Characterization of myeloid malignancies with TP53 mutations and comparison to P53 expression by immunohistochemical staining methods

2019 ◽  
Vol 42 (2) ◽  
Author(s):  
Kristin H. Karner ◽  
Jessica L. Kohan ◽  
Sheryl R. Tripp ◽  
Mohamed E. Salama
Keyword(s):  
Immunohistochemical Staining ◽  
P53 Expression ◽  
Tp53 Mutations ◽  
Myeloid Malignancies ◽  
Staining Methods

scholarly journals Immunohistochemical Markers and the Clinical Course of Adenosarcoma: a Series of Seven Cases

2020 ◽  
Author(s):  
Makiko Omi ◽  
Akiko Tonooka ◽  
Tomohiro Chiba ◽  
Hidetaka Nomura ◽  
Hiroyuki Kanao ◽  
...  
Keyword(s):  
Immunohistochemical Staining ◽  
Clinical Course ◽  
Abnormal Uterine Bleeding ◽  
P53 Expression ◽  
Prognostic Assessment ◽  
Immunohistochemical Markers ◽  
Recurrent Tumors ◽  
Gynecology And Obstetrics ◽  
Staining Methods ◽  
The Relationship

Abstract Background: Uterine adenosarcoma, a rare subtype of uterine tumor, is a biphasic tumor consisting of epithelial and mesenchymal elements. There is no research comparing histopathological features of primary and recurrent tumors, including immunohistochemistry; furthermore, the relationship between pathology and the clinical course is unclear. We reviewed the pathology and immunohistochemical features of 7 adenosarcoma cases and investigated the relevance of the histomorphological features to the clinical course. We also compared immunohistochemical features of primary and recurrent tumors.Methods: Seven patients with adenosarcoma who underwent surgery in our hospital were evaluated. We performed immunohistochemical staining for the estrogen receptor (ER), progesterone receptor (PR), p53, and two SWI/SNF chromatin-remodeling proteins (SMARCA4, BCOR), which were recently developed for the diagnosis of undifferentiated sarcomas in addition to conventional staining methods. Results: All patients were International Federation of Gynecology and Obstetrics stage 1B to 1C. All tumors were polypoid, and every patient presented with abnormal uterine bleeding. Six patients were over 50 years old and were menopausal; 1 patient was under 50 years old and was non-menopausal (average age 59.1 years). Histologically, the sarcomatous components were homologous in 6 patients and heterogenous in 1 patient. Four patients were recurrent patients; 3 were non-recurrent. All 4 recurrent patients showed high-grade morphology with sarcomatous overgrowth and were negative for ER and PR. Three recurrences could be evaluated by imaging, showing recurrence only in a distant area; biopsy specimens from these tissues revealed the identical mesenchymal component found in the primary tumor without a benign epithelial component. Immunohistochemical staining results were also the same as for the original tumor, except for the p53 expression in 1 patient. At the primary site, p53 was overexpressed in 2 recurrent patients and had a wild-type level in 1 recurrent patient; however, all 3 recurrent tissues showed overexpression of p53. None of the 7 cases showed SMARCA4 loss, and BCOR expression was positive in 1 case.Conclusions: Initial pathological analysis of the adenosarcoma with appropriate immunohistochemical staining is vital for prognostic assessment. Expression of p53 might increase at recurrence. SMARCA4 and BCOR could be an index of malignancy, regardless of sarcomatous overgrowth.

scholarly journals Mutated p53 in HGSC—From a Common Mutation to a Target for Therapy

Cancers ◽  
2021 ◽  
Vol 13 (14) ◽  
pp. 3465
Author(s):  
Aya Saleh ◽  
Ruth Perets
Keyword(s):  
Cancer Progression ◽  
Target Genes ◽  
P53 Protein ◽  
Genetic Alterations ◽  
Common Mutation ◽  
Missense Mutations ◽  
P53 Expression ◽  
Histologic Subtype ◽  
Tp53 Mutations

Mutations in tumor suppressor gene TP53, encoding for the p53 protein, are the most ubiquitous genetic variation in human ovarian HGSC, the most prevalent and lethal histologic subtype of epithelial ovarian cancer (EOC). The majority of TP53 mutations are missense mutations, leading to loss of tumor suppressive function of p53 and gain of new oncogenic functions. This review presents the clinical relevance of TP53 mutations in HGSC, elaborating on several recently identified upstream regulators of mutant p53 that control its expression and downstream target genes that mediate its roles in the disease. TP53 mutations are the earliest genetic alterations during HGSC pathogenesis, and we summarize current information related to p53 function in the pathogenesis of HGSC. The role of p53 is cell autonomous, and in the interaction between cancer cells and its microenvironment. We discuss the reduction in p53 expression levels in tumor associated fibroblasts that promotes cancer progression, and the role of mutated p53 in the interaction between the tumor and its microenvironment. Lastly, we discuss the potential of TP53 mutations to serve as diagnostic biomarkers and detail some more advanced efforts to use mutated p53 as a therapeutic target in HGSC.

Characterization of p53 expression in rainbow trout

2011 ◽  
Vol 154 (4) ◽  
pp. 326-332 ◽  
Author(s):  
Michelle Liu ◽  
Catherine Tee ◽  
Fanxing Zeng ◽  
James P. Sherry ◽  
Brian Dixon ◽  
...  
Keyword(s):  
Rainbow Trout ◽  
P53 Expression

scholarly journals Characterization of antibody against human liver guanase by immunoblotting and immunohistochemical staining of human liver guanase by a direct labeling antibody-enzyme method.

1989 ◽  
Vol 37 (5) ◽  
pp. 611-615 ◽  
Author(s):  
S Ito ◽  
A Iwasaki ◽  
J Syundo ◽  
Y Tamura ◽  
S Kishi ◽  
...  
Keyword(s):  
Liver Enzyme ◽  
Specific Antibody ◽  
Immunohistochemical Staining ◽  
Human Liver ◽  
Liver Extract ◽  
Precipitin Line ◽  
Tissue Sections ◽  
Immunohistochemical Reaction ◽  
Enzyme Method

Human liver guanase was purified and a specific antibody against it was raised in rabbits. The antiserum formed a single precipitin line with human liver extract, and also completely inhibited the activity of the liver enzyme. An immunoblotting study showed that the antibody bound specifically to one band of protein with guanase activity and not to other proteins. Therefore, we concluded that this antiserum against the liver enzyme was suitable for use in immunohistochemical demonstration of guanase. In tissue sections, the immunohistochemical reaction with this antibody was positive in the same locations as the histochemical guanase reaction with DAB (3,3'-diaminobenzidine tetrahydrochloride).

Connexins Within the Rat Larynx

2008 ◽  
Vol 139 (2_suppl) ◽  
pp. P95-P95
Author(s):  
Mark Van Deusen ◽  
Michael J Lyon
Keyword(s):  
Immunohistochemical Staining ◽  
Vocal Folds ◽  
Alcohol Ingestion ◽  
Smoke Inhalation ◽  
Rt Pcr ◽  
Pharmacologic Treatments ◽  
High Level

Problem To determine the various types of connexins and their localization within the rat larynx. Methods Eight larynges from 3–4 month old Fisher-344 rats were used. Four were immediately dissected to obtain the epiglottis, vocal folds, supraglottic and subglottic mucosa. RNA was extracted and used as a template for production of cDNA, which was used with primers for Cx26, Cx30, Cx32, Cx37, Cx40, and Cx43 and RT-PCR performed. Four others were serially sectioned and the sections processed for immunohistochemistry. Results RT-PCR revealed a high level of Cx43, Cx32, and Cx30 within epiglottis and Cx43 in the vocal folds. Immunohistochemical staining confirmed these results. Conclusion The rat epiglottis is rich in Cx43, Cx32, and Cx30 while the vocal folds contain Cx43. Their localizations suggest involvement in secretion for protective purposes and they may play a key role in laryngeal pathologies. Significance Cxs in the larynx may be disrupted by decreased pH, alcohol ingestion, and smoke inhalation. These three factors contribute significantly to the pathology that patients commonly present to the otolaryngologist. Potential pharmacologic treatments are on the horizon and further characterization of the laryngeal connexins needs to be carried out before such treatments can be utilized.

Cytoplasmic P53 Immunostaining With N-Terminus P53 Antibody And Absence Of Staining With C-Terminus P53 Antibody: A Report Of Two Pediatric Sarcomas With Distal Truncating TP53 Mutations Affecting Nuclear Localization Domain

2021 ◽  
pp. 106689692110651
Author(s):  
Hilda Mirbaha ◽  
Deyssy Carrillo ◽  
Midori Mitui ◽  
Matthew C. Hiemenz ◽  
Vivekanand Singh ◽  
...  
Keyword(s):  
Nuclear Localization ◽  
Immunohistochemical Staining ◽  
Precise Description ◽  
Cytoplasmic Staining ◽  
Tp53 Mutations ◽  
Localization Domain ◽  
C Terminus ◽  
Pediatric Sarcomas ◽  
N Terminus ◽  
P53 Antibody

P53 immunohistochemical staining with antibodies targeted to epitopes at or near the N-terminus are commonly used in diagnostic pathology practice as a surrogate for TP53 mutations. The abnormal staining patterns indicating TP53 mutations include nuclear overexpression, null, and the recently described cytoplasmic staining. The latter staining pattern occurs with the less common TP53 mutations affecting its nuclear localization and/or tetramerization domains that are located toward the C-terminus. Here we describe the first two cases of pediatric sarcomas with cytoplasmic staining with P53 antibody against N-terminus epitope and the absence of staining with P53 antibody against C-terminus epitope. We propose that a more precise description of P53 immunohistochemical staining patterns should include the nature of the antibody used.

Comprehensive molecular characterization of myeloid malignancies with 9q deletion

2019 ◽  
Vol 60 (10) ◽  
pp. 2591-2593
Author(s):  
Luise Hartmann ◽  
Torsten Haferlach ◽  
Manja Meggendorfer ◽  
Wolfgang Kern ◽  
Claudia Haferlach ◽  
...  
Keyword(s):  
Molecular Characterization ◽  
Myeloid Malignancies

scholarly journals Malignant or benign leukocytosis

Hematology ◽  
2012 ◽  
Vol 2012 (1) ◽  
pp. 475-484 ◽  
Author(s):  
Tracy I. George
Keyword(s):  
Blood Cell ◽  
Laboratory Finding ◽  
Complete Blood Cell Count ◽  
Blood Cell Count ◽  
Myeloid Malignancies ◽  
Monomorphic Population ◽  
Wbc Count ◽  
Ancillary Studies ◽  
Lymphoid Proliferation

Abstract Leukocytosis, or elevated WBC count, is a commonly encountered laboratory finding. Distinguishing malignant from benign leukocytosis is a critical step in the care of a patient, which initiates a vastly different decision tree. Confirmation of the complete blood cell count and the WBC differential is the first step. Examination of the PB smear is essential to confirming the automated blood cell differential or affirming the manual differential performed on the PB smear. Next is separation of the leukocytosis into a myeloid versus a lymphoid process. Distinguishing a reactive lymphoid proliferation from a lymphoproliferative disorder requires examination of lymphocyte morphology for pleomorphic lymphocytes versus a monomorphic population, with the latter favoring a lymphoproliferative neoplasm. Samples suspicious for lymphoproliferative disorders can be confirmed and characterized by flow cytometry, with molecular studies initiated in select cases; precursor lymphoid neoplasms (lymphoblasts) should trigger a BM examination. Myeloid leukocytosis triggers a differential diagnosis of myeloid leukemoid reactions versus myeloid malignancies. The manual differential is key, along with correct enumeration of blasts and blast equivalents, immature granulocytes, basophils, and eosinophils and identifying dysplasia to identify myeloid malignancies. Confirmation and characterization of myeloid malignancies should be performed with a BM examination and the appropriate ancillary studies. Myeloid leukemoid reactions commonly result from infections and show activated neutrophil changes on morphology; these should prompt evaluation for infection. Other causes of reactive myeloid leukocytoses are also discussed herein.

Significance of mortalin expression in gastric cancer with normal p53.

2012 ◽  
Vol 30 (4_suppl) ◽  
pp. 25-25
Author(s):  
Koji Ando ◽  
Eiji Oki ◽  
Zhao Yan ◽  
Hiroyuki Kitao ◽  
Hiroshi Saeki ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Multivariate Analysis ◽  
Prognostic Factor ◽  
Heat Shock Protein 70 ◽  
Immunohistochemical Staining ◽  
Cell Stress ◽  
Clinical Samples ◽  
Morbidity Rate ◽  
P53 Expression ◽  
Worse Prognosis

25 Background: Gastric cancer still has the highest morbidity rate and the second highest mortality rate. As chemotherapy confers only a minimal survival advantage, the prognosis of patients with advanced or recurrent gastric cancer remains poor. Studying the mechanisms and underlying molecules that drives gastric cancer malignant, could contribute to finding a remedy for gastric cancer. Mortalin is a heat non-inducible member of the heat shock protein 70 family. Mortalin binds to p53 and prevents p53 from entering the nucleus, as well as cell stress. To understand the significance of mortalin in gastric cancer, we investigated the expression of mortalin and p53. Methods: The expression of mortalin and p53 were examined by immunohistochemical staining of 182 clinical samples of gastric cancer. Results: Mortalin-positive and aberrant-p53-positive samples were found in 75.2% and 62.6% of cases, respectively. Mortalin-positive tumors were deeper in invasion and had more lymph node and liver metastases compared with mortalin-negative tumors (p < 0.01, p < 0.05, respectively). Mortalin-positive tumors had worse prognosis compared with mortalin-negative tumors (p = 0.035). Moreover, in tumors with normal p53 expression, mortalin-positive tumors had especially worse prognosis compared with mortalin-negative tumors (p = 0.013). With multivariate analysis, mortalin expression appeared to be an independent prognostic factor in gastric cancer with expression of normal p53 (p = 0.0174). Conclusions: Mortalin has a great impact on gastric cancer with normal p53. Therefore, mortalin is a target molecule for treatment of gastric cancer, as well as a promising prognostic factor, especially in tumors with normal p53.

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