Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04637 (p53)
 77,613 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this paper, we report 2 new cases of villoglandular papillary adenocarcinoma (VGPA) of the cervix, a rare, well-differentiated form of cervical adenocarcinoma. Both patients were without medical complications or history of oral contraceptive use and were nonsmokers. Extended hysterectomy was performed in both cases. Morphological criteria for a correct pathological diagnosis were emphasized. Immunohistochemical analysis was performed to clarify the phenotype of the neoplasms. Moreover, for the first time, we probed to establish if VGPA could be correlated to human papilloma virus (HPV) and herpes virus (HSV) types 1 and 2, using polymerase chain reaction amplification of tumoral DNA. Both neoplasms showed positivity for B72.3, Ca-125, carcinoembryonic antigen, keratin 7, and p16(INK4a) protein. Vimentin, P53, estrogen, and progesterone receptors, instead, were negative. Molecular study by polymerase chain reaction amplification of tumor DNA revealed a strong positive signal for HPV-DNA and no signal for HSV-DNA. It is reasonable to conclude that our cases of VGPA, in accordance with other examples reported in literature, are due to HPV infection. Behavioral cofactors, such as HSV infection (types 1 and 2), oral contraceptive use and smoking, involved in the pathogenesis of other cervical malignancies, can be excluded for the present cases.
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PMID:Villoglandular adenocarcinoma of the cervix: two new cases with morphological and molecular study. 1741 90

The differential diagnosis between carcinoma of the urinary bladder and adenocarcinoma of the prostate can be difficult, especially in the poorly differentiated forms infiltrating the neighboring organs. In this article, the authors report 2 cases that pose a diagnostic dilemma to the pathologist. The first is an infiltration of the bladder by a poorly differentiated adenocarcinoma of the prostate, which was clinically suspected as a papillary urothelial neoplasm. The second is a collision tumor composed of prostatic adenocarcinoma and urothelial carcinoma observed on a core needle biopsy of the prostate. In both cases, a large panel of immunohistochemical markers were used and demonstrated positivity for prostate-specific antigen and alpha methyl racemase in the prostatic carcinomas and immunoreactivity for CK7, CK20, Ag 34betaE12, and p53 in the urothelial carcinoma. The differentiating histological and immunohistochemical findings are discussed.
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PMID:Poorly differentiated adenocarcinomas of prostate versus high-grade urothelial carcinoma of the bladder: a diagnostic dilemma with immunohistochemical evaluation of 2 cases. 1747 86

Intrabiliary metastasis of colorectal carcinoma is not infrequent. We demonstrated interesting intraductal biliary epithelial lesions in two cases of colorectal carcinoma. The first case (65-year-old female) presented intrahepatic papillary adenocarcinoma with intrabiliary extension. While this biliary carcinoma was once diagnosed as intrabiliary metastasis of colon carcinoma, these carcinoma cells were positive for cytokeratin 7 (CK7, biliary cytokeratin) and negative for CK20 (intestinal cytokeratin). In addition, these carcinoma cells were oncocytic. Finally, a diagnosis of intraductal papillary cholangiocarcinoma of oncocytic variant was made. In the second case (74-year-old male), atypical biliary epithelial lesions were found near intrabiliary metastasis of colon carcinoma. The atypical lesions were immunohistochemically positive for CK7 but negative for CK20, and negative for p53. On the contrary, intraductal metastatic carcinoma was totally reversed, suggesting that atypical biliary lesions were not metastatic. Survey of such atypical biliary lesions in 6 consecutive cases with intrabiliary metastasis from colon carcinoma including this case disclosed that one third of such cases revealed such atypical biliary lesions. A variable type of biliary lesions should be carefully differentiated from intrabiliary metastatic colorectal carcinoma and a combined immunohistochemistry of CK7 and CK20 is useful for this differentiation.
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PMID:Intraductal papillary cholangiocarcinoma and atypical biliary epithelial lesions confused with intrabiliary extension of metastatic colorectal carcinoma. 1759 Oct 40

The 2004 WHO classification of lung tumours recognised basaloid carcinoma as a variant of squamous and large cell carcinoma. We report a unique case of primary pulmonary adenocarcinoma with a basaloid component. An 82-year-old man underwent pulmonary lobectomy for a 2.8 cm tumour. The patient is disease-free 13 months after diagnosis. Histologically, an invasive carcinoma having a glandular and a solid component was observed. The former was an adenocarcinoma with mucus containing spaces lined by columnar mucinous cells and basaloid cells. The solid component was an organoid proliferation of basaloid-type cells, as in cutaneous basal cell carcinoma. Basaloid cells, but not mucinous cells, were immunoreactive for high molecular weight cytokeratins (CK), CK 7 and, focally, for TTF-1. High Ki67 index, p53 and EGFR expression were also found. This tumour is unique in several respects: (1) The solid areas resemble a conventional basaloid carcinoma, except for the presence of small mucin-containing spaces. (2) The mucinous adenocarcinoma areas contain two layers of columnar and basaloid cells. (3) Both components are neoplastic based on cell morphology, invasive properties and phenotypic profile. These findings indicate that a basaloid variant of adenocarcinoma is also existing in the spectrum of basaloid carcinomas of the lung.
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PMID:Basaloid adenocarcinoma. A new variant of pulmonary adenocarcinoma. 1761 55

Anal gland carcinoma (AGC) is a rare perianal invasive cancer composed of tubular glands lined by cuboidal epithelium. The clinical features and histogenesis of AGC are not well understood and its origin from anal glands is often difficult to prove. Little is known about immunophenotypic features of AGC that could be useful in establishing the diagnosis. This study evaluated the immunohistochemical profile of 2 cases of AGC in comparison to anal glands from 11 hemorrhoidectomy specimens. Sections from the specimens were routinely processed and immunostained using commercial antibodies to cytokeratin (CK) 7, CK20, CK5/ 6, p63, CDX2, smooth muscle actin, calponin, heavy chain smooth muscle myosin, p53, and p16. In case 1 of AGC, radiation and chemotherapy preceded an abdominoperineal resection. In biopsies from this case, the neoplastic anal glands had a tubular pattern, whereas most glands in the resection specimen exhibited mucinous features. The histologic pattern in case 2 was tubular. Normal anal glands showed immunoreactivity for myoepithelial and basal cell markers CK5/6 and p63 in basal and parabasal cell layers and for CK7 in superficial cell layers. In contrast, both cases of AGC were negative for CK5/6 and p63 and were diffusely positive for CK7. Normal glands and both cases of AGC were negative for the intestinal differentiation marker CDX2, CK20, smooth muscle actin, calponin, smooth muscle myosin heavy chain, p16, and p53. Our data suggest that loss of p63 and CK5/6 expression is a feature of AGC. Anal gland carcinoma shares negativity for CDX2 and CK7+/CK20- profile with normal anal glands. No evidence of myoepithelial cells was found in normal or malignant anal glands. These data may be useful in establishing the diagnosis of AGC.
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PMID:Immunophenotypic characterization of anal gland carcinoma: loss of p63 and cytokeratin 5/6. 1883 5

We report a cribriform carcinoma of the left fossa poplitea in a 62-year-old woman. The patient did not present any symptoms, and the only complaint was the nodule, which was resected for diagnosis. After considering different diagnostic options, we decided that the most appropriate one was cribriform carcinoma, which is an entity described in 1998. The diagnostic criteria, which were provided in the few publications that refer to this entity, helped us to distinguish it from the main mimicker: cystic adenoid carcinoma. Owing to the cribriform pattern of the tumor, we also looked for a metastasis from other sites, mainly breast, vulva, and salivary glands, but all these were clinically excluded. The tumoral cells showed secretion by decapitation, as well as a positive stain of the luminal secretion by histochemical techniques of Alcian blue and periodic acid-Schiff. The tumor was negative for iron stain. In spite of these characteristics, which are, for some authors, indicative of an apocrine phenotype, the immunohistochemical study revealed some differences with the profile that has been described in cases of apocrine adenocarcinoma. The tumor did not express GCDFP-15 or CD 15. It was also negative for SMA, CEA, and PR. The pattern of cytokeratins expressed by our case was positive for AE1-AE3, CAM 5.2, and CK7, without any expression for CK20. Other markers expressed by the tumor were EMA, ER, c-erbB-2, p53, and S-100.
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PMID:Immunohistochemical phenotype of cutaneous cribriform carcinoma with a panel of 15 antibodies. 1808 81

We obtained 22 sessile serrated adenomas (SSAs) and 19 hyperplastic polyps (HPs) and performed immunolabeling for cytokeratins (CKs) 7 and 20, CDX2, beta-catenin, and p53 to determine the role of these markers in aiding distinction of lesions with neoplastic potential. Patients with SSAs more frequently had a prior or coexistent tubular adenoma (P = .004) that was right-sided (P = .00001) and larger (P = .03). No difference in CK7, CK20, or p53 labeling was found after correction for colonic location. However, CDX2 labeling was significantly lower in SSAs (P = .02) and was predominantly confined to the crypt bases, whereas it was diffusely positive in HPs (P < .001). Surprisingly, aberrant nuclear labeling for beta-catenin was found in 9 (41%) of the SSAs but in none of the HPs (P < .002). We propose that beta-catenin and/or CDX2 immunolabeling may have diagnostic usefulness in the evaluation of serrated polyps. These findings also suggest that Wnt signaling has a role in SSA development.
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PMID:Frequent beta-catenin nuclear labeling in sessile serrated polyps of the colorectum with neoplastic potential. 1828 64

We report 2 patients with conventional prostatic adenocarcinoma who developed sarcomatoid carcinoma of probable prostatic origin 6 and 2.5 years after radiation treatment (seed implantation and external beam). Our cases had histologic features consistent with those cases previously reported in the literature. The tumors consisted of spindle cells with large hyperchromatic nuclei and a pattern mimicking a sarcoma. Immunohistochemical studies showed the tumors to be weakly positive for EMA, CK7, and vimentin. Ki67 staining showed positivity in more than 50% of tumor cells. The tumors also stained diffusely positive for p53 and p63. PSA and PAP were negative. Clinically, the sarcomatoid carcinomas appeared to be of prostatic origin. The pathogenesis of the tumors is still uncertain but most likely represent a radiation-induced dedifferentiation of prostatic adenocarcinoma.
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PMID:Sarcomatoid carcinoma after radiation treatment of prostatic adenocarcinoma. 1832 77

Pagetoid spread of primary esophageal melanomas and several cases of pagetoid esophageal squamous cell carcinoma are known. However, true esophageal Paget disease (intraepithelial growth of neoplastic cells with glandular differentiation) has only rarely been reported. We encountered 3 endoscopic biopsy specimens containing Paget cells in squamous epithelium associated with adenocarcinomas in Barrett esophagus (BE) and in the esophagogastric junction. To determine the prevalence of Paget cells in the esophagus, we studied 81 endoscopic mucosal resections and 27 esophagectomies from patients with invasive or intramucosal adenocarcinoma, and compared the findings to a control group of 47 endoscopic mucosal resections and 25 esophagectomies from patients with high-grade dysplasia in BE. Paget cells were present in squamous epithelium overlying 5 (4.9%) of 108 adenocarcinomas but in none (0%) of 72 BE with high-grade dysplasia (P=0.16). A computerized search for primary Paget disease using the terms "Paget's and esophagus" or "pagetoid and esophagus" from 1994 to 2007 did not yield any additional cases. Among the 8 patients with Paget cells (including the 2 index biopsies) there were no differences in either sex distribution (7M:1F) or age (mean 62.4 y) as compared with 103 adenocarcinomas without Paget cells (93M:10F, P=0.58; mean age 69.2 y, P=0.78). Morphologically, all adenocarcinomas with Paget cells contained at least a component of diffuse, poorly differentiated adenocarcinoma, and 1 was a signet ring cell carcinoma. Paget cells involved only squamous epithelium directly above the poorly differentiated tumor foci. Histochemistry for periodic acid-Schiff with diastase (PAS-D) and mucicarmine, and immunohistochemistry for CK7, CK20, p53, and E-cadherin, were performed on 7 Paget cases with the following results: PAS-D+ (7 of 7, 100%), mucicarmine+ (6 of 7, 86%), CK7+ (7 of 7, 100%), CK20+ (5 of 7, 71%), p53 overexpression (3 of 7, 43%), and E-cadherin loss (complete loss in 1 and faint expression in 3, 57%). Overall, PAS-D was the most efficacious stain for highlighting Paget cells. A control group of 19 adenocarcinomas without Paget cells were also stained for E-cadherin; only 1 showed faint expression (5%) and none showed complete loss (P=0.01). These results demonstrate a low but significant prevalence (4.9%) of Paget cells in esophageal and esophagogastric junction adenocarcinomas. Unlike previously described cases of mammary, vulvar, and perianal Paget disease, esophageal Paget cells are almost universally associated with underlying adenocarcinoma and not with high grade dysplasia ("in situ" disease) or primary Paget disease. A commonality among cases with Paget cells is the presence of focal or diffuse, poorly differentiated adenocarcinoma with discohesive cells. E-cadherin alterations seem to play a less significant role.
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PMID:Paget cells in the esophagus: assessment of their histopathologic features and near-universal association with underlying esophageal adenocarcinoma. 1849 41

Small cell carcinoma of the urinary bladder is a rare entity known as an aggressive tumor. As it is rarely associated with transitional cell carcinoma in situ but more commonly with invasive transitional cell carcinoma, its origin is not well understood. We report a case of small cell carcinoma with coexisting transitional cell carcinoma in situ, where histologic mapping and parallel immunohistochemical and molecular analyses (TP53 mutation analyses, loss of heterozygosity) were performed. Immunohistochemical characterization (synaptophysin, thyroid transcription factor-1, chromogranin A, neuron specific enolase, CD56, CK, CK7, CK20, CD44v6, and p53) emphasized the morphology. Identical point mutations of TP53 were identified in invasive small cell carcinoma and transitional cell carcinoma in situ. No loss of heterozygosity of microsatellite markers D3S3050, D9S303, D9S304, D9S171, D9S775, D9S1748, D9S1751, D17S786, D17S918, and TP53alu was found in either component. We provide, for the first time, molecular evidence for the development of invasive small cell carcinoma out of transitional cell carcinoma in situ.
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PMID:Insights from a whole cystectomy specimen--association of primary small cell carcinoma of the bladder with transitional cell carcinoma in situ. 1854 17


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