Breast CancerNCT07607548
Assessment of the Effect of Probiotic Supplementation on Proinflammatory Mechanisms Induced by Systemic Treatment in Women With Breast Cancer
A study testing Probiotic in people with Breast Cancer and Probiotic Therapy, run by Poznan University of Medical Sciences at 1 site in Poland.
Trial summary
The gut microbiota and its role in cancer treatment are currently the subject of intensive research. It has long been known that interactions between the microbiome and the host are responsible for the proper functioning of many physiological processes and for maintaining systemic homeostasis. Read more about this study
- Who is it for?
- Ages 18 to 75 years, women only
- Conditions the study is for
- Breast Cancer, Probiotic Therapy
- What is being tested?
- Probiotic
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 60 participants
- Where
- 1 sitePoland
- Study dates
- 18 Oct 2022to 30 Apr 2024
- Phase
- Interventional
- Are there results?
- None posted in the registry
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 18 to 75 years
- Women only
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- first-time chemotherapy
- written consent to participate in the research
- no antibiotic and probiotic therapy in the last 3 months
Who cannot join
- serious comorbidities (chronic renal failure, diabetes, autoimmune diseasese, unstable coronary artery disease or other cancers)
- previous history of cancer
- smoking cigarettes or using other stimulants
- another probiotic supplementation
- qualification for another type of treatment - surgery or hormone therapy
Trial locations and contacts
1 site in 1 country.
About this study
Official title: A 8-week, Randomized, Double-blind, and Placebo-controlled Study Evaluating the Effect of Probiotic Supplementation on Proinflammatory Mechanisms Induced by Systemic Treatment in Women With Breast Cancer
The gut microbiota and its role in cancer treatment are currently the subject of intensive research. It has long been known that interactions between the microbiome and the host are responsible for the proper functioning of many physiological processes and for maintaining systemic homeostasis. Although the precise mechanisms underlying these interactions remain unclear, they appear to have a significant impact on the development and treatment of various diseases, including cancer.
One of the crucial functions regulated by the gut microbiota is the body's immune response. The appropriate quantitative and qualitative composition of the gut microbiota supports the maintenance of a critical balance between pro- and anti-inflammatory processes. Even a slight disruption of this balance can lead to systemic metabolic and biochemical changes, affecting the overall condition of the body and its systems.
Read more
Chemotherapy and immunotherapy are standard treatment protocols for cancer patients, including those with breast cancer. Despite their proven role in prolonging remission and improving patient survival, their effectiveness remains limited. Regardless of the regimen, the use of cytotoxic drugs does not fully prevent metastasis. In women with breast cancer, the risk of local recurrence or distant metastasis-primarily to the bones, lungs, and liver-is approximately 30% and increases over time following the initial diagnosis. Although the risk of cancer recurrence in this group is largely influenced by the baseline characteristics of the tumor, increasing attention is being paid to the immune response to treatment. The effectiveness of anticancer therapies depends not only on the response of cancer cells but also on the condition of the entire organism, particularly the host's immune system.
Recent studies indicate that chemotherapy induces a systemic inflammatory state that may persist long after treatment completion. Prolonged inflammation, along with increased levels of chemoattractants, cytokines, and metalloproteinases, creates an environment conducive to cancer progression and metastasis. Therefore, it is increasingly suggested that chemotherapy-induced chronic inflammation may be a significant factor limiting therapeutic effectiveness. Although the precise mechanisms underlying inflammation during chemotherapy are not fully understood, a growing body of evidence points to a key role of the gut microbiota in this process.
Cytotoxic drugs used during chemotherapy disrupt both the quantitative and qualitative composition of the gut microbiota, leading to dysbiosis. Dysbiosis is associated with the overgrowth of pathogenic species and alterations in the profile of microbial metabolites, often favoring those that negatively affect the intestinal barrier. Consequently, inflammation of the intestinal mucosa and increased intestinal permeability are observed during chemotherapy.
Bacterial components, collectively known as pathogen-associated molecular patterns (PAMPs), can enter the bloodstream through the compromised intestinal barrier, triggering immune cell activation and systemic inflammation. An important link between the gut microbiota and progressive inflammation involves Toll-like receptors (TLRs), particularly TLR4, which is expressed on the surface of monocytes and recognizes, among other ligands, lipopolysaccharide (LPS) produced by Gram-negative bacteria. This interaction activates transcription factors such as Nuclear factor-κB (NF-κB), leading to the expression of genes involved in the immune response, including pro-inflammatory cytokines such as Tumor Necrosis Factor-α (TNF-α), Interleukin-6 (IL-6), and Cyclooxygenase-2 (COX-2). These cytokines promote tumor progression and metastasis both directly, by acting on cancer cells, and indirectly, by enhancing cell proliferation and angiogenesis.
Several studies have reported increased expression and activity of TLR4 in various types of cancer, including breast cancer. Animal model studies have shown that blocking TLR4 reduces tumor metastasis and significantly decreases invasiveness. Therefore, inhibition of TLR4 signaling appears to be a promising therapeutic strategy for counteracting metastasis and chemoresistance. Probiotic therapy may contribute to this effect, as it has been shown to downregulate TLR4 expression and reduce levels of pro-tumor inflammatory mediators.
The aim of this study is to evaluate the impact of probiotic therapy on immunological, biochemical, morphological, and anthropometric parameters in a group of women with breast cancer undergoing chemotherapy or immunotherapy. The study will include two visits: one before treatment initiation and another eight weeks later. The main hypothesis is that probiotic supplementation will reduce inflammation associated with systemic breast cancer treatment.
- Conditions
- Breast Cancer, Probiotic Therapy
- Being tested
- Probiotic, Placebo
- Keywords
- systemic treatment, inflammation
- Medical subject headings
- Breast Neoplasms, Inflammation
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
ProbioticDietary supplement
The probiotic contained the Lactiplantibacillus plantarum 299v. It was prepared by Sanprobi Sp. z o.o., Sp. k., Szczecin, Poland; probiotic capsules manufacturer - Institute Rosell-Lallemand, Montreal, Canada; Lactiplantibacillus plantarum 299v strain owner - Probi AB, Lund, Sweden. Placebo supplementation began on the day of chemotherapy initiation, according to the following regimen: 1 capsule/day in the first week (1 x 1010 colony-forming unit (CFU)), and 2 capsules/day in the following weeks (2 x 1010 CFU). The supplementation period lasted eight weeks.
PlaceboDietary supplement
The placebo contained crystalline cellulose powder. It was prepared by Sanprobi Sp. z o.o., Sp. k., Szczecin, Poland.. Placebo supplementation began on the day of chemotherapy initiation and lasted eight weeks.
| Study group | Role | What they receive |
|---|---|---|
| Probiotic supplementation | Experimental | Not described Receives: Dietary Supplement: Probiotic |
| Placebo supplementation | Placebo comparator | Not described Receives: Dietary Supplement: Placebo |
What is being measured
The primary outcome is the main question the study is designed to answer.
Changes in serum levels of Tumor Necrosis Factor α (TNFα)
Measured: Baseline, 8 week
Changes in serum levels of interleukin-6 (IL-6)
Measured: Baseline, 8 week
Changes in serum levels of high-specific C-reactive protein (hsCRP)
Measured: Baseline, 8 week
Changes in Toll-like receptor 4 (TLR) expression on the surface of monocytes
Measured: Baseline, 8 week
Changes in the intracellular expression of cyclooxygenase 2 (COX-2)
Measured: Baseline, 8 week
Secondary outcomes (17)
Changes in the concentration of lymphocytes
Results expressed as G/L, marked routinely in the hospital laboratory
Measured: Baseline, 8 week
Changes in the concentration of leukocytes
Results expressed as [G/L], marked routinely in the hospital laboratory.
Measured: Baseline, 8 week
Changes in the concentration of monocytes
Results expressed as G/L, marked routinely in the hospital laboratory
Measured: Baseline, 8 week
Changes in the concentration of neutrophils
Results expressed as G/L, marked routinely in the hospital laboratory
Measured: Baseline, 8 week
Changes in the concentration of erythrocytes
Results expressed as [T/L], marked routinely in the hospital laboratory.
Measured: Baseline, 8 week
Changes in the concentration of hemoglobin
Results expressed as [g/dL], marked routinely in the hospital laboratory.
Measured: Baseline, 8 week
Changes in the levels of hematocrit
Results expressed as [L/L], marked routinely in the hospital laboratory.
Measured: Baseline, 8 week
Changes in the concentration of blood platelets
Results expressed as [G/L], marked routinely in the hospital laboratory.
Measured: Baseline, 8 week
Changes in serum levels of total cholesterol
Results expressed as [mg/dL], marked routinely in the hospital laboratory.
Measured: Baseline, 8 week
Changes in serum levels of low-density lipoprotein (LDL) cholesterol
Results expressed as [mg/dL], marked routinely in the hospital laboratory.
Measured: Baseline, 8 week
Changes in serum levels of high-density lipoprotein (HDL) cholesterol
Results expressed as [mg/dL], marked routinely in the hospital laboratory.
Measured: Baseline, 8 week
Changes in serum levels of triglycerides (TG)
Results expressed as [mg/dL], marked routinely in the hospital laboratory.
Measured: Baseline, 8 week
Changes in body weight
Results presented in kg, measured with a certified body composition analyzer
Measured: Baseline, 8 week
Body height measurement
Results presented in m, measured with a certified height gauge
Measured: Baseline
Changes of body fat content
Results presented in kg of body weight, measured with a certified body composition analyzer
Measured: Baseline, 8 week
Changes of free fat mass content
Results presented in kg, measured with a certified body composition analyzer
Measured: Baseline, 8 week
Changes of total body water
Results presented in kg, measured with a certified body composition analyzer
Measured: Baseline, 8 week
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted26 May 2026
- Study start18 Oct 2022
- Primary completion30 Apr 2024
- Study completion30 Apr 2024
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (19)Papers the sponsor has linked to this study.
- Other trials for Breast CancerStudies of the same condition, open and under way.
- 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
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Quadruple blind
- Who is masked
- Participant, Care provider, Investigator, Outcomes assessor
- Enrolment
- 60 participants (actual)
Sponsor and investigators
- Lead sponsor
- Poznan University of Medical Sciences
- Sponsor type
- University, hospital or other
- Collaborators
- Sanprobi Sp. z o.o., Sp. k., Szczecin, Poland
- Responsible party
- Sponsor
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT07607548
- Sponsor's protocol ID
- 551/22
- Status last verified
- Feb 2026
- First submitted
- 27 Feb 2026
- Last updated
- 26 May 2026
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Yang X, Fu Y, Liu J, Ren HY. Impact of probiotics on toll-like receptor 4 expression in an experimental model of ulcerative colitis. J Huazhong Univ Sci Technolog Med Sci. 2013 Oct;33(5):661-665. doi: 10.1007/s11596-013-1177-9. Epub 2013 Oct 20.
PubMed 24142717Khademalhosseini M, Arababadi MK. Toll-like receptor 4 and breast cancer: an updated systematic review. Breast Cancer. 2019 May;26(3):265-271. doi: 10.1007/s12282-018-00935-2. Epub 2018 Dec 12.
PubMed 30543015Ahmed A, Redmond HP, Wang JH. Links between Toll-like receptor 4 and breast cancer. Oncoimmunology. 2013 Feb 1;2(2):e22945. doi: 10.4161/onci.22945.
PubMed 23526132Yiu JH, Dorweiler B, Woo CW. Interaction between gut microbiota and toll-like receptor: from immunity to metabolism. J Mol Med (Berl). 2017 Jan;95(1):13-20. doi: 10.1007/s00109-016-1474-4. Epub 2016 Sep 17.
PubMed 27639584Velloso LA, Folli F, Saad MJ. TLR4 at the Crossroads of Nutrients, Gut Microbiota, and Metabolic Inflammation. Endocr Rev. 2015 Jun;36(3):245-71. doi: 10.1210/er.2014-1100. Epub 2015 Mar 26.
PubMed 25811237Ge Y, Wang X, Guo Y, Yan J, Abuduwaili A, Aximujiang K, Yan J, Wu M. Gut microbiota influence tumor development and Alter interactions with the human immune system. J Exp Clin Cancer Res. 2021 Jan 25;40(1):42. doi: 10.1186/s13046-021-01845-6.
PubMed 33494784Secombe KR, Coller JK, Gibson RJ, Wardill HR, Bowen JM. The bidirectional interaction of the gut microbiome and the innate immune system: Implications for chemotherapy-induced gastrointestinal toxicity. Int J Cancer. 2019 May 15;144(10):2365-2376. doi: 10.1002/ijc.31836. Epub 2018 Oct 1.
PubMed 30155890Montassier E, Gastinne T, Vangay P, Al-Ghalith GA, Bruley des Varannes S, Massart S, Moreau P, Potel G, de La Cochetiere MF, Batard E, Knights D. Chemotherapy-driven dysbiosis in the intestinal microbiome. Aliment Pharmacol Ther. 2015 Sep;42(5):515-28. doi: 10.1111/apt.13302. Epub 2015 Jul 6.
PubMed 26147207Wei L, Wen XS, Xian CJ. Chemotherapy-Induced Intestinal Microbiota Dysbiosis Impairs Mucosal Homeostasis by Modulating Toll-like Receptor Signaling Pathways. Int J Mol Sci. 2021 Aug 31;22(17):9474. doi: 10.3390/ijms22179474.
PubMed 34502383Oh B, Boyle F, Pavlakis N, Clarke S, Guminski A, Eade T, Lamoury G, Carroll S, Morgia M, Kneebone A, Hruby G, Stevens M, Liu W, Corless B, Molloy M, Libermann T, Rosenthal D, Back M. Emerging Evidence of the Gut Microbiome in Chemotherapy: A Clinical Review. Front Oncol. 2021 Sep 16;11:706331. doi: 10.3389/fonc.2021.706331. eCollection 2021.
PubMed 34604043Zheng D, Liwinski T, Elinav E. Interaction between microbiota and immunity in health and disease. Cell Res. 2020 Jun;30(6):492-506. doi: 10.1038/s41422-020-0332-7. Epub 2020 May 20.
PubMed 32433595Lee KA, Luong MK, Shaw H, Nathan P, Bataille V, Spector TD. The gut microbiome: what the oncologist ought to know. Br J Cancer. 2021 Oct;125(9):1197-1209. doi: 10.1038/s41416-021-01467-x. Epub 2021 Jul 14.
PubMed 34262150Cheng WY, Wu CY, Yu J. The role of gut microbiota in cancer treatment: friend or foe? Gut. 2020 Oct;69(10):1867-1876. doi: 10.1136/gutjnl-2020-321153. Epub 2020 Aug 5.
PubMed 32759302Edwardson DW, Boudreau J, Mapletoft J, Lanner C, Kovala AT, Parissenti AM. Inflammatory cytokine production in tumor cells upon chemotherapy drug exposure or upon selection for drug resistance. PLoS One. 2017 Sep 15;12(9):e0183662. doi: 10.1371/journal.pone.0183662. eCollection 2017.
PubMed 28915246Xu MM, Pu Y, Zhang Y, Fu YX. The Role of Adaptive Immunity in the Efficacy of Targeted Cancer Therapies. Trends Immunol. 2016 Feb;37(2):141-153. doi: 10.1016/j.it.2015.12.007. Epub 2016 Jan 7.
PubMed 26778079
Study at a glance
From the registry record, last updated by the sponsor on 26 May 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- A 8-week, Randomized, Double-blind, and Placebo-controlled Study Evaluating the Effect of Probiotic Supplementation on Proinflammatory Mechanisms Induced by Systemic Treatment in Women With Breast Cancer
- ClinicalTrials.gov ID
- NCT07607548
- Acronym / sponsor ID
- 551/22
- Conditions
- Breast Cancer, Probiotic Therapy
- Keywords
- systemic treatment, inflammation
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 60 participants (actual)
- Lead sponsor
- Poznan University of Medical SciencesUniversity, hospital or other
- Collaborators
- Sanprobi Sp. z o.o., Sp. k., Szczecin, Poland
- Study start
- 18 Oct 2022 (actual)
- Primary completion
- 30 Apr 2024 (actual)
- Study completion
- 30 Apr 2024 (actual)
- First posted
- 26 May 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 gut microbiota and its role in cancer treatment are currently the subject of intensive research. It has long been known that interactions between the microbiome and the host are responsible for the proper functioning of many physiological processes and for maintaining systemic homeostasis. Although the precise mechanisms underlying these interactions remain unclear, they appear to have a significant impact on the development and treatment of various diseases, including cancer.
One of the crucial functions regulated by the gut microbiota is the body's immune response. The appropriate quantitative and qualitative composition of the gut microbiota supports the maintenance of a critical balance between pro- and anti-inflammatory processes. Even a slight disruption of this balance can lead to systemic metabolic and biochemical changes, affecting the overall condition of the body and its systems.
Chemotherapy and immunotherapy are standard treatment protocols for cancer patients, including those with breast cancer. Despite their proven role in prolonging remission and improving patient survival, their effectiveness remains limited. Regardless of the regimen, the use of cytotoxic drugs does not fully prevent metastasis. In women with breast cancer, the risk of local recurrence or distant metastasis-primarily to the bones, lungs, and liver-is approximately 30% and increases over time following the initial diagnosis. Although the risk of cancer recurrence in this group is largely influenced by the baseline characteristics of the tumor, increasing attention is being paid to the immune response to treatment. The effectiveness of anticancer therapies depends not only on the response of cancer cells but also on the condition of the entire organism, particularly the host's immune system.
Recent studies indicate that chemotherapy induces a systemic inflammatory state that may persist long after treatment completion. Prolonged inflammation, along with increased levels of chemoattractants, cytokines, and metalloproteinases, creates an environment conducive to cancer progression and metastasis. Therefore, it is increasingly suggested that chemotherapy-induced chronic inflammation may be a significant factor limiting therapeutic effectiveness. Although the precise mechanisms underlying inflammation during chemotherapy are not fully understood, a growing body of evidence points to a key role of the gut microbiota in this process.
Cytotoxic drugs used during chemotherapy disrupt both the quantitative and qualitative composition of the gut microbiota, leading to dysbiosis. Dysbiosis is associated with the overgrowth of pathogenic species and alterations in the profile of microbial metabolites, often favoring those that negatively affect the intestinal barrier. Consequently, inflammation of the intestinal mucosa and increased intestinal permeability are observed during chemotherapy.
Bacterial components, collectively known as pathogen-associated molecular patterns (PAMPs), can enter the bloodstream through the compromised intestinal barrier, triggering immune cell activation and systemic inflammation. An important link between the gut microbiota and progressive inflammation involves Toll-like receptors (TLRs), particularly TLR4, which is expressed on the surface of monocytes and recognizes, among other ligands, lipopolysaccharide (LPS) produced by Gram-negative bacteria. This interaction activates transcription factors such as Nuclear factor-κB (NF-κB), leading to the expression of genes involved in the immune response, including pro-inflammatory cytokines such as Tumor Necrosis Factor-α (TNF-α), Interleukin-6 (IL-6), and Cyclooxygenase-2 (COX-2). These cytokines promote tumor progression and metastasis both directly, by acting on cancer cells, and indirectly, by enhancing cell proliferation and angiogenesis.
Several studies have reported increased expression and activity of TLR4 in various types of cancer, including breast cancer. Animal model studies have shown that blocking TLR4 reduces tumor metastasis and significantly decreases invasiveness. Therefore, inhibition of TLR4 signaling appears to be a promising therapeutic strategy for counteracting metastasis and chemoresistance. Probiotic therapy may contribute to this effect, as it has been shown to downregulate TLR4 expression and reduce levels of pro-tumor inflammatory mediators.
The aim of this study is to evaluate the impact of probiotic therapy on immunological, biochemical, morphological, and anthropometric parameters in a group of women with breast cancer undergoing chemotherapy or immunotherapy. The study will include two visits: one before treatment initiation and another eight weeks later. The main hypothesis is that probiotic supplementation will reduce inflammation associated with systemic breast cancer treatment.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Quadruple blind (participant, care provider, investigator, outcomes assessor)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Probiotic supplementation | Experimental | Dietary Supplement: Probiotic |
| Placebo supplementation | Placebo comparator | Dietary Supplement: Placebo |
Who may qualify
- Ages
- 18 to 75 years
- Sex
- Female only
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (3 listed)
- first-time chemotherapy
- written consent to participate in the research
- no antibiotic and probiotic therapy in the last 3 months
Key exclusion criteria (5 listed)
- serious comorbidities (chronic renal failure, diabetes, autoimmune diseasese, unstable coronary artery disease or other cancers)
- previous history of cancer
- smoking cigarettes or using other stimulants
- another probiotic supplementation
- qualification for another type of treatment - surgery or hormone therapy
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 |
|---|---|---|
| ProbioticThe probiotic contained the Lactiplantibacillus plantarum 299v. It was prepared by Sanprobi Sp. z o.o., Sp. k., Szczecin, Poland; probiotic capsules manufacturer - Institute Rosell-Lallemand, Montreal, Canada; Lactiplantibacillus plantarum 299v strain owner - Probi AB, Lund, Sweden. Placebo supplementation began on the day of chemotherapy initiation, according to the following regimen: 1 capsule/day in the first week (1 x 1010 colony-forming unit (CFU)), and 2 capsules/day in the following weeks (2 x 1010 CFU). The supplementation period lasted eight weeks. | Dietary supplement | Probiotic supplementation |
| PlaceboThe placebo contained crystalline cellulose powder. It was prepared by Sanprobi Sp. z o.o., Sp. k., Szczecin, Poland.. Placebo supplementation began on the day of chemotherapy initiation and lasted eight weeks. | Dietary supplement | Placebo supplementation |
Primary outcome
Changes in serum levels of Tumor Necrosis Factor α (TNFα)
Time frame: Baseline, 8 week
Changes in serum levels of interleukin-6 (IL-6)
Time frame: Baseline, 8 week
Changes in serum levels of high-specific C-reactive protein (hsCRP)
Time frame: Baseline, 8 week
Changes in Toll-like receptor 4 (TLR) expression on the surface of monocytes
Time frame: Baseline, 8 week
Changes in the intracellular expression of cyclooxygenase 2 (COX-2)
Time frame: Baseline, 8 week
17 secondary outcomes
Changes in the concentration of lymphocytes
Time frame: Baseline, 8 week
Changes in the concentration of leukocytes
Time frame: Baseline, 8 week
Changes in the concentration of monocytes
Time frame: Baseline, 8 week
Changes in the concentration of neutrophils
Time frame: Baseline, 8 week
Changes in the concentration of erythrocytes
Time frame: Baseline, 8 week
Changes in the concentration of hemoglobin
Time frame: Baseline, 8 week
Changes in the levels of hematocrit
Time frame: Baseline, 8 week
Changes in the concentration of blood platelets
Time frame: Baseline, 8 week
Changes in serum levels of total cholesterol
Time frame: Baseline, 8 week
Changes in serum levels of low-density lipoprotein (LDL) cholesterol
Time frame: Baseline, 8 week
Changes in serum levels of high-density lipoprotein (HDL) cholesterol
Time frame: Baseline, 8 week
Changes in serum levels of triglycerides (TG)
Time frame: Baseline, 8 week
Changes in body weight
Time frame: Baseline, 8 week
Body height measurement
Time frame: Baseline
Changes of body fat content
Time frame: Baseline, 8 week
Changes of free fat mass content
Time frame: Baseline, 8 week
Changes of total body water
Time frame: Baseline, 8 week
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 26 May 2026.
- Background: PubMed 24142717Yang X, Fu Y, Liu J, Ren HY. Impact of probiotics on toll-like receptor 4 expression in an experimental model of ulcerative colitis. J Huazhong Univ Sci Technolog Med Sci. 2013 Oct;33(5):661-665. doi: 10.1007/s11596-013-1177-9. Epub 2013 Oct 20.
- Background: PubMed 30543015Khademalhosseini M, Arababadi MK. Toll-like receptor 4 and breast cancer: an updated systematic review. Breast Cancer. 2019 May;26(3):265-271. doi: 10.1007/s12282-018-00935-2. Epub 2018 Dec 12.
- Background: PubMed 23526132Ahmed A, Redmond HP, Wang JH. Links between Toll-like receptor 4 and breast cancer. Oncoimmunology. 2013 Feb 1;2(2):e22945. doi: 10.4161/onci.22945.
- Background: PubMed 27639584Yiu JH, Dorweiler B, Woo CW. Interaction between gut microbiota and toll-like receptor: from immunity to metabolism. J Mol Med (Berl). 2017 Jan;95(1):13-20. doi: 10.1007/s00109-016-1474-4. Epub 2016 Sep 17.
- Background: PubMed 25811237Velloso LA, Folli F, Saad MJ. TLR4 at the Crossroads of Nutrients, Gut Microbiota, and Metabolic Inflammation. Endocr Rev. 2015 Jun;36(3):245-71. doi: 10.1210/er.2014-1100. Epub 2015 Mar 26.
- Background: PubMed 33494784Ge Y, Wang X, Guo Y, Yan J, Abuduwaili A, Aximujiang K, Yan J, Wu M. Gut microbiota influence tumor development and Alter interactions with the human immune system. J Exp Clin Cancer Res. 2021 Jan 25;40(1):42. doi: 10.1186/s13046-021-01845-6.
- Background: PubMed 30155890Secombe KR, Coller JK, Gibson RJ, Wardill HR, Bowen JM. The bidirectional interaction of the gut microbiome and the innate immune system: Implications for chemotherapy-induced gastrointestinal toxicity. Int J Cancer. 2019 May 15;144(10):2365-2376. doi: 10.1002/ijc.31836. Epub 2018 Oct 1.
- Background: PubMed 26147207Montassier E, Gastinne T, Vangay P, Al-Ghalith GA, Bruley des Varannes S, Massart S, Moreau P, Potel G, de La Cochetiere MF, Batard E, Knights D. Chemotherapy-driven dysbiosis in the intestinal microbiome. Aliment Pharmacol Ther. 2015 Sep;42(5):515-28. doi: 10.1111/apt.13302. Epub 2015 Jul 6.
- Background: PubMed 34502383Wei L, Wen XS, Xian CJ. Chemotherapy-Induced Intestinal Microbiota Dysbiosis Impairs Mucosal Homeostasis by Modulating Toll-like Receptor Signaling Pathways. Int J Mol Sci. 2021 Aug 31;22(17):9474. doi: 10.3390/ijms22179474.
- Background: PubMed 34604043Oh B, Boyle F, Pavlakis N, Clarke S, Guminski A, Eade T, Lamoury G, Carroll S, Morgia M, Kneebone A, Hruby G, Stevens M, Liu W, Corless B, Molloy M, Libermann T, Rosenthal D, Back M. Emerging Evidence of the Gut Microbiome in Chemotherapy: A Clinical Review. Front Oncol. 2021 Sep 16;11:706331. doi: 10.3389/fonc.2021.706331. eCollection 2021.
- Background: PubMed 32433595Zheng D, Liwinski T, Elinav E. Interaction between microbiota and immunity in health and disease. Cell Res. 2020 Jun;30(6):492-506. doi: 10.1038/s41422-020-0332-7. Epub 2020 May 20.
- Background: PubMed 34262150Lee KA, Luong MK, Shaw H, Nathan P, Bataille V, Spector TD. The gut microbiome: what the oncologist ought to know. Br J Cancer. 2021 Oct;125(9):1197-1209. doi: 10.1038/s41416-021-01467-x. Epub 2021 Jul 14.
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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. This study is not recruiting at the moment.
The record lists no contact. Use the official record to reach the sponsor.
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Probiotic in people with Breast Cancer and Probiotic Therapy, run by Poznan University of Medical Sciences at 1 site in Poland.
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 3 inclusion and 5 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: finished, as of the sponsor's last update on 26 May 2026. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Poland. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. Some participants in this study may receive a placebo. 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?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Changes in serum levels of Tumor Necrosis Factor α (TNFα) (time frame: Baseline, 8 week). The study lists 5 primary outcomes in all. 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 NCT07607548, which also lists 19 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 26 May 2026.