DigitalUM :: Browsing by Subject "p53"

Browsing by Subject "p53"

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Open Access
Aging and uterine serous carcinoma
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Hachisuga, Toru
Uterine serous carcinoma (USC) is closely associated with advanced age in patients. The p53 signature (p53S) is considered the earliest indication for the presence of carcinogenesis of USC. Based on our previous studies, the presence of p53Ss have almost always been found in elderly women and are suspected of being responsible for the imbalance between the proliferation and apoptosis of endometrial epithelial cells with advanced age. We have summarized the current state of knowledge regarding the association between age and cancer and propose an age-related type of endometrial cancer instead of Type II estrogenindependent endometrial cancer.
Open Access
ATRX loss in adult supratentorial diffuse astrocytomas correlates with p53 over expression and IDH1 mutation and predicts better outcome in p53 accumulated patients
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Shao, Li-Wei; Pan, Yi; Qi, Xue-Ling; Ma, Xiao Long; Yi, Wei-Ning; Zhang, Jing; Zhong, Yan-Feng; Chang, Qing
Background: IDH1/2 mutation, 1p/19qcodeletion and MGMT hypermethylation are well known molecular markers for gliomas. ATRX and p53 alterations are two lineage-specific genetic aberrations in diffuse astrocytic tumors. The aim of the present study is to clarify the significance of ATRX loss and its correlation with p53 overexpression, IDH1/2 mutations, 1p/19q-codeletion and MGMT hypermethylation in supertentorial astrocytoma, and to determine the prognostic value of these factors in Chinese patients. Methods and Results: A total of 135 adult supertentorial astrocytomas were evaluated. ATRX loss was detected by immunohistochemistry (IHC) and was shown to be much less frequent in pGBs (3.5%) than in grade II, III astrocytomas and IV sGBs (31%). Direct sequencing and/or IHC analysis of the IDH1R132H gene mutation and p53 accumulation demonstrated correlation with age. Strong correlations were found between ATRX loss and IDH1R132H mutation, p53 overexpression as well as MGMT hypermethylation. 1p/19q-codeletion detected by fluorescence in situ hybridization (FISH) showed mutually exclusive with ATRX loss and p53 accumulation. In addition, patients with p53 overexpression combined with ATRX alterations demonstrated substantially longer survival than patients with wild-type ATRX. Conclusions: There may be interactions among these distinct molecules in astrocytoma development. ATRX loss may predict better clinical outcome in astrocytoma patients with p53 overexpression as compared to patients with wild-type ATRX. Tumors with astrocytoma phenotype accompanied by 1p/19q-codeletion and IDH1R132H mutation are mutually exclusive with ATRX and p53 alterations. Routine IHC can be used for evaluation of ATRX loss, p53 protein accumulation and IDH1R132H mutation, which may allow a means of classification of astrocytoma outcome.
Open Access
Bcl-2 expression in colorectal tumours. Correlation with p53, mdm-2, Rb proteins and proliferation indices
(Murcia : F. Hernández, 2000) Goussia, A.C.; Loachim, E.; Agnantis, N.J.; Mahera, M.; Tsianos, E.V.
Immunostaining for bcl-2 protein was performed in 27 colorectal adenomas and 108 colorectal adenocarcinomas. The aim of the study was to determine bcl-2 expression in correlation with p53, mdm-2 and Rb expression, with proliferation indices (Ki-67-LI, PCNALI) as well as with conventional clinicopathological variables. A higher proportion of adenomas (30.8%) than carcinomas (16.7%) expressed bcl-2 and conversely, a lower proportion of adenomas (7.4%) than carcinomas expressed p53 (57.1 %), the difference being statistically significant (p<0.0001). No correlation of bcl-2 expression with p53 expression (parallel or inverse) as well as with the other parameters studied was observed in any tumour. The bcl-2+/p53- subgroup of cancers showed a trend for correlation with negative lymph node status. Our data suggest, that bcl-2 expression may be involved in the early phase of colorectal carcinogenesis regardless of p53 status, while p53 function may be involved in a late stage of the adenoma-carcinoma sequence. P53 is apparently not involved in the regulation of apoptosis in the colorectal neoplasias or perhaps bcl-2 expression, as an early event in colorectal tumours, may occur before changes of p53 take place. Tumours with bcl-2+/p53- immunophenotype are frequently associated with negative lymph node status and seem to have a less aggressive behavior.
Open Access
Downregulation of nuclear ING3 expression and translocalization to cytoplasm promotes tumorigenesis and progression in head and neck squamous cell carcinoma (HNSCC)
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Li, Xiaohan; Zhang, Qun; Zhang, Mingming; Luo, Yusong
ING3 (inhibitor of growth gene 3) is a member of the ING gene family, and is considered as a candidate tumor suppressor gene. In order to explore the roles of ING3 in tumorigenesis and cancer progression of head and neck squamous cell carcinoma (HNSCC), ING3 expression was assessed in 173 cases of HNSCC by immunohistochemistry. The expression of ING3 was also compared to clinicopathological variables, and the expression of several tumorigenic markers. Nuclear expression of ING3 in HNSCC was significantly lower than that in dysplasia and normal epithelium, and was negatively correlated with a poor-differentiated status, T staging and TNM staging. In contrast, cytoplasmic expression of ING3 was significantly increased in HNSCC, and was statistically associated with lymph node metastasis and 14-3-3η expression. In addition, nuclear expression of ING3 was positively correlated with the expression of p300, p21 and acetylated p53. In conclusion, decreases in nuclear ING3 may play important roles in tumorigenesis, progression and tumor differentiation in HNSCC. Increases in cytoplasmic ING3 may be due to 14-3-3η binding and may also be involved in malignant progression. Nuclear ING3 may modulate the transactivation of target genes, promoting apoptosis through interactions with p300 and p21. Moreover, ING3 may interact with p300 to upregulate the level of acetylation of p53, and promote p53- mediated cell cycle arrest, senescence and/or apoptosis. Therefore, ING3 may be a potential tumor suppressor and a possible therapeutic target in HNSCC
Open Access
Expression of p53 and selected proliferative markers (Ki-67, MCM3, PCNA, and topoisomerase IIα) in borderline ovarian tumors: Correlation with clinicopathological features
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Ciepliński, Klaudiusz; Jóźwik, Maciej; Semczuk Sikora, Anna; Gogacz, Marek; Lewkowicz, Dorota; Ignatov, Atanas; Semczuk, Andrzej
Background. The expression of p53 has been studied not only in primary human ovarian carcinomas, but also in borderline ovarian tumors, however, the results were discordant. Expression patterns of proteins involved in cell proliferation and apoptosis have been investigated in various human neoplasms, including female genital tract neoplasms. Objective. The aim of this investigation was to assess the staining pattern and immunolocalization of p53 and selected proliferative markers (Ki-67, MCM3, PCNA, and topoisomerase IIα) in borderline ovarian tumors (BOTs). Design. The study group consisted of 42 women who underwent pelvic surgery between 2006-2015. The median patients’ age was 46 years. The immunoperoxidase technique was employed using antibodies against p53, Ki-67, MCM3, PCNA, and topoisomerase IIα. Results. For p53, nuclear expression was observed in BOTs, however, cytoplasmatic immunoreactivity was also detected. Altogether, 25 (60%) tumors demonstrated positive p53 immunostaining, including overexpression found in 6 (14%). There were no significant differences in p53 expression between subgroups of clinicopathological variables. Immunoexpression of Ki-67, MCM3, PCNA, and topoisomerase IIα was nuclear. Ki67 expression was positive in 12 (29%) cases and there was a trend towards a relationship between patients’ age and Ki-67 staining (P=0.08). Interestingly, a significantly higher Ki-67 expression was found in tumors of ≥10 cm in diameter compared to smaller tumors (P=0.008). MCM3 expression was detected in 38 (90%) tumors, and PCNA expression in 28 (67%), yet none of clinico-pathological factors was related to them. Topoisomerase IIα expression was present in 14 (33%) cases and, interestingly, its significantly higher expression was observed in BOTs of ≥10 cm in diameter compared to smaller tumors (P=0.008). Moreover, Spearman’s correlation revealed highly significant positive associations between Ki-67 and topoisomerase IIα (R=0.403, P=0.008) and Ki-67 and MCM3 (R=0.469, P=0.001). Conclusions. We report a high positive immunostaining rate for p53, suggesting a role of TP53 alterations in the development of BOTs in humans. The new finding of higher topoisomerase IIα immunostaining positivity in BOTs of ≥10 cm may be clinically relevant and requires further studies on larger patient groups.
Open Access
Expression of p53 family members and CD44 in oral squamous cell carcinoma (OSCC) in relation to tumorigenesis
(Murcia : F. Hernández, 2010) Bidaud, Pauline; Chasle, Jacques; Sichel, François; Rousseau, Stéphane; Petit, Pascal; Pottier, Didier; Picquenot, Jean Michel; Louis, Marie-Yolande; Lechevrel, Mathilde
Oral squamous cell carcinomas (OSCCs) aredescribed as the result of a multistep tumorigenesisprocess. In order to develop useful diagnosis of pre-malignant lesions, expression of p53 family membersand the cancer stem cell (CSCs) marker, CD44v6, werestudied in histologically normal oral epithelium,precancerous lesions and succeeding invasive OSCCs.p53 was expressed focally in normal epithelium adjacentto tumors, while expression was high in intra-epithelialneoplasia and moderate in OSCC. p63 nuclear stainingwas important in basal and suprabasal layers ofhistologically normal oral mucosa and in immaturecompartments of premalignant lesions and cancer. Inepithelium without neoplasia, intense p73 staining wasobserved in the basal layer, while focal expression waspresent in suprabasal layers. Most immature dysplasticareas showed either high or moderate staining, whereasthose in OSCCs expressed low and moderate p73 levelexpression. CD44v6 was only expressed in poorlydifferentiated areas of epithelium, altered or not. p53,p63 and p73 positive stainings were statistically relatedin intra-epithelial neoplasia to tumours. Analysis ofTP53 mutations in 17% of tumours principally revealedG>A and A>G transitions. No relation was observedbetween this mutational profile and differentimmunostainings. In conclusion, our results support thatimmunostaining of p53 family members might behelpful in diagnosis and monitoring of high-risk pre-malignant lesions of oral epithelium. The combination ofstaining patterns of p63, p73αand CD44v6 enabled us to isolate phenotypic undifferentiated or transientamplifying areas, reflecting the immaturity of the tumourcell lineage. While CD44v6 expression is an interestingmarker of such epithelial cells, it is not specific enoughto be useful alone and other phenotypic markers areneeded.
Open Access
Expression of p53 in endometrial polyps with special reference to the p53 signature
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Sho, Tomoko; Hachisuga, Toru; Kawagoe, Toshinori; Urabe, Rie; Kurita, Tomoko; Kagami, Seiji; Shimajiri, Shohei; Fujino, Yoshihisa
We herein examined the significance of the p53 expression in endometrial polyps (EMPs). A total of 133 EMPs, including 62 premenopausal and 71 postmenopausal women with EMP, were immunohistochemically studied for the expression of estrogen receptor (ER)-alpha, Ki-67 and p53. Apoptotic cells were identified using a TUNEL assay. A DNA sequence analysis of TP53 exons 5 to 9 was performed. Among the premenopausal EMPs, a multivariate analysis showed the labeling index (LI) for Ki-67 to correlate significantly with that for p53 (P<0.001), but not that for apoptosis. On the contrary, among the postmenopausal EMPs, the LI for Ki-67 correlated significantly with that for apoptosis (P<0.001). The p53 signature (p53S) was defined by endometrial epithelial cells, which are morphologically benign in appearance but display 12 or more consecutive epithelial cell nuclei with strong p53 immunostaining. The p53S was found in nine (12.7%) postmenopausal EMPs (mean age: 70.2 years). The median Ki-67 index for the p53S was 7%, with no significant difference from that of the glands of the postmenopausal EMPs without the p53S (P=0.058). The median apoptotic index for the p53S was 0%, which was significantly lower than that of the postmenopausal EMPs without the p53S (P=0.002). Two of four p53Ss showed TP53 mutations according to the DNA sequence analysis. The presence of the p53S is not rare in postmenopausal EMPs with an advanced age. Among postmenopausal EMPs, the LI of Ki-67 significantly correlates with that of apoptosis. However, such a positive correlation between the LI of Ki-67 and apoptosis is not observed in p53S.
Open Access
Gain of function properties of mutant p53 proteins at the mitotic spindle cell cycle checkpoint
(Murcia : F. Hernández, 2000) Hixon, M.L.; Flores, A.; Wagner, M.; Gualberto, A.
Mutations in the p53 tumor suppressor gene locus predispose human cells to chromosomal instability. This is due in part to interference of mutant p53 proteins with the activity of the mitotic spindle and postmitotic cell cycle checkpoints. Recent data demonstrates that wild type p53 is required for postmitotic checkpoint activity, but plays no role at the mitotic spindle checkpoint. Likewise, structural dominant p53 mutants demonstrate gain-of-function properties at the mitotic spindle checkpoint and dominant negative properties at the postmitotic checkpoint. At mitosis, mutant p53 proteins interfere with the control of the metaphase-toanaphase progression by up-regulating the expression of CKsl, a protein that mediates activatory phosphorylation of the anaphase promoting complex (APC) by Cdc2. Cells that carry mutant p53 proteins overexpress CKsl and are unable to sustain APC inactivation and mitotic arrest. Thus, mutant p53 gain-of-function at mitosis constitutes a key component to the origin of chromosomal instability in mutant p53 cells.
Open Access
Immunohistochemical expression of p53 in animal tumors: a methodological study using four anti-human p53 antibodies
(2001) Albaric, O.; Bret, L.; Amardeihl, M.; Delverdier, M.
Mutations in the p53 tumor suppressor gene are the most common genetic alterations in human cancers. These mutations usually lead to strongly enhanced protein stabilization and allow detection by immunohistochemistry. Two monoclonal (DO-7 and PAb-240) and two polyclonal (Ab-7 and CM-l) antibodies were evaluated by standard immunoperoxidase method in domestic animal tumors, chiefly squamous cell carcinomas (Scq, and osteosarcomas as positive controls. Immunoreactivity was detected in SCC of cattle, sheep, horse and cat as well as in feline actinic keratosis, with PAb-240 and CM-l antibodies. One polyclonal antibody (Ab-7) did not give positive result at all, whereas DO-7 monoclonal antibody did not react in dogs and cats. Immunodetection of p53 protein is thus possible in all domestic species tested, especially with CM-l and PAb-240 antibodies, and p53 alterations seem to occur early in carcinogenesis of feli ne SCC as in comparable human lesions.
Open Access
lmmunohistochemical study of p53 expression in cancer tissues from patients undergoing radiation therapy
(Murcia : F. Hernández, 1995) Hamada, N.; Ogawal, Y.; Seguchi, H.; Terashima, M.; Nishioka, A.; Inomata, T.; Yoshida, S.; Kishimoto, S.; Saito, H.
Immunostaining using p53 monoclonal antibodies (p53(Ab-3) recognizes mutant type and p53(Ab-6) the wild type of p53 protein) was performed on frozen sections of biopsy specimens obtained before and during preoperative radiotherapy from 23 patients with head and neck squamous cell carcinoma. The positive staining rates of p53(Ab-3) before radiotherapy and at radiation doses of 4Gy, lOGy and 20Gy were 30.0%, 38.9%, 25.0% and 6.25%, and those of p53(Ab- 6) 10,5%, 11.8%, 5.0% and 0% respectively. The relationship between the immunohistochemical findings and antitumor effect at radiation dose of 20Gy was examined on the correspondent haematoxylin-eosin sections. In patients whose p53(Ab-3) stainings were positive at any doses of radiotherapy, the antitumor effect at the cumulative dose of 20Gy was either remarkable or effective. Moreover, the frequency of the expression of mutant type p53 protein tended to increase in rather radiosensitive tumors. As for wild type p53 protein, there was no remarkable relationship between the staining of p53(Ab-6) and the antitumor effect.
Open Access
p53 mutation and protein alteration in 50 gliomas. Retrospective study by DNA-sequencing techniques and immunohistochemistry
(Murcia : F. Hernández, 1997) von Eckardstein, K.; Gries, H.; Bolik, E.; Cervós-Navarro, J.; Tschairkin, I.N.; Patt, Stephan
Alterations of the p53 protein, which is a 53 kD phosphoprotein and gene product of the p53 gene, has been found to play a major role in the genesis of a variety of human malignancies including tumors of the central nervous system. We investigated 50 tumor specimens from primary central nervous system neoplasms. Tissue samples were screened for mutations by the single-strand conformation polymorphism method and detected mutations were sequenced. Al1 tissue specimens were stained immuno- ' histochemically for p53 protein, which when altered accumulates in the nucleus due to prolonged halflife. Mutations were found in six cases, including one pilocytic astrocytoma World Health Organisation (WHO) grade 1, two astrocytomas WHO grade 11, two anaplastic astrocytomas WHO grade 111, and one primitive neuroectodermal tumor (PNET). In terms of relative frequency mutations were found mostly in the group of anaplastic astrocytomas WHO grade 111. Interestingly, no mutations were found in the group of investigated glioblastomas. P53 immunopositivity did not correlate with the mutations found, whereas the staining index was significantly higher in the cases with detected mutations than in those without. When p53 alteration is seen as an indicator for different pathogenic pathways in glioma formation, this study gives evidence for a difference between anaplastic astrocytoma and glioblastoma. However, since there was a great overlap in p53 immunopositivity and p53 mutation in tumors of different WHO grades and entities, it seems that p53 will not act as a marker molecule neither for tumor entities nor for tumor malignancy.
Open Access
p53, latent membrane protein 1, bcl-2, and prognosis in nasopharyngeal carcinoma: a meta-analysis
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2019) Yang, Guang Da; Wang, Zhi Chao; Chen, Qian Ya; Zhang, Hai Liang; Lin, Xian Gan; Huang, Tie Jun; Qian, Chao Nan; Huang, Bi Jun
The controversy of (p53) in nasopharyngeal carcinoma persists, despite the fact that many studies have been conducted on its correlation with latent membrane protein 1 (LMP1), bcl-2, and prognosis. To better understand this postulated relationship, a metaanalysis was performed based on existing relevant studies. A total of 19 individual studies with a total of 1189 patients were included in the meta-analysis. Overall, the results revealed a significant association of p53-positive status with a poor 5-year survival of nasopharyngeal carcinoma (NPC) patients as the risk difference (RD) was -0.17 (95% CI, -0.31, -0.03; P=0.02, Pheterogeneity=0.01).The overall odds ratio (OR) for LMP1 in the p53 positive group vs. negative group revealed that a significantly elevated risk of positive LMP1 in the former was achieved (OR 5.52 95% CI, 2.66-11.46; P<0.00001, Pheterogeneity=0.78). Similarly, a strong correlation between bcl-2 and p53 was found with an OR 6.85 (95% CI, 2.37-19.74; P=0.0004, Pheterogeneity=0.48). However, there did not appear to be any correlations with clinical parameters such as gender, tumor site, lymph node metastasis, pathological type and TNM stage. In conclusion, p53 expression is related to the survival of nasopharyngeal carcinoma. It can be considered as the auxiliary detection index in treatment and prognosis of nasopharyngeal carcinoma
Open Access
Prognostic value of p53 protein expression and clinicopathological factors in infiltrating ductal carcinoma of the breast. A study of 192 patients
(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2001) Sirvent, J. J.; Fortuño Mar, A.; Olana, M.; Ortí, A.
The p53 gene is located on the short arm of chromosome 17. It encodes a 53-kd nuclear protein (p53) found in scant amounts in normal tissue. Mutations of the p53 gene have been reported in different human tumours. In breast cancer, it has been noted that the overexpression of p53 protein in the nucleus is an indicator of poor prognosis, although there is a high degree of variability, which may be due to different immunohistochemical techniques, varying assessment of results a nd the type of monoclonal antibody used. This study is an immunohistochemical analysis of p53 expression in 192 cases of infiltrating ductal carcinoma of the breast, correlating it with clinicopathological factors and the clinical course of the disease. Of all the breast-cancer tissue analysed, stains for p53 antibody were found in 87 tumours (45.3%). The results of multivariate ana lysis show that the independent predictors related to recurrence are tumour size, Iymphnode metastasis and p53, while those related to death are necrosis, lymph-node metastasis and p53. In summary, our series showed prognostic significance between the expression of p53 and shorter survival time and disease-free interval for all patients in general as well as those who prese nted lymph-node metastases at the time of diagnosis.
Open Access
Role of miRNAs in endometrial cancer
(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Li, Shuangdi; Zhang, Jiarong; Wan, Xiaoping
Endometrial cancer (EC) is the most common gynecologic malignancy. MicroRNAs (miRNAs) were recently associated with carcinogenesis and progression of EC. In this review, we discuss recent advances and the emerging role of miRNAs in EC and their clinical implications, with special emphasis on the differences between deregulated miRNAs in type I and type II EC, as well as the impact of this dysregulation on EC initiation and progression.
Open Access
The ARF-p53 senescence pathway in mouse and human cells
(Murcia : F. Hernández, 2004) Wadhwa, R.; Sugahara, T.; Taira, K.; Kaul, S.C.
Mouse and human cells have most frequently been used for studies that have led to the elucidation of various molecular pathways involved in senescence. The ARF–p53 pathway has been assigned as one of the major protagonists in these phenomena. ARF is an alternative reading frame protein encoded along with p16INK4A by the INK4a locus on human chromosome 9p21 and the corresponding locus on mouse chromosome 4. Whereas the mouse ARF (p19ARF) consists of 169 amino acids, the human ARF (p14ARF) consists of 132 amino acids, truncated at the C-terminus. Molecular studies on the regulation of ARF activity by its binding partners have revealed that mouse ARF protein, but not human ARF protein, interacts with a cytoplasmic protein, Pex19p. This interaction of mouse ARF with Pex19p results in its milder p53 activation function in mouse cells as compared to human cells and thus accounts, at least in part, for the weaker tumor surveillance and frequent immortalization of mouse cells.
Open Access
The clinical translational potential of p53-related alterations as cancer biomarkers
(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Xiao, Meng; Wang, Xu; Chen, Wantao
We aimed to analyse and summarise the potential value of the clinical use of p53-related alterations as cancer biomarkers. A systematic search and collection of the published meta-analyses on p53- related alterations and cancers in the past 5 years was conducted through appropriate queries in the PubMed database. We then composed “grey-scale” tables to show the significant levels for each variant, and the potential heterogeneity was subsequently discussed. The data show that p53-related alterations are extremely complex biomarkers in terms of their clinical translation. Together with the experimental studies on p53-related alterations, a gold-standard approach is still in need of development, with more evidence from clinical studies with large, prospectively planned cohorts, to fully understand its potential as a cancer biomarker.
Open Access
The diverse oncogenic and tumour suppressor roles of p63 and p73 in cancer: a review by cancer site
(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Orzol, Paulina; Holcakova, Jitka; Nekulova, Marta; Nenutil, Rudolf; Vojtesek, Borivoj; Coates, Philip J.
p63 and p73, the two other members of the p53 family, were identified almost 15 years ago. Here, we review their potential use for diagnosis, prognosis and prediction of response to therapy in various cancers. The two genes show distinct expression patterns in both normal and cancer tissues and each gene gives rise to multiple protein isoforms with different activities, including those with tumour-suppressor or oncogenic effects. Despite such complexity, some common themes emerge; p63 is commonly overexpressed as the ΔNp63 isoform and sometimes associated with TP63 amplification, whereas p73 is often reduced (by methylation or gene loss), or there is an increase in the ratio of ΔNp73 to TAp73. These generalisations do not apply universally; TAp63 is overexpressed in haematological malignancies, TP63 mis-sense mutations have been reported in squamous cancers and TP63 translocations occur in lymphomas and some lung adenocarcinomas. There are associations with disease prognosis and response to specific therapies in individual cancer types for both p63 and p73, making their analysis of clinical relevance. We also discuss their utility for aiding in differential diagnosis, which has been demonstrated for p63, but not yet for p73. Throughout, we highlight the discrepant nature of many studies due to the variable methodologies employed, the lack of systematic evaluation of isoforms and the problems of poor antibody characterization and crossreactions within the p63/p73 family. Finally, we emphasize the value of recently developed isoformspecific reagents that have clear advantages for the study of p63 and p73 experimentally and clinically.

Browsing by Subject "p53"

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