Clinical trial · Observational
CDK and Body Composition Study
Pilot Study Assessing the Effect of Cyclin-dependent Kinase 4/6 Inhibitors on Body Composition in Patients With ER+/HER2- Metastatic Breast Cancer
NCT03697577CI-TRIAL-00112990completedClinicalTrials.gov clinicaltrialsProvenance
- Source
- ClinicalTrials.gov
- Retrieved
- Sep 26, 2026
- Layer
- normalized (units and labels harmonized; values unchanged)
- Run
- ING-CLINICALTRIALS-20260926-000001
Summary
Brief summary (as posted)
The goal of this study is to evaluate changes in body composition among patients who are treated with cyclin-dependent kinase (CDK) 4/6 inhibitors (abemaciclib, ribociclib, or palbociclib).
Conditions
Conditions (1)
Free-text conditions as registered, with the CancerIndex entity they were reconciled to and the match type.
| Condition (as posted) | Mapped entity | Match | Confidence |
|---|---|---|---|
| Breast Cancer | Malignant Breast Neoplasm | CURATED_EXACT | 0.92 |
Interventions
Interventions (2)
| Intervention | Type | Mapped drug | Match |
|---|---|---|---|
| CT scans | Diagnostic Test | — | UNRESOLVED |
| DEXA scan | Diagnostic Test | — | UNRESOLVED |
Design
Arms and outcomes
Arms (1)
- label
- ER+/HER2- metastatic breast cancer
- description
- Subjects have metastatic ER+/HER2- breast cancer, and their doctor is offering treatment with CDK 4/6 inhibitors as standard of care treatment. It is hypothesized that cyclin-dependent kinase (CDK) 4/6 inhibitors decrease fat mass among women with ER+/HER2- metastatic breast cancer without significant effect in the skeletal mass. Body composition will be obtained from CT scans (CT or PETCT) as part of standard of care, and body fat mass will be obtained from DEXA scan (DEXA will be performed only if available)
- interventionNames
- Diagnostic Test: CT scans
- Diagnostic Test: DEXA scan
Primary outcomes (1)
- measure
- Change in Total adipose tissue (TAT)
- timeFrame
- From Baseline and 6 months after CDK 4/6 inhibitor therapy
- description
- Total Adipose tissue (TAT) is defined as the sum of intramuscular adipose tissue (IMAT), visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT) obtained from L3 cross section from CT scans. Only patients who complete 24 weeks of CDK 4/6 inhibitor treatment and have no radiological/clinical signs of disease progression will be included in the analysis of primary endpoint. Results will be calculated and summarized in area (cm²).
Eligibility
Eligibility (as posted)
- Sex
- All
- Minimum age
- 18 Years
Show eligibility criteria text
Inclusion Criteria: * Histologically confirmed adenocarcinoma of the breast that is Estrogen Receptor (ER) and/or Progesterone Receptor (PR) positive based on current American Society of Clinical Oncology-College of American Pathologists (ASCO-CAP) guidelines * Metastatic or locally advanced/inflammatory, unresectable breast cancer not amenable to potentially curative surgery * Measurable and/or non-measurable as defined by RECIST 1.1 criteria * Patients must be a candidate to start an FDA approved CDK 4/6 inhibitor (palbociclib, ribociclib, abemaciclib) as part of standard of care treatment * Female, or male patients, and age \>=18 years * Eastern Cooperative Oncology Group (ECOG) performance status 0-2 * Ability to understand and the willingness to sign a written informed consent document * Concomitant therapy with bisphosphonates, RANKL inhibitors or growth-colony-stimulating factor (G-CSF) is allowed as per physician decision Exclusion Criteria: * History of allergic reactions attributed to compounds of similar chemical or biologic composition to CDK 4/6 inhibitors or other agents used in the study (e.g., fulvestrant, letrozole, anastrozole, exemestane) * BMI \< 18.5 * Prior CDK 4/6 use in any setting * Inability to undergo anthropometric measurements * Inability to undergo CT scan imaging * Women of child-bearing potential must not be pregnant or breast feeding. They must also agree to use adequate contraception (hormonal or barrier method of birth control) and not be breast feeding prior to study entry, for the duration of study participation, and for up to 10 days after completion of all protocol therapy. Should a woman become pregnant or suspect she is pregnant while participating in this study or up to 10 days after completion of protocol therapy, she should inform her treating physician immediately * Intercurrent illness that would substantially increase the risk of treatment associated complications (e.g., active infection, uncontrolled diabetes mellitus or hypertension) * Psychiatric illness/social situations that would interfere with the patient's ability to comply with the treatment regimen * Patients with untreated brain metastasis are excluded. Patients with a prior history of brain metastasis are eligible if they have received prior brain radiation (whole brain or stereotactic radiosurgery) or surgery, have stable intracranial disease for at least 3 months after completion of local therapy, and are not taking corticosteroids for treatment of brain metastasis * Patients who have not recovered (i.e., CTCAE Grade ≤1 or baseline) from an adverse event due to a previously administered agent, excluding alopecia * Patients with inability to swallow and retain pills * Malabsorption syndrome or other gastrointestinal illness that could affect oral absorption * Patients with active implanted medical devices (cardiac pacemakers, defibrillators or patients connected to electronic life support devices)
References
Publications (47)
- BACKGROUNDFlegal KM, Carroll MD, Ogden CL, Curtin LR. Prevalence and trends in obesity among US adults, 1999-2008. JAMA. 2010 Jan 20;303(3):235-41. doi: 10.1001/jama.2009.2014. Epub 2010 Jan 13. PMID 20071471
- BACKGROUNDRyan DH, Kushner R. The state of obesity and obesity research. JAMA. 2010 Oct 27;304(16):1835-6. doi: 10.1001/jama.2010.1531. Epub 2010 Oct 9. No abstract available. PMID 20935336
- BACKGROUNDRenehan AG, Tyson M, Egger M, Heller RF, Zwahlen M. Body-mass index and incidence of cancer: a systematic review and meta-analysis of prospective observational studies. Lancet. 2008 Feb 16;371(9612):569-78. doi: 10.1016/S0140-6736(08)60269-X. PMID 18280327
- BACKGROUNDFinkelstein EA, Khavjou OA, Thompson H, Trogdon JG, Pan L, Sherry B, Dietz W. Obesity and severe obesity forecasts through 2030. Am J Prev Med. 2012 Jun;42(6):563-70. doi: 10.1016/j.amepre.2011.10.026. PMID 22608371
- BACKGROUNDMyers MG Jr, Heymsfield SB, Haft C, Kahn BB, Laughlin M, Leibel RL, Tschop MH, Yanovski JA. Challenges and opportunities of defining clinical leptin resistance. Cell Metab. 2012 Feb 8;15(2):150-6. doi: 10.1016/j.cmet.2012.01.002. PMID 22326217
- BACKGROUNDRing LE, Zeltser LM. Disruption of hypothalamic leptin signaling in mice leads to early-onset obesity, but physiological adaptations in mature animals stabilize adiposity levels. J Clin Invest. 2010 Aug;120(8):2931-41. doi: 10.1172/JCI41985. Epub 2010 Jul 1. PMID 20592471
- BACKGROUNDDhillon H, Zigman JM, Ye C, Lee CE, McGovern RA, Tang V, Kenny CD, Christiansen LM, White RD, Edelstein EA, Coppari R, Balthasar N, Cowley MA, Chua S Jr, Elmquist JK, Lowell BB. Leptin directly activates SF1 neurons in the VMH, and this action by leptin is required for normal body-weight homeostasis. Neuron. 2006 Jan 19;49(2):191-203. doi: 10.1016/j.neuron.2005.12.021.