11, 19, 19, and 9 cases, respectively. Altogether 15 cases (71%) (11 SCNEC, 4 LCNEC) exhibited nuclear positivity, often diffuse, with TTF1. All but 1 case was diffusely positive with p16. p63 was positive in 9 cases, including 5 with diffuse nuclear immunoreactivity. Ten and 4 neoplasms were positive with CK7 and CK20, respectively. Neurofilament was positive in 7 tumors. The 4 neoplasms that were CK20 positive were stained with the monoclonal antibody CM2B4, generated against an antigenic epitope on the Merkel cell polyomavirus T antigen; all were negative. CD99 was positive in 6 cases. In 2 cases, adjacent foci of adenocarcinoma in situ (AIS) contained scattered individual chromogranin positive cells, raising the possibility that some cervical neuroendocrine carcinomas arise from neuroendocrine cells in AIS. Four of 13 cases of pure AIS also contained scattered chromogranin positive cells. Our results illustrate that a proportion of cervical neuroendocrine carcinomas are negative with broad spectrum cytokeratins and some of the commonly used neuroendocrine markers. TTF1 positivity is extremely common and may be a useful marker of a neuroendocrine carcinoma. It is of no value in exclusion of a pulmonary primary. p16 is almost always positive in cervical neuroendocrine carcinomas, possibly owing to an association with oncogenic human papillomavirus, although other mechanisms of expression are also possible. Cervical neuroendocrine carcinomas may be p63 positive, illustrating that this marker is not specific for squamous differentiation. CK20 and neurofilament positivity in some cervical neuroendocrine carcinomas is in keeping with a Merkel cell immunophenotype, similar to that described in SCNECs in other organs. However, the absence of staining with CM2B4 argues against a true Merkel cell tumor. CD99 staining in a cervical neuroendocrine carcinoma should not result in misdiagnosis as a neoplasm in the Ewing family of tumors.
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PMID:An immunohistochemical study of cervical neuroendocrine carcinomas: Neoplasms that are commonly TTF1 positive and which may express CK20 and P63. 2018 42

Often the distinction of primary adnexal carcinoma from metastatic adenocarcinoma to skin from breast, lung, and other sites can be a diagnostic dilemma. Current markers purportedly of utility as diagnostic adjuncts include p63 and D2-40; however, their expression has been demonstrated in 11-22% and 5% of metastatic cutaneous metastases, respectively. Both cytokeratin (CK) 15 and nestin have been reported as follicular stem cell markers. We performed CK15 and nestin, as well as previously reported stains (such as p63, D2-40, and calretinin) on 113 cases (59 primary adnexal carcinomas and 54 cutaneous metastases). Expressions of p63, CK15, nestin, D2-40, and calretinin were observed in 91, 40, 37, 44, and 14% of primary adnexal carcinoma, respectively, and in 8, 2, 8, 4, and 10% of cutaneous metastases, respectively. p63 appeared to be the most sensitive marker (with a sensitivity of 91%) in detecting primary adnexal carcinomas. CK15 appeared to be the most specific marker with a specificity of 98%. Using chi(2) analysis, statistically significant P-values (<0.05) were observed for p63, CK15, nestin, and D2-40 in the distinction of primary adnexal carcinoma versus cutaneous metastases. In logistic regression and stepwise selection for predicting a primary adnexal carcinoma, statistical significance was observed for p63, CK15, and D2-40 (P-values: <0.001, 0.0275, and 0.0298, respectively) but not for nestin (P-value=0.4573). Our study indicates that diagnostic sensitivity and specificity are significantly improved using a selected panel of immunohistochemical markers, including p63, CK15, and D2-40. Positive staining with all three markers argues in favor of a primary cutaneous adnexal neoplasm.
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PMID:The diagnostic utility of immunohistochemistry in distinguishing primary skin adnexal carcinomas from metastatic adenocarcinoma to skin: an immunohistochemical reappraisal using cytokeratin 15, nestin, p63, D2-40, and calretinin. 2019 Jul 34

Cystic change in adenocarcinoma of the prostate is unusual and may be confused with benign cystic atrophy. Limited data exist on the pathologic attributes of microcystic change in malignant prostatic glands. The aim of this study was to assess histologic and immunohistologic characteristics of microcystic adenocarcinoma of the prostate. This alteration was defined as cystic dilatation and rounded expansion of the malignant gland profile, with a flat luminal cell lining layer. We identified 53 cases with microcystic change from a survey of 472 radical prostatectomy cases, for an incidence of 11.2%. The greatest diameter of the dilated cancer glands was 0.4 to 0.9 mm, with a mean diameter 10-fold greater than adjacent small malignant glands. The microcystic glands were typically adjacent to usual small acinar adenocarcinoma. Atrophic features were seen at least focally in all cases, although many microcystic adenocarcinoma epithelia exhibited a moderate amount of cytoplasm. Gleason grade 3 was the predominant grade of the adjacent nonmicrocystic malignant glands. Intraluminal crystalloids, and wispy blue intraluminal mucin were seen in all cases. Ninety-six percent of the microcystic cases showed alpha-methylacyl CoA racemase overexpression and all cases showed complete basal cell loss (using 34betaE12 and p63 antibodies) in immunohistochemistry. Microcystic adenocarcinoma of the prostate is a distinctive histomorphologic presentation of prostatic adenocarcinoma that is deceptively benign-looking at low magnifications. Detection of intraluminal crystalloids or wispy blue mucin at low magnification, immunostains for alpha-methylacyl CoA racemase, and basal cells, and a search for adjacent usual small acinar adenocarcinoma are helpful diagnostic aids. Diagnostic awareness of this growth pattern of prostatic carcinoma is important to avoid underdiagnosis of adenocarcinoma of the prostate.
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PMID:Microcystic adenocarcinoma of the prostate: a variant of pseudohyperplastic and atrophic patterns. 2021 81

A lipid-rich carcinoma of the mammary gland was diagnosed in a female Djungarian hamster (Phodopus sungorus), which was kept as an indoor pet. The animal underwent surgery for a primary tumor arising in the mammary gland at the age of 16 months, and also for a recurrent tumor 6 months later. Histologically, the primary neoplasm was composed of 2 different cell populations: nonvacuolated glandular neoplastic cells with moderate atypia, and vacuolated neoplastic cells with marked atypia. Transition from the nonvacuolated glandular cells to the vacuolated cells was frequently seen. The recurrent neoplasm was composed predominantly of vacuolated neoplastic cells that often invaded the surrounding soft tissue. The cytoplasmic vacuoles contained neutral lipids, as confirmed by oil red O and Nile blue staining. The vacuolated neoplastic cells were immunopositive for cytokeratin and negative for vimentin, alpha-smooth muscle actin, p63, estrogen receptor alpha, and androgen receptor. Presumably, this high-grade, lipid-rich mammary carcinoma had developed from a low-grade mammary adenocarcinoma.
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PMID:Lipid-rich carcinoma in the mammary gland of a Djungarian hamster (Phodopus sungorus). 2022 99

Carcinomas may arise as a disorder of regeneration, so that a malignant cell may represent a failure to fully attain the characteristics of differentiated tissue. We hypothesized that there is a differential distribution of progenitor cell markers among different histological types of lung cancers, with poorly differentiated tumors being more likely to express progenitor stem cell markers. The study was limited to paraffin-embedded archival material of resected untreated pulmonary carcinomas, including adenocarcinoma, squamous cell carcinoma, large cell carcinoma, and small cell carcinoma. The sections were stained for putative stem cells markers (Musashi-1, Musashi-2, CD34, CD21, KIT, CD133, p63, and OCT-4). Positivity was read as isolated, focal, or diffuse staining. Stem cell markers were detected in all histological types of pulmonary carcinomas. There was a difference in the expression of markers among the histological types. Small cell carcinoma showed diffuse positivity for most of the markers; in contrast to focal or negative staining in other histological groups. An inverse relationship between CD21 and Musashi-1 was observed. No staining for OCT-4 and CD34 was seen in any of the tumor types. Hierarchical clustering based on marker expression separated tumors into two groups, with one group marked by high expression of Musashi-1 and KIT, contained most of the poorly differentiated adenocarcinomas and small cell carcinomas. Therefore, stem cell markers are expressed in lung cancers with different patterns seen for different histological types and degrees of differentiation.
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PMID:Progenitor stem cell marker expression by pulmonary carcinomas. 2030 19

In lung cancer, integrating translational data from various histologies obtained in different patients under different conditions can increase their robustness. This is a meta-analysis of cDNA array data obtained in 688 tumor patients (541 non-small cell lung cancer, 33 small cell lung cancer and 114 others) and 205 controls. 1,206 genes were found to be dysregulated in one of the 12 transcriptomics studies available. 748 results (62%) were obtained only once and might be questioned. 38% of observations could be reproduced twice or more. 346 genes were reported twice, 80 three times, 27 four and 5 five times. A common set of genes dysregulated in lung cancer was obtained, including BPA1, DUSP6, ASCL1, RNAS1 and S100P. p63 and CK 5/6 p63 are useful for differentiating adenocarcinoma and small cell lung cancer from squamous cell carcinoma. TFF-3 and MUC1 are over-expressed in adenocarcinoma. INSM1, SGNE1 and H2AFZ are typical for small cell lung cancer. Using a meta-analysis approach, it was possible to detect a robust set of genes differentially expressed in lung cancer and to determine a limited number of key genes linked to subtypes in lung cancer molecular pathology.
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PMID:Key genes in lung cancer translational research: a meta-analysis. 2033 65

Localized gingival enlargement is often associated with specific systemic medication, abscess formation, trauma or reactive lesions. Scant literature is available reporting enlargement of gingiva due the metastasis of adenocarcinoma from lung. The case report presents a unique case of an adenocarcinoma in the lung metastasizing to the buccal and lingual interdental papillae of teeth numbering 34 and 35. A 72-year-old female was referred to the Mayo Clinic with a recent diagnosis of metastatic stage IV adenocarcinoma of the left lung presented with an abnormal mass located on the left posterior buccal keratinized tissue adjacent to teeth numbering 34-35. Biopsy of the lesion was performed for CK7, CK20, TTF-1 and p63. The tumor cells were positive for CK7 and TTF-1, and weakly positive for p63 suggesting a diagnosis of adenocarcinoma. The periodontist may be in the unique position to be the first oral health care provider to evaluate any biopsy suspicious intra-oral lesions.
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PMID:A case report of metastatic adenocarcinoma of the gingiva. 2037 44


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