2006
DOI: 10.1016/j.advenzreg.2006.01.004
|View full text |Cite
|
Sign up to set email alerts
|

Roles of the RAF/MEK/ERK and PI3K/PTEN/AKT pathways in malignant transformation and drug resistance

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

21
478
0
5

Year Published

2007
2007
2019
2019

Publication Types

Select...
10

Relationship

0
10

Authors

Journals

citations
Cited by 568 publications
(504 citation statements)
references
References 97 publications
21
478
0
5
Order By: Relevance
“…The fact that not all effectors of Ras mediate the same biological effects of Ras is consistent with previous studies that showed, for example, that the Raf/Mek pathway predominantly mediates proliferation whereas the PI3K/Akt drives survival. [27][28][29][30][31][32] Furthermore, our results are consistent with other reports that demonstrated that the RalGDS/RalA-RalB pathway downstream of Ras may be more important at mediating Ras-driven malignant transformation than the PI3K/Akt and the Raf-1/Mek pathways in some but not all tumors. 27 Interestingly, we have found that depletion of RalA and RalB in some tumors, particularly those of pancreatic origin, such as Panc-1 and MiaPacca-2 cells, does not result in decreasing survivin levels.…”
Section: Discussionsupporting
confidence: 92%
“…The fact that not all effectors of Ras mediate the same biological effects of Ras is consistent with previous studies that showed, for example, that the Raf/Mek pathway predominantly mediates proliferation whereas the PI3K/Akt drives survival. [27][28][29][30][31][32] Furthermore, our results are consistent with other reports that demonstrated that the RalGDS/RalA-RalB pathway downstream of Ras may be more important at mediating Ras-driven malignant transformation than the PI3K/Akt and the Raf-1/Mek pathways in some but not all tumors. 27 Interestingly, we have found that depletion of RalA and RalB in some tumors, particularly those of pancreatic origin, such as Panc-1 and MiaPacca-2 cells, does not result in decreasing survivin levels.…”
Section: Discussionsupporting
confidence: 92%
“…To enhance anticancer activity of sorafenib, the combination of sorafenib and doxorubicin was evaluated in several studies. Sorafenib plus doxorubicin is an attractive regimen since inhibition of Ras/Raf/MEK/ERK signaling pathway by sorafenib may suppress expression of MDR-1 (70). Therefore, the combination can increase area under the curve (AUC) of doxorubicin without worsening toxicities (71).…”
Section: Combination With Sorafenibmentioning
confidence: 99%
“…A complete loss of PTEN is more frequent in metastatic than in primary tumors 16 In vitro and clinical studies confirmed that deregulation of the PI3K/PTEN/Akt pathway was associated with resistance to doxorubicin and tamoxifen, drugs commonly used in metastatic breast cancer therapy. 18 This may have significant implications since chemotherapy and hormonal therapy are basic modalities for the treatment of metastatic breast carcinoma. On the other side, specific mutations we detected in our case, give new insights in both breast carcinogenesis and novel therapeutic modalities.…”
Section: Discussionmentioning
confidence: 99%