Breast Cancer - ER+, HER2-, PIK3CA Gene Mutationp-AKT p-S6NCT07387861
PI3K Pathway Activation Markers in ER-Positive, HER2-Negative Breast Cancer: A Clinicopathologic Study
An observational study of Breast Cancer - ER+, HER2-, PIK3CA Gene Mutation, run by Assiut University.
Trial summary
The goal of this observational study is to examine whether markers of PI3K pathway activation are associated with endocrine therapy response and clinicopathologic features in estrogen receptor-positive, HER2-negative breast cancer. Read more about this study
- Who is it for?
- Any age
- Conditions the study is for
- Breast Cancer - ER+, HER2-, PIK3CA Gene Mutation
- What is being tested?
- Not applicable- observational study
- How many people
- 70 participants
- Where
- No sites listed yet
- Study dates
- Mar 2026to Mar 2028
- Phase
- Observational
- Are there results?
- Not yet: the study is under way
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages Any age
- All sexes
- No healthy volunteers
- Child, Adult, Older adult
Study population: Patients with estrogen receptor-positive (ER+), HER2-negative invasive breast cancer who received adjuvant endocrine therapy and have available formalin-fixed, paraffin-embedded (FFPE) tumor tissue archived in the Surgical Pathology Laboratory of Assiut University Hospital, as well as corresponding clinical follow-up data in the medical records of the Oncology Department at Assiut University Hospital.
Who may be able to join
- Patients diagnosed with invasive breast carcinoma.
- ER-positive and HER2-negative tumor status.
- Received adjuvant endocrine therapy as part of routine clinical care.
- Archived formalin-fixed paraffin-embedded (FFPE) tumor tissue available from excisional specimens (mastectomy).
- Available medical records documenting treatment history and follow-up outcomes.
Who cannot join
- Cases with missing or unavailable FFPE tissue blocks.
- Cases with insufficient tissue quality for immunohistochemistry (e.g., severely degraded or exhausted FFPE block).
- Cases with unknown or incomplete follow-up or treatment data.
Trial locations and contacts
No sites are listed yet. Contact the study team or a site near you to ask about taking part.
About this study
Official title: Immunohistochemical Evaluation of p-AKT and p-S6 as Surrogate Markers of PI3K/AKT/mTOR Pathway Activation in ER-Positive, HER2-Negative Breast Carcinoma
The goal of this observational study is to examine whether markers of PI3K pathway activation are associated with endocrine therapy response and clinicopathologic features in estrogen receptor-positive, HER2-negative breast cancer. The main questions it aims to answer are:
Are immunohistochemical levels of phosphorylated AKT (p-AKT) and phosphorylated S6 (p-S6) different between endocrine-sensitive and endocrine-resistant breast cancer cases? Do different levels of p-AKT and p-S6 show distinct clinicopathologic and histologic characteristics, including features of the tumor microenvironment?
Archived tumor tissue from patients who received adjuvant endocrine therapy as part of routine clinical care will be analyzed. Biomarker expression will be correlated with clinicopathologic parameters, including tumor-infiltrating lymphocyte density, tumor budding, and other histologic features, to explore associations with tumor behavior and outcomes.
Read the detailed description
Endocrine therapy is the cornerstone of treatment for estrogen receptor-positive breast cancer; however, a substantial proportion of patients develop resistance during the disease course. Activation of the PI3K/AKT/mTOR signaling pathway has been implicated as a key mechanism underlying resistance to endocrine therapy and disease progression. While genomic alterations in PI3K pathway-related genes are commonly assessed, they do not consistently reflect pathway activation or predict therapeutic response, highlighting the need for practical surrogate biomarkers.
The aim of this study is to evaluate immunohistochemical markers of PI3K pathway activation in estrogen receptor-positive, HER2-negative invasive breast carcinoma and to explore their associations with endocrine therapy response and clinicopathologic characteristics. Specifically, the study examines whether levels of phosphorylated AKT (p-AKT) and phosphorylated S6 (p-S6) differ between endocrine-sensitive and endocrine-resistant cases and whether these markers correlate with histologic features related to tumor biology and the tumor microenvironment.
This is a retrospective observational study including patients with estrogen receptor-positive, HER2-negative invasive breast carcinoma who received adjuvant endocrine therapy as part of routine clinical care. Archived formalin-fixed, paraffin-embedded (FFPE) tissue blocks from excisional surgical specimens will be retrieved, and clinicopathologic and follow-up data will be collected from medical records.
Cases will be classified into endocrine-sensitive and endocrine-resistant groups based on international consensus definitions using the timing of disease recurrence relative to endocrine therapy. Immunohistochemical staining for p-AKT and p-S6 will be performed on FFPE tissue sections and evaluated using a semi-quantitative scoring system. Histopathologic assessment will include standard reporting parameters as well as additional features such as tumor-infiltrating lymphocyte density, tumor budding, lymphovascular invasion, perineural invasion, and tumoral necrosis. Associations between biomarker expression, clinicopathologic features, and follow-up outcomes will be explored.
- Being tested
- Not applicable- observational study
- Keywords
- Breast Cancer, PI3K/AKT/mTOR pathway, Phospho-AKT, Phospho-S6, Endocrine therapy, Tumor budding, TILs
- Medical subject headings
- Breast Neoplasms
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Not applicable- observational studyOther
Not Applicable. This is an observational study; no interventions are assigned.
| Study group | Role | What they receive |
|---|---|---|
| Endocrine-Resistant Breast Cancer | Patients with ER-positive, HER2-negative invasive breast carcinoma who developed primary or secondary resistance to adjuvant endocrine therapy. Receives: Other: Not applicable- observational study | |
| Endocrine-Sensitive Breast Cancer | Patients with ER-positive, HER2-negative invasive breast carcinoma who remained relapse-free during adjuvant endocrine therapy and for ≥12 months after completion, with sufficient follow-up. Receives: Other: Not applicable- observational study |
What is being measured
The primary outcome is the main question the study is designed to answer.
Immunohistochemical expression of PI3K pathway activation markers: p-AKT and p-S6.
Semi-quantitative assessment of phosphorylated AKT (Ser473) and phosphorylated S6 ribosomal protein in FFPE breast carcinoma tissue sections, scored using H-score, to compare expression levels between endocrine-sensitive and endocrine-resistant ER-positive, HER2-negative cases.
Measured: At the time of immunohistochemical staining of archived tissue (single time point).
Secondary outcomes (3)
Correlation of p-AKT and p-S6 expression with endocrine therapy response.
Description: Association of biomarker expression with endocrine therapy response (sensitive vs resistant) and time to recurrence or progression.
Measured: through study completion, an average of 2 years
Correlation of p-AKT and p-S6 expression with histologic features
Association of biomarker expression with tumor grade, histologic type, luminal subtype, tumor budding, tumor-infiltrating lymphocyte (TIL) density, lymphovascular invasion, perineural invasion, and tumor necrosis.
Measured: through study completion, an average of 2 years
Correlation of p-AKT and p-S6 expression with clinicopathologic features
Description: Association of biomarker expression with patient age, menopausal status, tumor size, nodal status, and stage at presentation.
Measured: through study completion, an average of 2 years
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted4 Feb 2026
- Study startMar 2026 (estimated)
- Primary completionJan 2028 (estimated)
- Study completionMar 2028 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (14)Papers the sponsor has linked to this study.
- Other trials for Breast Cancer - ER+, HER2-, PIK3CA Gene MutationStudies of the same condition, open and under way.
- More trials run by Assiut UniversityThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Case-control
- Time perspective
- Retrospective
- Enrolment
- 70 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Assiut University
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Roaa Ahmed Mohamed Elnaffar, Assiut University
- Investigators
- Roaa A Elnaffar, MBBS, Principal investigator, Assiut University, Faculty of Medicine
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT07387861
- Sponsor's protocol ID
- Pending
- Acronym
- p-AKT p-S6
- Status last verified
- Jan 2026
- First submitted
- 25 Jan 2026
- Last updated
- 4 Feb 2026
- Results posted
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided: Individual participant-level data will not be publicly shared because the study uses archived clinical and pathology records containing sensitive patient information. Although the data will be de-identified, sharing it broadly could risk patient privacy and confidentiality. Data may be shared on a case-by-case basis with qualified researchers after institutional review and approval.
Publications
Lv W, Du C, Zhang Y, Wu F, Jin Y, Chen X, Liu X, Feng C, Ma X, Zhang S. Clinicopathological characteristics and prognostic analysis of PIK3CA mutation in breast cancer patients in Northwest China. Pathol Res Pract. 2022 Oct;238:154063. doi: 10.1016/j.prp.2022.154063. Epub 2022 Aug 10.
PubMed 35994807Adamo B, Deal AM, Burrows E, Geradts J, Hamilton E, Blackwell KL, Livasy C, Fritchie K, Prat A, Harrell JC, Ewend MG, Carey LA, Miller CR, Anders CK. Phosphatidylinositol 3-kinase pathway activation in breast cancer brain metastases. Breast Cancer Res. 2011;13(6):R125. doi: 10.1186/bcr3071. Epub 2011 Dec 1.
PubMed 22132754Maruyama N, Miyoshi Y, Taguchi T, Tamaki Y, Monden M, Noguchi S. Clinicopathologic analysis of breast cancers with PIK3CA mutations in Japanese women. Clin Cancer Res. 2007 Jan 15;13(2 Pt 1):408-14. doi: 10.1158/1078-0432.CCR-06-0267. Epub 2007 Jan 3.
PubMed 17202311Sakr RA, Weigelt B, Chandarlapaty S, Andrade VP, Guerini-Rocco E, Giri D, Ng CK, Cowell CF, Rosen N, Reis-Filho JS, King TA. PI3K pathway activation in high-grade ductal carcinoma in situ--implications for progression to invasive breast carcinoma. Clin Cancer Res. 2014 May 1;20(9):2326-37. doi: 10.1158/1078-0432.CCR-13-2267. Epub 2014 Mar 14.
PubMed 24634376Rasti AR, Guimaraes-Young A, Datko F, Borges VF, Aisner DL, Shagisultanova E. PIK3CA Mutations Drive Therapeutic Resistance in Human Epidermal Growth Factor Receptor 2-Positive Breast Cancer. JCO Precis Oncol. 2022 Mar;6:e2100370. doi: 10.1200/PO.21.00370.
PubMed 35357905Pierobon M, Ramos C, Wong S, Hodge KA, Aldrich J, Byron S, Anthony SP, Robert NJ, Northfelt DW, Jahanzeb M, Vocila L, Wulfkuhle J, Gambara G, Gallagher RI, Dunetz B, Hoke N, Dong T, Craig DW, Cristofanilli M, Leyland-Jones B, Liotta LA, O'Shaughnessy JA, Carpten JD, Petricoin EF. Enrichment of PI3K-AKT-mTOR Pathway Activation in Hepatic Metastases from Breast Cancer. Clin Cancer Res. 2017 Aug 15;23(16):4919-4928. doi: 10.1158/1078-0432.CCR-16-2656. Epub 2017 Apr 26.
PubMed 28446508Creighton CJ, Fu X, Hennessy BT, Casa AJ, Zhang Y, Gonzalez-Angulo AM, Lluch A, Gray JW, Brown PH, Hilsenbeck SG, Osborne CK, Mills GB, Lee AV, Schiff R. Proteomic and transcriptomic profiling reveals a link between the PI3K pathway and lower estrogen-receptor (ER) levels and activity in ER+ breast cancer. Breast Cancer Res. 2010;12(3):R40. doi: 10.1186/bcr2594. Epub 2010 Jun 22.
PubMed 20569503Cascardo F, Vivanco M, Perrone MC, Werbach A, Enrico D, Mando P, Amat M, Martinez-Vazquez P, Burruchaga J, Mac Donnell M, Lanari C, Zwenger A, Waisberg F, Novaro V. Higher risk of recurrence in early-stage breast cancer patients with increased levels of ribosomal protein S6. Sci Rep. 2024 Oct 24;14(1):25136. doi: 10.1038/s41598-024-75154-1.
PubMed 39448637Miller TW, Rexer BN, Garrett JT, Arteaga CL. Mutations in the phosphatidylinositol 3-kinase pathway: role in tumor progression and therapeutic implications in breast cancer. Breast Cancer Res. 2011;13(6):224. doi: 10.1186/bcr3039. Epub 2011 Nov 1.
PubMed 22114931Skolariki A, D'Costa J, Little M, Lord S. Role of PI3K/Akt/mTOR pathway in mediating endocrine resistance: concept to clinic. Explor Target Antitumor Ther. 2022;3(2):172-199. doi: 10.37349/etat.2022.00078. Epub 2022 Apr 24.
PubMed 36046843Toska E, Osmanbeyoglu HU, Castel P, Chan C, Hendrickson RC, Elkabets M, Dickler MN, Scaltriti M, Leslie CS, Armstrong SA, Baselga J. PI3K pathway regulates ER-dependent transcription in breast cancer through the epigenetic regulator KMT2D. Science. 2017 Mar 24;355(6331):1324-1330. doi: 10.1126/science.aah6893.
PubMed 28336670Vasan N, Toska E, Scaltriti M. Overview of the relevance of PI3K pathway in HR-positive breast cancer. Ann Oncol. 2019 Dec 1;30(Suppl_10):x3-x11. doi: 10.1093/annonc/mdz281.
PubMed 31859348Lei JT, Anurag M, Haricharan S, Gou X, Ellis MJ. Endocrine therapy resistance: new insights. Breast. 2019 Nov;48 Suppl 1(Suppl 1):S26-S30. doi: 10.1016/S0960-9776(19)31118-X.
PubMed 31839155Hanker AB, Sudhan DR, Arteaga CL. Overcoming Endocrine Resistance in Breast Cancer. Cancer Cell. 2020 Apr 13;37(4):496-513. doi: 10.1016/j.ccell.2020.03.009.
PubMed 32289273
Study at a glance
From the registry record, last updated by the sponsor on 4 Feb 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Immunohistochemical Evaluation of p-AKT and p-S6 as Surrogate Markers of PI3K/AKT/mTOR Pathway Activation in ER-Positive, HER2-Negative Breast Carcinoma
- ClinicalTrials.gov ID
- NCT07387861
- Acronym / sponsor ID
- p-AKT p-S6 / Pending
- Keywords
- Breast Cancer, PI3K/AKT/mTOR pathway, Phospho-AKT, Phospho-S6, Endocrine therapy, Tumor budding, TILs
- Study type
- Observational
- Recruitment status
- Not yet recruiting
- Enrolment
- 70 participants (estimated)
- Lead sponsor
- Assiut UniversityUniversity, hospital or other
- Study start
- Mar 2026 (estimated)
- Primary completion
- Jan 2028 (estimated)
- Study completion
- Mar 2028 (estimated)
- First posted
- 4 Feb 2026 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The goal of this observational study is to examine whether markers of PI3K pathway activation are associated with endocrine therapy response and clinicopathologic features in estrogen receptor-positive, HER2-negative breast cancer. The main questions it aims to answer are:
Are immunohistochemical levels of phosphorylated AKT (p-AKT) and phosphorylated S6 (p-S6) different between endocrine-sensitive and endocrine-resistant breast cancer cases? Do different levels of p-AKT and p-S6 show distinct clinicopathologic and histologic characteristics, including features of the tumor microenvironment?
Archived tumor tissue from patients who received adjuvant endocrine therapy as part of routine clinical care will be analyzed. Biomarker expression will be correlated with clinicopathologic parameters, including tumor-infiltrating lymphocyte density, tumor budding, and other histologic features, to explore associations with tumor behavior and outcomes.
Detailed description
Endocrine therapy is the cornerstone of treatment for estrogen receptor-positive breast cancer; however, a substantial proportion of patients develop resistance during the disease course. Activation of the PI3K/AKT/mTOR signaling pathway has been implicated as a key mechanism underlying resistance to endocrine therapy and disease progression. While genomic alterations in PI3K pathway-related genes are commonly assessed, they do not consistently reflect pathway activation or predict therapeutic response, highlighting the need for practical surrogate biomarkers.
The aim of this study is to evaluate immunohistochemical markers of PI3K pathway activation in estrogen receptor-positive, HER2-negative invasive breast carcinoma and to explore their associations with endocrine therapy response and clinicopathologic characteristics. Specifically, the study examines whether levels of phosphorylated AKT (p-AKT) and phosphorylated S6 (p-S6) differ between endocrine-sensitive and endocrine-resistant cases and whether these markers correlate with histologic features related to tumor biology and the tumor microenvironment.
This is a retrospective observational study including patients with estrogen receptor-positive, HER2-negative invasive breast carcinoma who received adjuvant endocrine therapy as part of routine clinical care. Archived formalin-fixed, paraffin-embedded (FFPE) tissue blocks from excisional surgical specimens will be retrieved, and clinicopathologic and follow-up data will be collected from medical records.
Cases will be classified into endocrine-sensitive and endocrine-resistant groups based on international consensus definitions using the timing of disease recurrence relative to endocrine therapy. Immunohistochemical staining for p-AKT and p-S6 will be performed on FFPE tissue sections and evaluated using a semi-quantitative scoring system. Histopathologic assessment will include standard reporting parameters as well as additional features such as tumor-infiltrating lymphocyte density, tumor budding, lymphovascular invasion, perineural invasion, and tumoral necrosis. Associations between biomarker expression, clinicopathologic features, and follow-up outcomes will be explored.
Study design
- Observational model
- Case-control
- Time perspective
- Retrospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Endocrine-Resistant Breast Cancer | – | Other: Not applicable- observational studyPatients with ER-positive, HER2-negative invasive breast carcinoma who developed primary or secondary resistance to adjuvant endocrine therapy. |
| Endocrine-Sensitive Breast Cancer | – | Other: Not applicable- observational studyPatients with ER-positive, HER2-negative invasive breast carcinoma who remained relapse-free during adjuvant endocrine therapy and for ≥12 months after completion, with sufficient follow-up. |
Who may qualify
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child, Adult, Older adult
- Study population
- Patients with estrogen receptor-positive (ER+), HER2-negative invasive breast cancer who received adjuvant endocrine therapy and have available formalin-fixed, paraffin-embedded (FFPE) tumor tissue archived in the Surgical Pathology Laboratory of Assiut University Hospital, as well as corresponding clinical follow-up data in the medical records of the Oncology Department at Assiut University Hospital.
Key inclusion criteria (5 listed)
- Patients diagnosed with invasive breast carcinoma.
- ER-positive and HER2-negative tumor status.
- Received adjuvant endocrine therapy as part of routine clinical care.
- Archived formalin-fixed paraffin-embedded (FFPE) tumor tissue available from excisional specimens (mastectomy).
- Available medical records documenting treatment history and follow-up outcomes.
Key exclusion criteria (3 listed)
- Cases with missing or unavailable FFPE tissue blocks.
- Cases with insufficient tissue quality for immunohistochemistry (e.g., severely degraded or exhausted FFPE block).
- Cases with unknown or incomplete follow-up or treatment data.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Not applicable- observational studyNot Applicable. This is an observational study; no interventions are assigned. | Other | Endocrine-Resistant Breast Cancer, Endocrine-Sensitive Breast Cancer |
Primary outcome
Immunohistochemical expression of PI3K pathway activation markers: p-AKT and p-S6.
Time frame: At the time of immunohistochemical staining of archived tissue (single time point).
Semi-quantitative assessment of phosphorylated AKT (Ser473) and phosphorylated S6 ribosomal protein in FFPE breast carcinoma tissue sections, scored using H-score, to compare expression levels between endocrine-sensitive and endocrine-resistant ER-positive, HER2-negative cases.
3 secondary outcomes
Correlation of p-AKT and p-S6 expression with endocrine therapy response.
Time frame: through study completion, an average of 2 years
Correlation of p-AKT and p-S6 expression with histologic features
Time frame: through study completion, an average of 2 years
Correlation of p-AKT and p-S6 expression with clinicopathologic features
Time frame: through study completion, an average of 2 years
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 4 Feb 2026.
- Background: PubMed 35994807Lv W, Du C, Zhang Y, Wu F, Jin Y, Chen X, Liu X, Feng C, Ma X, Zhang S. Clinicopathological characteristics and prognostic analysis of PIK3CA mutation in breast cancer patients in Northwest China. Pathol Res Pract. 2022 Oct;238:154063. doi: 10.1016/j.prp.2022.154063. Epub 2022 Aug 10.
- Background: PubMed 22132754Adamo B, Deal AM, Burrows E, Geradts J, Hamilton E, Blackwell KL, Livasy C, Fritchie K, Prat A, Harrell JC, Ewend MG, Carey LA, Miller CR, Anders CK. Phosphatidylinositol 3-kinase pathway activation in breast cancer brain metastases. Breast Cancer Res. 2011;13(6):R125. doi: 10.1186/bcr3071. Epub 2011 Dec 1.
- Background: PubMed 17202311Maruyama N, Miyoshi Y, Taguchi T, Tamaki Y, Monden M, Noguchi S. Clinicopathologic analysis of breast cancers with PIK3CA mutations in Japanese women. Clin Cancer Res. 2007 Jan 15;13(2 Pt 1):408-14. doi: 10.1158/1078-0432.CCR-06-0267. Epub 2007 Jan 3.
- Background: PubMed 24634376Sakr RA, Weigelt B, Chandarlapaty S, Andrade VP, Guerini-Rocco E, Giri D, Ng CK, Cowell CF, Rosen N, Reis-Filho JS, King TA. PI3K pathway activation in high-grade ductal carcinoma in situ--implications for progression to invasive breast carcinoma. Clin Cancer Res. 2014 May 1;20(9):2326-37. doi: 10.1158/1078-0432.CCR-13-2267. Epub 2014 Mar 14.
- Background: PubMed 35357905Rasti AR, Guimaraes-Young A, Datko F, Borges VF, Aisner DL, Shagisultanova E. PIK3CA Mutations Drive Therapeutic Resistance in Human Epidermal Growth Factor Receptor 2-Positive Breast Cancer. JCO Precis Oncol. 2022 Mar;6:e2100370. doi: 10.1200/PO.21.00370.
- Background: PubMed 28446508Pierobon M, Ramos C, Wong S, Hodge KA, Aldrich J, Byron S, Anthony SP, Robert NJ, Northfelt DW, Jahanzeb M, Vocila L, Wulfkuhle J, Gambara G, Gallagher RI, Dunetz B, Hoke N, Dong T, Craig DW, Cristofanilli M, Leyland-Jones B, Liotta LA, O'Shaughnessy JA, Carpten JD, Petricoin EF. Enrichment of PI3K-AKT-mTOR Pathway Activation in Hepatic Metastases from Breast Cancer. Clin Cancer Res. 2017 Aug 15;23(16):4919-4928. doi: 10.1158/1078-0432.CCR-16-2656. Epub 2017 Apr 26.
- Background: PubMed 20569503Creighton CJ, Fu X, Hennessy BT, Casa AJ, Zhang Y, Gonzalez-Angulo AM, Lluch A, Gray JW, Brown PH, Hilsenbeck SG, Osborne CK, Mills GB, Lee AV, Schiff R. Proteomic and transcriptomic profiling reveals a link between the PI3K pathway and lower estrogen-receptor (ER) levels and activity in ER+ breast cancer. Breast Cancer Res. 2010;12(3):R40. doi: 10.1186/bcr2594. Epub 2010 Jun 22.
- Background: PubMed 39448637Cascardo F, Vivanco M, Perrone MC, Werbach A, Enrico D, Mando P, Amat M, Martinez-Vazquez P, Burruchaga J, Mac Donnell M, Lanari C, Zwenger A, Waisberg F, Novaro V. Higher risk of recurrence in early-stage breast cancer patients with increased levels of ribosomal protein S6. Sci Rep. 2024 Oct 24;14(1):25136. doi: 10.1038/s41598-024-75154-1.
- Background: PubMed 22114931Miller TW, Rexer BN, Garrett JT, Arteaga CL. Mutations in the phosphatidylinositol 3-kinase pathway: role in tumor progression and therapeutic implications in breast cancer. Breast Cancer Res. 2011;13(6):224. doi: 10.1186/bcr3039. Epub 2011 Nov 1.
- Background: PubMed 36046843Skolariki A, D'Costa J, Little M, Lord S. Role of PI3K/Akt/mTOR pathway in mediating endocrine resistance: concept to clinic. Explor Target Antitumor Ther. 2022;3(2):172-199. doi: 10.37349/etat.2022.00078. Epub 2022 Apr 24.
- Background: PubMed 28336670Toska E, Osmanbeyoglu HU, Castel P, Chan C, Hendrickson RC, Elkabets M, Dickler MN, Scaltriti M, Leslie CS, Armstrong SA, Baselga J. PI3K pathway regulates ER-dependent transcription in breast cancer through the epigenetic regulator KMT2D. Science. 2017 Mar 24;355(6331):1324-1330. doi: 10.1126/science.aah6893.
- Background: PubMed 31859348Vasan N, Toska E, Scaltriti M. Overview of the relevance of PI3K pathway in HR-positive breast cancer. Ann Oncol. 2019 Dec 1;30(Suppl_10):x3-x11. doi: 10.1093/annonc/mdz281.
- Individual participant dataSharing planned: Undecided. Individual participant-level data will not be publicly shared because the study uses archived clinical and pathology records containing sensitive patient information. Although the data will be de-identified, sharing it broadly could risk patient privacy and confidentiality. Data may be shared on a case-by-case basis with qualified researchers after institutional review and approval.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part.
Roaa A Elnaffar, MBBS principal investigator
Assiut University, Faculty of Medicine
Questions about this trial
What is this clinical trial studying?
An observational study of Breast Cancer - ER+, HER2-, PIK3CA Gene Mutation, run by Assiut University.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 5 inclusion and 3 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: opening soon, as of the sponsor's last update on 4 Feb 2026. Status can change between updates, so confirm with the study contact before making plans.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Roaa A Elnaffar, MBBS (+20 1281071748, roaaelnaffar@aun.edu.eg), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Immunohistochemical expression of PI3K pathway activation markers: p-AKT and p-S6. (time frame: At the time of immunohistochemical staining of archived tissue (single time point).). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT07387861, which also lists 14 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 4 Feb 2026.