Clinical trial · Observational
Evaluation of Prognostic Factors: From Breast Cancer to Bone Metastases
- Source
- ClinicalTrials.gov
- Retrieved
- Sep 8, 2026
- Layer
- normalized (units and labels harmonized; values unchanged)
- Run
- ING-CLINICALTRIALS-20260908-000001
Summary
Brief summary (as posted)
Bone metastases represent a frequent complication of some solid tumours, particularly prostate, breast and lung carcinomas. Bone metastases can cause pain and give rise to the so-called "Skeletal-related Events" (SRE) such as pathological fractures and nerve compression. Despite advances in cancer treatment in general, treatment options for bone metastases remain inadequate and generally palliative. It is therefore necessary to identify patients at "high risk" of developing metastases at an early stage of neoplastic disease in order to counteract it. Therefore, the identification of changes in the expression of proteins that could be variously involved in the progression of breast cancer is of primary importance since they could act as prognostic factors and therefore address the therapeutic strategy. The aim of the investigators is to clarify the role of de-regulation of post-translational events (such as SUMOylation) in the progression of breast cancer.
Conditions
Conditions (2)
Free-text conditions as registered, with the CancerIndex entity they were reconciled to and the match type.
| Condition (as posted) | Mapped entity | Match | Confidence |
|---|---|---|---|
| Bone Metastases | — | UNRESOLVED | — |
| Breast Cancer Metastatic | — | UNRESOLVED | — |
Interventions
Interventions (2)
| Intervention | Type | Mapped drug | Match |
|---|---|---|---|
| Bone metastasis | Other | — | UNRESOLVED |
| Breast cancer metastatic to bone | Other | — | UNRESOLVED |
Design
Arms and outcomes
Arms (2)
- label
- Breast cancer metastatic to bone
- description
- No direct intervention(s) will be administer to the patients. We will use the sample (slides) recovered from the surgery on primary tumor (breast cancer responsible for metastatic disease).
- interventionNames
- Other: Breast cancer metastatic to bone
- label
- Bone metastasis
- description
- No direct intervention(s) will be administer to the patients. Waste material will be analysed for the expression of specific proteins
- interventionNames
- Other: Bone metastasis
Primary outcomes (1)
- measure
- SENP1 expression
- timeFrame
- 6 months
- description
- The expression of SENP1 in bone metastatic mammary carcinomas will be studied. The evaluation of the expression of SENP1 in bone metastases will be finalized to define a possible use as a therapeutic target. The expression of SENP1 in bone metastatic breast carcinoma samples will be compared with the expression of SENP1 in non-metastatic breast cancer (commercial source).
Eligibility
Eligibility (as posted)
- Sex
- Female
- Minimum age
- 18 Years
Show eligibility criteria text
Inclusion Criteria: * Adult women (≥ 18 years) candidates for excisional surgery and bone consolidation due to osteolytic bone metastases from breast cancer. * Female * Ability to understand the experimental study and willingness to sign the written consent Exclusion Criteria: \- Retraction of written consent
References
Publications (6)
- BACKGROUNDSowder ME, Johnson RW. Bone as a Preferential Site for Metastasis. JBMR Plus. 2019 Jan 15;3(3):e10126. doi: 10.1002/jbm4.10126. eCollection 2019 Mar. PMID 30918918
- BACKGROUNDYeh ET. SUMOylation and De-SUMOylation: wrestling with life's processes. J Biol Chem. 2009 Mar 27;284(13):8223-7. doi: 10.1074/jbc.R800050200. Epub 2008 Nov 13. PMID 19008217
- BACKGROUNDWang Z, Jin J, Zhang J, Wang L, Cao J. Depletion of SENP1 suppresses the proliferation and invasion of triple-negative breast cancer cells. Oncol Rep. 2016 Oct;36(4):2071-8. doi: 10.3892/or.2016.5036. Epub 2016 Aug 24. PMID 27573572
- BACKGROUNDFeng Y, Yao Z, Klionsky DJ. How to control self-digestion: transcriptional, post-transcriptional, and post-translational regulation of autophagy. Trends Cell Biol. 2015 Jun;25(6):354-63. doi: 10.1016/j.tcb.2015.02.002. Epub 2015 Mar 8. PMID 25759175
- BACKGROUNDMathew R, Karp CM, Beaudoin B, Vuong N, Chen G, Chen HY, Bray K, Reddy A, Bhanot G, Gelinas C, Dipaola RS, Karantza-Wadsworth V, White E. Autophagy suppresses tumorigenesis through elimination of p62. Cell. 2009 Jun 12;137(6):1062-75. doi: 10.1016/j.cell.2009.03.048. PMID 19524509
- BACKGROUNDMoscat J, Diaz-Meco MT. p62 at the crossroads of autophagy, apoptosis, and cancer. Cell. 2009 Jun 12;137(6):1001-4. doi: 10.1016/j.cell.2009.05.023. PMID 19524504