Delta Np73 expression in thyroid neoplasms originating from follicular cells

Ito, Yasuhiro; Uramoto, Hidetaka; Funa, Keiko; Yoshida, Hiroshi; Jikuzono, Tomoo; Asahi, Shuji; Higashiyama, Takuya; Tomoda, Chisato; Takamura, Yuuki; Miya, Akihiro; Kobayashi, Kaoru; Matsuzuka, Fumio; Kuma, Kanji; Miyauchi, Akira

doi:10.1080/00313020600696298

Cited by 7 publications

(2 citation statements)

References 17 publications

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“…One model of deregulated interaction among p53 family members is represented by thyroid cancer cells, which may express TAp63a, DNp73a and may harbor p53 mutations (37)(38)(39)(40)(41)(42)(43)(44)(45)(46). It is noteworthy that the ectopic expression of p53 by gene delivery in thyroid cancer cells harboring p53 mutations is not able to fully restore p53 tumor suppressor function (47)(48)(49)(50)(51).…”

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confidence: 99%

TAp73α Increases p53 Tumor Suppressor Activity in Thyroid Cancer Cells via the Inhibition of Mdm2-Mediated Degradation

Malaguarnera

Vella

Pandini

et al. 2008

Molecular Cancer Research

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p53 family proteins include p53 tumor suppressor, p63, and p73. Despite the high similarity in structure and function with p53, p63, and p73 function in tumor suppression is still controversial. Here, we show that TAp73A, a transcriptionally active p73 isoform, is able to synergize p53 tumor suppressor function in thyroid cancer cells. Indeed, depletion of p73 by small interfering RNA in thyroid cancer cells resulted in a reduced transcriptional activity of p53.

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confidence: 99%

TAp73α Increases p53 Tumor Suppressor Activity in Thyroid Cancer Cells via the Inhibition of Mdm2-Mediated Degradation

Malaguarnera

Vella

Pandini

et al. 2008

Molecular Cancer Research

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“…Controversial results are also found regarding thyroid neoplasms. Ferru and collaborators observed downregulation of TAp73 and Δ Np73 in 60 adenomas and in differentiated carcinomas (Ferru et al, ), while upregulation of Δ Np73 and its correlation with carcinoma progression was reported in 223 thyroid tumors (Ito et al, ).…”

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confidence: 98%

The TP73 complex network: Ready for clinical translation in cancer?

Soldevilla

Millán

Bonilla

et al. 2013

Genes Chromosomes & Cancer

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TP73 is a member of the TP53 family, whose deregulated expression has been reported in a wide variety of cancers and linked to patients' outcome. The fact that TP73 encodes a complex number of isoforms (TAp73 and ΔTAp73) with opposing functions and the cross-talk with other members of the family (TP53 and TP63) make it difficult to determine its clinical relevance. Here, we review the molecular mechanisms driving TAp73 and ΔTAp73 expression and how these variants inhibit or promote carcinogenesis. We also highlight the intricate interplay between TP53 family members. In addition, we comment on current pharmacological approaches targeting the TP73 pathway and those affecting the TAp73/ΔTAp73 ratio. Finally, we discuss the current data available in the literature that provide evidence on the role of TP73 variants in predicting prognosis. To date, most of the studies that evaluate the status levels of TP73 isoforms have been based on limited-size series. Despite this limitation, these publications highlight the correlation between high levels of the oncogenic forms and failure to respond to chemotherapy and/or shorter survival. Finally, we emphasize the need for studies to evaluate the significance of combining the deregulation of various members of the TP53 family in order to define patient outcome or their responsiveness to specific therapies.

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Clinical implications of the deregulated TP73 isoforms expression in cancer

et al. 2017

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TP73 is a member of the TP53 family whose expression has been observed altered in most human cancers and associated with the prognosis. TP73 translates into a complex number of isoforms with both oncogenic and tumour-suppressor functions and presents a complex cross-talk with other members of the family (TP53 and TP63). In this revision, we focus on the evidence that may support TP73 variants as prognostic markers in cancer. Nowadays, most publications in this topic highlight the association between overexpression of the oncogenic variants and failure to respond to chemotherapy and/or shorter survival. In addition, we comment on the putative possibilities that the detection through a liquid biopsy of TP73 variants may provide, and finally, the significance of determining the value of the combined alteration of the TP53 family members in the clinical setting.

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Delta Np73 expression in thyroid neoplasms originating from follicular cells

Cited by 7 publications

References 17 publications

TAp73α Increases p53 Tumor Suppressor Activity in Thyroid Cancer Cells via the Inhibition of Mdm2-Mediated Degradation

TAp73α Increases p53 Tumor Suppressor Activity in Thyroid Cancer Cells via the Inhibition of Mdm2-Mediated Degradation

The TP73 complex network: Ready for clinical translation in cancer?

Clinical implications of the deregulated TP73 isoforms expression in cancer

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