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)

The author reports herein a case of occult very small lung carcinoma with a solitary brain metastasis that is clinically diagnosed as cavernous hemangioma, with an emphasis on pathologic findings. A 48-year-old Japanese man was admitted to our hospital complaining of mild paresis of left leg. Brain CT and MRI showed a solitary tumor (2 cm) with features of cavernous hemangioma in the right temporal lobe. Tumorectomy was performed, and it was pathologically undifferentiated carcinoma. An immunohistochemical analysis reveled that the carcinoma cells were positive for four types of pancytokeratin, cytokeratin (CK) 5/6, CK7, CK18, CK19, p63, and Ki-67 (78%). They were negative for high molecular weight CK, CK14, CK20, TTF-1, PE-10, melanosome, S100 protein, EMA, vimentin, CD34, myoglobin, CEA, p53, desmin, alpha-smooth muscle actin, chromogranin, synaptophysin, CD56, neuron-specific enolase, CD68, KIT, and PDGFRA. The positive CK7 and negative CK20 suggested lung origin, and cytokeratin profiles and positive CK5/6 and p63 suggested a squamous differentiation. The pathological diagnosis was undifferentiated carcinoma with squamous differentiation probably of lung origin. Later, systemic CT, MRI and PET were performed, and they detected a small lung tumor (8 mm) in the right apex. The lung biopsy revealed an undifferentiated carcinoma with focal squamous differentiation; the immunohistochemical findings were the same as those of the brain tumor. These findings suggest that occult very small lung carcinoma can metastasize to brain and such a metastasis may mimic cavernous hemangioma radiologically. Pathologic observations using many antibodies are very useful to determine the origin and histological type in solitary brain nodule.
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PMID:Occult very small lung carcinoma with a solitary brain metastasis that is clinically diagnosed as cavernous hemangioma: a case report. 1982 73

The central granular cell odontogenic tumor (CGCOT) is a rare lesion that usually affects the posterior region of the mandible of young adults. We present a case of CGCOT involving the mandible of a 20-year-old white woman, emphasizing the immunohistochemical characteristics using a large panel of antibodies. The lesion was removed surgically, and after 4 years of follow-up, there are no evidences of recurrences. The odontogenic epithelium (OE) showed positivity for cytokeratins (CKs) AE1/AE3, 34betaE12, CK5, CK7, CK8, CK14, CK19, E-cadherin, beta-catenin, CD138, and p63. The granular cells were positive for vimentin, CD68, lysozyme, muscle-specific actin, alpha-smooth muscle actin, calponin, neuron-specific enolase (NSE), CD138, and bcl-2. Dendritic-like cells surrounding the OE displayed positivity for vimentin, CD1a, S100, CD68, and bcl-2, but it was negative for factor XIIIa, supporting a Langerhans cell phenotype. Ki-67 labeling index was 1.8%, whereas p53 was negative. These data confirm the benign nature of CGCOT, the association of OE with Langerhans cells, and a variable phenotype of the granular cells.
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PMID:Central granular cell odontogenic tumor: a histopathologic and immunohistochemical study. 1991 79

The author herein reports histopathologic features of 31 surgical cases of gastrointestinal stromal tumor (GIST) of the digestive organs. The 31 cases of GIST were diagnosed in our pathology laboratory. They consisted of 24 cases of gastric GIST, 1 case of hepatic GIST, 1 case of small intestinal GIST, 4 cases of colon GIST, and 1 case of rectal GIST. The age of the patients ranged from 56 year to 84 years with a mean of 71 years. Male to female ratio was 21:10. The presenting symptoms were gastrointestinal bleeding in 13 cases, abdominal pain and discomfort in 13 cases, and asymptomatic in 5 cases. Endoscopy and imaging modalities including US, CT and MRI were useful to detect the tumors in all cases, and biopsies confirmed the GIST diagnosis in 21 cases. The size of GIST ranged from 1 cm to 12 cm with a mean of 4.3 cm. Grossly, 23 cases were submucosal tumors, 6 serosa-side tumors, 1 solid tumor in the liver, and 1 rectal polyp. Histologically, 28 cases were of spindle cell type and 3 of epithelioid type. According to mitotic counts and tumor size, the malignant risk was very low in 4 cases, low in 14 cases, intermediate in 9 cases, and high in 4 cases. Immunohistochemically, all cases were positive for KIT and vimentin, 30 cases for CD34, and 4 cases for alpha-smooth muscle actin. None were positive for desmin and S100 protein. Ki-67 labeling ranged from 2% to 18%. P53 protein was negative in all cases. PDGFRA was positive in 20 cases among 24 cases examined. Genetic analysis using PCR-direct sequencing method was performed in 5 GISTs; all the 5 GISTs showed point mutations or deletions in KIT gene, but did not in PDGFRA gene. The 5 cases of GIST were positive for PDGFRA protein, suggesting that PDGFRA overexpression is not associated with PDGFRA gene mutations. Four of the 31 cases showed metastases. The chemotherapy was imatinib mesylate in 6 cases, and none in 25 cases. Four cases of high risk died of GIST, and 27 cases are alive now without tumors.
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PMID:Gastrointestinal stromal tumor of the digestive organs: a histopathologic study of 31 cases in a single Japanese institute. 2012 84

The author herein reports a very rare case of large cell neuroendocrine carcinoma (LCNEC) with sarcomatous changes of the endometrium. A 40-year-old woman was admitted to our hospital because of abnormal uterine bleeding. Gynecologic examination and imaging modalities revealed a polypoid tumor of the uterine corpus. Uterine curettage biopsy revealed a sarcomatous undifferentiated carcinoma. Simple hysterectomy, salpingo-oophorectomy, extensive lymph node dissection, and omentectomy were performed. The patient was diagnosed as having FIGO stage Ib (T1N0M0) carcinoma, and adjuvant chemotherapy was performed. The patient is now alive 16 months after the operation. Pathologically, a polypoid tumor measuring 3x2x2 cm(3) was found in the uterine corpus. Histologically, the tumor consisted of relatively large-sized carcinoma cells without differentiation. The tumor cells have abundant cytoplasm and prominent nucleoli. It was composed of a spindle cell component (40%) and an epithelioid component (60%). A gradual transition between the two was recognized. Immunohistochemically, both elements showed the same immunophenotypes. The carcinoma cells were positive for cytokeratin, vimentin, CA125, CD34, estrogen receptor, progesterone receptor, p53 protein, Ki-67 antigen (80%), synaptophysin, CD56, KIT, and PDGFRA. They were negative for epithelial membrane antigen, CEA, desmin, S100 protein, melanosome, alpha-smooth muscle actin, chromogranin, and neuron-specific enolase. A molecular genetic analysis revealed no mutations of KIT (exons 9, 11, 13, and 17) and PDGFRA (exons 12 and 18) genes. The final diagnosis was LCNEC with sarcomatous changes.
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PMID:Large cell neuroendocrine carcinoma with sarcomatous changes of the endometrium: a case report with immunohistochemical studies and molecular genetic study of KIT and PDGFRA. 2018 18

The author reports herein a case of small cell carcinoma of the brain without extracranial tumors by serial imaging modalities. A 75-year-old man presented with headache. Brain CT and MRI revealed a solitary cystic tumor (5 x 6 x 7 cm) in the left occipital lobe. Blood laboratory test revealed no significant findings. Preoperative diagnosis was a primary or metastatic brain tumor. Preoperative systemic examinations including CT, MRI and PET revealed no extracranial tumors. Tumorectomy was performed. Pathologically, the tumor was small cell carcinoma positive for four types of pancytokeratins, cytokeratin (CK) 7, CK 18, thyroid transcriptional factor-1 (TTF-1), CD56, chromogranin, synaptophysin, neuron-specific enolase, p53 protein, KIT, PDGFRA, and Ki-67 antigen (labeling = 100%). It was negative for high molecular weight CK, CK5/6, CK14, CK19, CK20, PE10, epithelial membrane antigen, vimentin, CEA, desmin, S100 protein, CA19-9, alpha-smooth muscle actin, CD34, p63, and CD68. The pathologic examination strongly suggested primary small cell lung carcinoma. However, repeated serial imaging modalities including systemic CT, MRI and PET revealed no extracranial tumors. The serial sputum cytology was always negative. The patient was treated with radiation and cisplatin-based chemotherapy, and no tumors were found seven months after the operation. The present case suggests that there are small cell carcinomas with a solitary brain metastasis without a radiologically detected primary site. In the present case, primary small cell brain carcinoma cannot be excluded completely, although such a case has not been reported in the literature.
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PMID:Small cell carcinoma of the brain without extracranial involvement by serial CT, MRI and PET. 2022 32

We previously reported that the telomere-targeting drug telomestatin induces apoptosis accompanied by G-tail reduction and dissociation of binding protein TRF2 from telomeres in cancer cell lines but not normal or human telomerase reverse transcriptase (hTERT)-immortalized cells. Because telomere-targeting drugs induce growth arrest in normal cells at higher doses, their development is dependent on the ability to predict toxicity before in vivo use, but no models for this are available. Here, we established two new cell lines, telomerase immortalized human fetal hepatocytes, Hc3716-hTERT, and telomerase immortalized hepatic stellate cells, NPC-hTERT. Examinations showed that Hc3716-hTERT maintained normal mammalian cell morphology, cell growth, albumin expression, and wild-type p53 responsiveness, whereas NPC-hTERT maintained hepatic stellate-like morphology, expression of hepatic stellate markers, alpha-smooth muscle actin, and secretion of type I collagen, an extracellular matrix protein. Given our finding that telomere G-tail length in Hc3716 cells was decreased in senescence and increased by hTERT infection, we next examined the effect of high-dose telomestatin-induced telomere dysfunction and G-tail shortening on cellular functions in Hc3716-hTERT cells. Interestingly, telomestatin decreased expression of cytochrome P450 (CYP) family members CYP3A3/4, CYP3A5, and CYP3A7, mRNA and induced albumin expression at both mRNA and protein levels. These gene expression responses to telomestatin were similar to those of the normal parental cell Hc3716. These established cell lines thus represent the first model for predicting the side-effects of telomere-targeting drugs in normal cells, and should be powerful tools in the development of these drugs.
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PMID:Establishment of functional telomerase immortalized human hepatocytes and a hepatic stellate cell line for telomere-targeting anticancer drug development. 2045 67

The author reports a case of CD34-positive malignant myxoid sarcoma in the retroperitoneum with a dilemma of differential diagnosis in multiple biopsy specimens of different locations. A 79-year-old man was diagnosed with right renal pelvic carcinoma and nephrectomy was performed. The carcinoma was urothelial carcinoma (2 cm in diameter) without invasion. The patient was followed up, and a large retroperitoneal tumor was found two years after the operation. Multiple needle biopsies were performed. The patient then showed a hepatic metastasis, and died of cachexia one year after the detection of the retroperitoneal tumor. The needle biopsy specimens showed spindle cell sarcoma in the myxomatous stroma (80%) and in the non-myxomatous stroma (20%). Immunohistochemically, the tumor cells were positive for vimentin, CD34, CD99, bcl-2 and p53 protein. They were negative for cytokeratins, desmin, alpha-smooth muscle actin, S100 protein, melanosome, CEA, neuron specific enolase, CD68, factor VIII-related antigen, CD31, KIT, and PDGFRA. Ki67 labeling was 30%. A genetic analysis for KIT gene (exons 9, 11, 13 and 17) and PDGFRA gene (exons 12 and 18) showed no mutations. Although the differential diagnosis is problematic and difficult, the present case is probably dedifferentiated liposarcoma. The needle biopsy diagnosis of sarcomas is difficult and limited because sarcomas show heterogeneous histologies with regard to locations in the same tumor.
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PMID:CD34-positive myxoid sarcoma of the retroperitoneum: a dilemma in differential diagnosis of multiple biopsy specimens. 2055 46

Three myoepitheliomas (MEOs) derived from the salivary glands were examined immunohistochemically. Proliferating cell nuclear antigen (PCNA)-positive cells were very rare (less than 2% of all tumor cells) in localized tumors of case 1 (epithelioid) (E-oid) cells) and case 2 (plasmacytoid) (P-toid) cells with a small number of spindle-shaped cells), but the percentage of PCNA-positive cells was high (21.8%) in case 3 (clear cells) exhibiting bone destruction. Strong c-myc expression was detected in all the tumors, but p53 or c-erbB-2 protein was not detected in any of the cases. More than half of the clear cells were positive for epidermal growth factor (EGF), while fewer tumor cells in cases 1 and 2 expressed EGF. A few tumor cells in cases 2 and 3 were positive for EGF-receptor (R). Keratin was most prominent in the E-oid cells, The P-toid cells were most strongly positive for S-100 protein followed by the E-oid and clear cells. More than half of the spindle-shaped cells and one-third of the E-oid cells were positive for alpha-smooth muscle actin (alpha-SMA), but less than 5% of the clear cells and none of the P-toid cells were positive for alpha-SMA. These results suggest that tumor cells in MEO are heterogenous and have different proliferation activities.
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PMID:Benign and malignant myoepithelioma of salivary-gland - an immunohistochemical evaluation. 2155 64

Aggressive angiomyxoma is a distinctive and very rare soft tissue tumor occurring almost exclusively in women. Only seven cases occurring in men have been previously reported. We herein report a case of a 74-year-old man who was admitted to our hospital presenting with a huge right inguinal mass that had grown over a 14-year period, in order to undergo surgical treatment for gastric cancer. The inguinal tumor was well-defined and demonstrated a glistening appearance on the cut surface. Histologically, the tumor was composed of bland-looking spindle and stellate cells with delicate cytoplasmic processes, which sparsely populated the fibromyxoid matrix. A prominent vascular component was also present. Immunohistochemically, the stromal cells stained consistently for vimentin and variably for muscle-specific actin, but not for alpha-smooth muscle actin, desmin, and S-100 protein. The gastric cancer was microscopically diagnosed to be papillary adenocarcinoma with serosal invasion and showing immunoreactivity for p53 protein, but not for aggressive angiomyxoma.
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PMID:Aggressive angiomyxoma of the inguinal region. 2159 Jan 83

The immunohistochemical profiles of 16 cases of phyllodes tumor of the breast (9 benign and 7 malignant) from 15 patients were examined by the labeled streptavidin biotin method. The expression of Ki-67, p53, bcl-2, alpha-smooth muscle actin (alpha-SMA), desmin, S-100 protein, estrogen receptor (ER), and progesterone receptor (PgR) was analyzed. The number of Ki-67-positive stromal cell nuclei of malignant phyllodes tumor were significantly more prominent than the benign tumors. The p53 expression on the stromal cell nuclei showed a significant difference between malignant and benign cases (86% vs 22%; p<0.05). bcl-2 was regularly seen on the luminal cell cytoplasm and stromal cell labeling showed no significant difference between malignant and benign cases (29% vs 33%). Stromal cells were alpha-SMA positive but refractory among cases, and desmin and S-100 protein were negative. PgR was expressed in all 16 cases and ER in most cases (12/16) the expression of which was restricted to luminal epithelial cell nuclei. These findings indicate that the Ki-67 labeling index and p53 expression in the stroma would be a good diagnostic parameter distinguishing benign tumors from malignant tumors. However, the absence of steroid receptor expression in stromal cells suggests the ineffectiveness of hormonal therapy for phyllodes tumor of the breast.
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PMID:Immunohistochemical profile of phyllodes tumors of the breast. 2159 34


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