Clinicopathologic and molecular significance of phospho-Akt expression in early invasive breast cancer

Aleskandarany, Mohammed A.; Rakha, Emad A.; Ahmed, Mohamed A.; Powe, Desmond G.; Ellis, Ian O.; Green, Andrew

doi:10.1007/s10549-010-1012-y

Cited by 54 publications

(50 citation statements)

References 36 publications

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“…Higher proportions of luminal tumors were pAKT positive relative to TNBCs/basal subtypes. 19 There is a positive correlation between pAKT and hormone receptors, which suggested the possible mechanism of endocrine resistance in ER-positive breast cancer.9 In our study, pAKT expression was demonstrated in 85.7 % (30/35) of TNBCs. High pAKT expression was observed in the ST subtype.…”

supporting

confidence: 49%

Immunohistoochemical evaluation of GATA-3, pAKT and Ki-67 in triple negative breast carcinoma

Aryal

Aryal²,

Soejima³

et al. 2017

J Pathol Nep

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Background: Triple-negative breast cancers lack expression of estrogen receptor, progesterone receptor, and human epidermal growth factor receptor -2. These tumors have been known to be clinically aggressive. We evaluate GATA-3, pAKT and Ki-67 expression in 35 triple negative breast carcinomas. Materials and Methods: A total of 35 triple negative breast carcinomas were included in this study. The histological subtyping was done according to Japanese guidelines for breast cancer. Results: GATA-3 was positive in 60% (21/35) of tumors. High GATA-3 expression was observed in ductal carcinoma in situ. pAKT expression was demonstrated in 85.7 % (30/35) of TNBCs. The levels of expression of GATA-3 and pAKT showed no significant association with nuclear grading. (P=0.761 and P=0.487, respectively). Ki-67 labeling index was positively correlated with nuclear grading (p<0.001).Conclusion: GATA-3 expression has no relation with ER and PR expression and pAKT and GATA-3 are strongly expressed in triple negative breast cancers.

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supporting

confidence: 49%

Immunohistoochemical evaluation of GATA-3, pAKT and Ki-67 in triple negative breast carcinoma

Aryal

Aryal²,

Soejima³

et al. 2017

J Pathol Nep

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“…These studies have only analyzed the expression of p-Akt (27,33). Although our study may be limited by the small number of patients, to our knowledge, this study is the first to detect the two signaling proteins, p-Akt and PI3K, in ACC.…”

Section: Discussionmentioning

confidence: 96%

“…In ACC, few studies exist regarding the expression of signaling proteins of the PI3K/Akt pathway (27,33). These studies have only analyzed the expression of p-Akt (27,33).…”

Section: Discussionmentioning

confidence: 99%

Recurrent prognostic factors and expression of GLUT-1, PI3K and p-Akt in adenoid cystic carcinomas of the head and neck: Clinicopathological features and biomarkers of adenoid cystic carcinoma

et al. 2012

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Abstract. The purpose of this study was to explore the factors associated with the recurrence of adenoid cystic carcinomas (ACCs). We examined the recurrence values of clinicopathological variables and GLUT-1, p-Akt and PI3K expression in 42 patients with ACC. Of the 42 patients, 17 developed recurrence following initial surgery. The positive rates of GLUT-1, PI3K and p-Akt protein expression in ACC were 38.1, 38.1 and 50.0%, respectively. The expression of GLUT-1, p-Akt or PI3K protein in ACC was higher than that in inflammatory lesions or benign tumors. Our study demonstrated that T stage, a positive resection margin, perineural invasion, surgery without postoperative radiotherapy and the expression of GLUT-1, PI3K and p-Akt were factors predictive of recurrence by univariate analyses. In multivariate analyses, perineural invasion, a positive resection margin and p-Akt were significant predictors of recurrence. Initial surgery is very significant in the recurrence of ACC. Overexpression of GLUT-1, PI3K and p-Akt may also play a role in its development and recurrence.

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“…157 In addition, approximately 5% of breast cancers may harbour activating mutations in AKT. 158 The fact that strong immunostaining for Akt has been associated with a poor prognosis in breast cancer patients independent of adjuvant therapy [159][160][161] indicates a general prognostic role for activation of the PI3K/Akt system in breast cancer. Notably, experimental evidence has linked activation of the Akt/mTOR pathway to a number of biological processes; overexpressing Akt has been shown to enhance lymphangiogenesis and confer resistance to cyclophosphamide as well as doxorubicin in murine models, 162 effects that are reversed by blocking Akt's downstream effector mTOR by rapamycin.…”

Section: Activating Mutations In the Pten/pi3k/mtor Pathway As A Causmentioning

confidence: 99%

Mapping genetic alterations causing chemoresistance in cancer: identifying the roads by tracking the drivers

Lønning

Knappskog

2013

Oncogene

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Although new agents are implemented to cancer therapy, we lack fundamental understandings of the mechanisms of chemoresistance, the main obstacle to cure in cancer. Here we review clinical evidence linking molecular defects to drug resistance across different tumour forms and discuss contemporary experimental evidence exploring these mechanisms. Although evidence, in general, is sparse and fragmentary, merging knowledge links drug resistance, and also sensitivity, to defects in functional pathways having a key role in cell growth arrest or death and DNA repair. As these pathways may act in concert, there is a need to explore multiple mechanisms in parallel. Taking advantage of massive parallel sequencing and other novel high-throughput technologies and base research on biological hypotheses, we now have the possibility to characterize functional defects related to these key pathways and to design a new generation of studies identifying the mechanisms controlling resistance to different treatment regimens in different tumour forms.

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Clinicopathologic and molecular significance of phospho-Akt expression in early invasive breast cancer

Cited by 54 publications

References 36 publications

Immunohistoochemical evaluation of GATA-3, pAKT and Ki-67 in triple negative breast carcinoma

Immunohistoochemical evaluation of GATA-3, pAKT and Ki-67 in triple negative breast carcinoma

Recurrent prognostic factors and expression of GLUT-1, PI3K and p-Akt in adenoid cystic carcinomas of the head and neck: Clinicopathological features and biomarkers of adenoid cystic carcinoma

Mapping genetic alterations causing chemoresistance in cancer: identifying the roads by tracking the drivers

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