FAP-Familial Adenomatous PolyposisPhase 4NCT02354560
Erythromycin Treatment for Readthrough of APC Gene Stop Codon Mutation in Familial Adenomatous Polyposis-minors' Adjusted Version
A Phase 4 study testing Erythromycin in people with FAP-Familial Adenomatous Polyposis, run by michal roll.
Trial summary
Colorectal cancer (CRC) is a leading cause for cancer related mortality in the western world with a lifetime risk of 6%. Etiology is complex, while genetic background significantly affects the risk. Read more about this study
- Who is it for?
- Ages 10 to 17 years
- Conditions the study is for
- FAP-Familial Adenomatous Polyposis
- What is being tested?
- Erythromycin
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 15 participants
- Where
- No sites listed yet
- Study dates
- Jun 2015to Dec 2017
- Phase
- Phase 4
- 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 10 to 17 years
- All sexes
- No healthy volunteers
- Child
Who may be able to join
- ages: 10-17 years old.
- A lack of known sensitivity to ERYTHROMYCIN or other macrolide.
- at the relevant subgroup - existence of polyps in the colon or Ileo-anal pouch that classified as adenomas and the size isn't bigger than 10 mm and there's no high grade dysplasia and that not yet need immediate resection of the colon rectal but just a surveillance.
- In the relevant subgroup- existence of polyps in the duodenum that do not require surgery and aren't bigger than 10 mm and with out high grade dysplasia.
- In the relevant subgroup- a tumor that classified as stomach or pelvic desmoid that not yet need immediate resection and which can be measured by ultrasound or MRI.
Who cannot join
- below 10 years old or above 18 years old.
- sensitivity to ERYTHROMYCIN or other macrolide.
- Ileo-anal pouch without adenomas.
- existence of polyps that are classified as adenomas which are bigger than 10 mm and/or with histological of high grade dysplasia.
- Taking medicines that have interactions with ERYTHROMYCIN such as: Carbamazepine, Cyclosporine, barbiturate, PHENYTOIN, Disopyramide, Lovastatin, Bromocriptine: it is recommended to keep careful attention over their Concentrations in the blood and to match the dose.
- significant personal of familial history of ventricular arrhythmia and/or Long QT interval per ECG, or consumption of drugs that may cause prolonged QT.
- Recruitment of children whom suffer from FAP in addition to other diseases is subject to a joint decision of the PI and the study pediatrician.
Trial locations and contacts
No sites are listed yet.
About this study
Official title: Erythromycin Treatment for Readthrough of APC Gene Stop Codon Mutation in Familial Adenomatous Polyposis-protocol is Identical to Study No. 0519-10-TLV- Minors' Adjusted Version
Colorectal cancer (CRC) is a leading cause for cancer related mortality in the western world with a lifetime risk of 6%. Etiology is complex, while genetic background significantly affects the risk. Around one third of all genetic disorders as well as most cases of Familial Adenomatous Polyposis (FAP) and a large proportion of all sporadic CRC cases occur as a result of premature nonsense mutations (creating a stop codon) in an individual's adenomatous polyposis coli (APC) gene. Nonsense mutations are single-point alterations in the DNA that prematurely halt the protein translation process, producing a shortened, nonfunctional protein. In many of these cases, if the cell can be 'persuaded' to ignore the premature stop codon signal, the resulting protein may be able to ameliorate or stop the disease.
Recently, members of the aminoglycoside family of antibiotics have been found to induce ribosomal read-through of nonsense mutations, leading to expression of a full length, functional protein. Investigators have recently shown that members of the aminoglycoside and macrolide antibiotic families can induce read-through of the nonsense mutations in the APC gene and lead to reduced oncogenic phenotypes in CRC cells and in different mice models.
Read more
The aim of this project is to determine the ability of the macrolide antibiotic-erythromycin to induce read-through of the nonsense mutations in the APC gene and to induce expression of a full length, functional APC protein in patients suffering from FAP and to tests its effect on adenoma number and size and on desmoid tumors in these patients. The future goal is to maximize the effect of stop-codon suppressors on APC while minimizing side effects.
In this study investigators will select FAP patients which carry APC nonsense mutations, treat them with erythromycin PO for 4-6 months and examine colonic and duodenal adenomas as well as abdominal desmoid tumors, that will be documented before during and after treatment. In parallel, investigators will test polyp, adenoma and desmoid tissue samples as well as blood samples from these patients for changes in expression levels of the APC protein and related oncogenic markers.
Suppression of nonsense mutations within the APC gene should be of benefit for patients suffering from FAP, attenuated FAP or multiple adenomas and for patients with advanced or diffuse CRC. Furthermore, given the rapid progress being made in the identification of different nonsense mutations in human genes that lead to mostly un-curable disease, the identification of clinically approved compounds that suppress nonsense mutations and that can be administered long-term without significant side effects would open new venues in the treatment of genetic human diseases that arise from pre-mature stop codons in important coding sequences.
Immediate goal: establish the ability of erythromycin to read-through APC nonsense mutation in FAP patients. The read-through effect of erythromycin will be clinically tested by counting and measuring the number and size of both colonic and duodenal adenomas before and over treatment and by measuring the size of known desmoid tumors. Samples of the adenomas and desmoid tumors will be tested by western blot, immunofluorescence and immunohistochemistry for restoration of APC expression and changes in oncogenic markers. These experiments should be conducted within 6 month.
Long term objective:
- Determine the lowest dose of erythromycin that can inhibit growth of colonic neoplasia and CRC in patients expressing a truncated APC protein due to nonsense mutations.
- Examine the ability of a panel of additional macrolide antibiotics to induce APC nonsense mutation suppression using in-vitro methods. Investigators will focus on macrolide antibiotics that are currently in clinical use and are administrated for long terms. These objectives should take around 6 month and will be conducted in parallel.
- Conditions
- FAP-Familial Adenomatous Polyposis
- Being tested
- Erythromycin
- Keywords
- Erythromycin, Familial Adenomatous Polyposis (FAP), APC gene, nonsense mutations
- Medical subject headings
- Adenomatous Polyposis Coli
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
ErythromycinDrug
Oral Treatment with Erythromycin 250-500mg, twice daily, for 16 weeks.Exact dose is subjected to body weight and will be determined by the study's pediatrician.
| Study group | Role | What they receive |
|---|---|---|
| Erythromycin | Experimental | Oral treatment with Erythromycin 250-500mg (will be determined according to body weight) twice a day. Receives: Drug: Erythromycin |
What is being measured
The primary outcome is the main question the study is designed to answer.
Evaluation of changes in number of adenomas measured by upper endoscopy
Change in number of adenomas from baseline will be measured by endoscopic and histological evaluation. response will be tested by upper and lower endoscopies after 8 ,16-20 weeks and 12 months of treatment.
Measured: After 8,16 weeks and 12 months
Evaluation of changes in size of adenomas measured by lower endoscopy
Change in number of adenomas from baseline will be measured by endoscopic and histological evaluation. response will be tested by upper and lower endoscopies after 8 ,16-20 weeks and 12 months of treatment.
Measured: After 8,16 weeks and 12 months
Evaluation of changes in size of desmoid tumors
Desmoids imaging (US or CT or MRI) will be performed to determine the size at the begining of the study and to evaluate the change from baseline after 4-6 months of treatment.
Measured: At the begining of the trial (before treatment) and at the end of the treatment (after 4-6 months)
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted3 Feb 2015 (estimated)
- Study startJun 2015
- Primary completionDec 2017 (estimated)
- Study completionDec 2017 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (11)Papers the sponsor has linked to this study.
- Other trials for FAP-Familial Adenomatous PolyposisStudies 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 4
- Primary purpose
- Treatment
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Enrolment
- 15 participants (estimated)
Sponsor and investigators
- Lead sponsor
- michal roll
- Sponsor type
- Other government
- Responsible party
- Sponsor-investigator, michal roll, Tel-Aviv Sourasky Medical Center
- Investigators
- Revital Kariv, MD, Study director, Department of Gastroenterol Tel Aviv Medical Center, Sackler Faculty of Medicine, Tel Aviv University.Rina Rosin-Arbeseld, Ph.D, Study director, Department of Anatomy Sackler Faculty of Medicine, Tel Aviv University.
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02354560
- Sponsor's protocol ID
- 0377-14-TLV
- Status last verified
- Jan 2015
- First submitted
- 21 Jan 2015
- Last updated
- 3 Feb 2015
- Results posted
- No
- Data monitoring committee
- No
Publications
Smith KJ, Johnson KA, Bryan TM, Hill DE, Markowitz S, Willson JK, Paraskeva C, Petersen GM, Hamilton SR, Vogelstein B, et al. The APC gene product in normal and tumor cells. Proc Natl Acad Sci U S A. 1993 Apr 1;90(7):2846-50. doi: 10.1073/pnas.90.7.2846.
PubMed 8385345Miyoshi Y, Nagase H, Ando H, Horii A, Ichii S, Nakatsuru S, Aoki T, Miki Y, Mori T, Nakamura Y. Somatic mutations of the APC gene in colorectal tumors: mutation cluster region in the APC gene. Hum Mol Genet. 1992 Jul;1(4):229-33. doi: 10.1093/hmg/1.4.229.
PubMed 1338904Jasperson KW, Tuohy TM, Neklason DW, Burt RW. Hereditary and familial colon cancer. Gastroenterology. 2010 Jun;138(6):2044-58. doi: 10.1053/j.gastro.2010.01.054.
PubMed 20420945Nieuwenhuis MH, Mathus-Vliegen EM, Baeten CG, Nagengast FM, van der Bijl J, van Dalsen AD, Kleibeuker JH, Dekker E, Langers AM, Vecht J, Peters FT, van Dam R, van Gemert WG, Stuifbergen WN, Schouten WR, Gelderblom H, Vasen HF. Evaluation of management of desmoid tumours associated with familial adenomatous polyposis in Dutch patients. Br J Cancer. 2011 Jan 4;104(1):37-42. doi: 10.1038/sj.bjc.6605997. Epub 2010 Nov 9.
PubMed 21063417Zilberberg A, Lahav L, Rosin-Arbesfeld R. Restoration of APC gene function in colorectal cancer cells by aminoglycoside- and macrolide-induced read-through of premature termination codons. Gut. 2010 Apr;59(4):496-507. doi: 10.1136/gut.2008.169805. Epub 2009 Dec 1.
PubMed 19951906Lai CH, Chun HH, Nahas SA, Mitui M, Gamo KM, Du L, Gatti RA. Correction of ATM gene function by aminoglycoside-induced read-through of premature termination codons. Proc Natl Acad Sci U S A. 2004 Nov 2;101(44):15676-81. doi: 10.1073/pnas.0405155101. Epub 2004 Oct 21.
PubMed 15498871Wilschanski M, Yahav Y, Yaacov Y, Blau H, Bentur L, Rivlin J, Aviram M, Bdolah-Abram T, Bebok Z, Shushi L, Kerem B, Kerem E. Gentamicin-induced correction of CFTR function in patients with cystic fibrosis and CFTR stop mutations. N Engl J Med. 2003 Oct 9;349(15):1433-41. doi: 10.1056/NEJMoa022170.
PubMed 14534336Kerem E, Hirawat S, Armoni S, Yaakov Y, Shoseyov D, Cohen M, Nissim-Rafinia M, Blau H, Rivlin J, Aviram M, Elfring GL, Northcutt VJ, Miller LL, Kerem B, Wilschanski M. Effectiveness of PTC124 treatment of cystic fibrosis caused by nonsense mutations: a prospective phase II trial. Lancet. 2008 Aug 30;372(9640):719-27. doi: 10.1016/S0140-6736(08)61168-X. Epub 2008 Aug 20.
PubMed 18722008West NJ, Clark SK, Phillips RK, Hutchinson JM, Leicester RJ, Belluzzi A, Hull MA. Eicosapentaenoic acid reduces rectal polyp number and size in familial adenomatous polyposis. Gut. 2010 Jul;59(7):918-25. doi: 10.1136/gut.2009.200642. Epub 2010 Mar 26.
PubMed 20348368Lips DJ, Barker N, Clevers H, Hennipman A. The role of APC and beta-catenin in the aetiology of aggressive fibromatosis (desmoid tumors). Eur J Surg Oncol. 2009 Jan;35(1):3-10. doi: 10.1016/j.ejso.2008.07.003. Epub 2008 Aug 21.
PubMed 18722078Markowitz SD, Bertagnolli MM. Molecular origins of cancer: Molecular basis of colorectal cancer. N Engl J Med. 2009 Dec 17;361(25):2449-60. doi: 10.1056/NEJMra0804588. No abstract available.
PubMed 20018966
Study at a glance
From the registry record, last updated by the sponsor on 3 Feb 2015. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Erythromycin Treatment for Readthrough of APC Gene Stop Codon Mutation in Familial Adenomatous Polyposis-protocol is Identical to Study No. 0519-10-TLV- Minors' Adjusted Version
- ClinicalTrials.gov ID
- NCT02354560
- Acronym / sponsor ID
- 0377-14-TLV
- Conditions
- FAP-Familial Adenomatous Polyposis
- Keywords
- Erythromycin, Familial Adenomatous Polyposis (FAP), APC gene, nonsense mutations
- Phase
- Phase 4
- Study type
- Interventional
- Recruitment status
- Unknown status
- Enrolment
- 15 participants (estimated)
- Lead sponsor
- michal rollOther government
- Study start
- Jun 2015
- Primary completion
- Dec 2017 (estimated)
- Study completion
- Dec 2017 (estimated)
- First posted
- 3 Feb 2015 (estimated)
- 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.
Colorectal cancer (CRC) is a leading cause for cancer related mortality in the western world with a lifetime risk of 6%. Etiology is complex, while genetic background significantly affects the risk. Around one third of all genetic disorders as well as most cases of Familial Adenomatous Polyposis (FAP) and a large proportion of all sporadic CRC cases occur as a result of premature nonsense mutations (creating a stop codon) in an individual's adenomatous polyposis coli (APC) gene. Nonsense mutations are single-point alterations in the DNA that prematurely halt the protein translation process, producing a shortened, nonfunctional protein. In many of these cases, if the cell can be 'persuaded' to ignore the premature stop codon signal, the resulting protein may be able to ameliorate or stop the disease.
Recently, members of the aminoglycoside family of antibiotics have been found to induce ribosomal read-through of nonsense mutations, leading to expression of a full length, functional protein. Investigators have recently shown that members of the aminoglycoside and macrolide antibiotic families can induce read-through of the nonsense mutations in the APC gene and lead to reduced oncogenic phenotypes in CRC cells and in different mice models.
The aim of this project is to determine the ability of the macrolide antibiotic-erythromycin to induce read-through of the nonsense mutations in the APC gene and to induce expression of a full length, functional APC protein in patients suffering from FAP and to tests its effect on adenoma number and size and on desmoid tumors in these patients. The future goal is to maximize the effect of stop-codon suppressors on APC while minimizing side effects.
In this study investigators will select FAP patients which carry APC nonsense mutations, treat them with erythromycin PO for 4-6 months and examine colonic and duodenal adenomas as well as abdominal desmoid tumors, that will be documented before during and after treatment. In parallel, investigators will test polyp, adenoma and desmoid tissue samples as well as blood samples from these patients for changes in expression levels of the APC protein and related oncogenic markers.
Suppression of nonsense mutations within the APC gene should be of benefit for patients suffering from FAP, attenuated FAP or multiple adenomas and for patients with advanced or diffuse CRC. Furthermore, given the rapid progress being made in the identification of different nonsense mutations in human genes that lead to mostly un-curable disease, the identification of clinically approved compounds that suppress nonsense mutations and that can be administered long-term without significant side effects would open new venues in the treatment of genetic human diseases that arise from pre-mature stop codons in important coding sequences.
Immediate goal: establish the ability of erythromycin to read-through APC nonsense mutation in FAP patients. The read-through effect of erythromycin will be clinically tested by counting and measuring the number and size of both colonic and duodenal adenomas before and over treatment and by measuring the size of known desmoid tumors. Samples of the adenomas and desmoid tumors will be tested by western blot, immunofluorescence and immunohistochemistry for restoration of APC expression and changes in oncogenic markers. These experiments should be conducted within 6 month.
Long term objective:
- Determine the lowest dose of erythromycin that can inhibit growth of colonic neoplasia and CRC in patients expressing a truncated APC protein due to nonsense mutations.
- Examine the ability of a panel of additional macrolide antibiotics to induce APC nonsense mutation suppression using in-vitro methods. Investigators will focus on macrolide antibiotics that are currently in clinical use and are administrated for long terms. These objectives should take around 6 month and will be conducted in parallel.
Study design
- Primary purpose
- Treatment
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| Erythromycin | Experimental | Drug: ErythromycinOral treatment with Erythromycin 250-500mg (will be determined according to body weight) twice a day. |
Who may qualify
- Ages
- 10 to 17 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child
Key inclusion criteria (5 listed)
- ages: 10-17 years old.
- A lack of known sensitivity to ERYTHROMYCIN or other macrolide.
- at the relevant subgroup - existence of polyps in the colon or Ileo-anal pouch that classified as adenomas and the size isn't bigger than 10 mm and there's no high grade dysplasia and that not yet need immediate resection of the colon rectal but just a surveillance.
- In the relevant subgroup- existence of polyps in the duodenum that do not require surgery and aren't bigger than 10 mm and with out high grade dysplasia.
- In the relevant subgroup- a tumor that classified as stomach or pelvic desmoid that not yet need immediate resection and which can be measured by ultrasound or MRI.
Key exclusion criteria (7 listed)
- below 10 years old or above 18 years old.
- sensitivity to ERYTHROMYCIN or other macrolide.
- Ileo-anal pouch without adenomas.
- existence of polyps that are classified as adenomas which are bigger than 10 mm and/or with histological of high grade dysplasia.
- Taking medicines that have interactions with ERYTHROMYCIN such as: Carbamazepine, Cyclosporine, barbiturate, PHENYTOIN, Disopyramide, Lovastatin, Bromocriptine: it is recommended to keep careful attention over their Concentrations in the blood and to match the dose.
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 |
|---|---|---|
| ErythromycinOral Treatment with Erythromycin 250-500mg, twice daily, for 16 weeks.Exact dose is subjected to body weight and will be determined by the study's pediatrician. | Drug | Erythromycin |
Primary outcome
Evaluation of changes in number of adenomas measured by upper endoscopy
Time frame: After 8,16 weeks and 12 months
Change in number of adenomas from baseline will be measured by endoscopic and histological evaluation. response will be tested by upper and lower endoscopies after 8 ,16-20 weeks and 12 months of treatment.
Evaluation of changes in size of adenomas measured by lower endoscopy
Time frame: After 8,16 weeks and 12 months
Change in number of adenomas from baseline will be measured by endoscopic and histological evaluation. response will be tested by upper and lower endoscopies after 8 ,16-20 weeks and 12 months of treatment.
Evaluation of changes in size of desmoid tumors
Time frame: At the begining of the trial (before treatment) and at the end of the treatment (after 4-6 months)
Desmoids imaging (US or CT or MRI) will be performed to determine the size at the begining of the study and to evaluate the change from baseline after 4-6 months of treatment.
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 3 Feb 2015.
- Background: PubMed 8385345Smith KJ, Johnson KA, Bryan TM, Hill DE, Markowitz S, Willson JK, Paraskeva C, Petersen GM, Hamilton SR, Vogelstein B, et al. The APC gene product in normal and tumor cells. Proc Natl Acad Sci U S A. 1993 Apr 1;90(7):2846-50. doi: 10.1073/pnas.90.7.2846.
- Background: PubMed 1338904Miyoshi Y, Nagase H, Ando H, Horii A, Ichii S, Nakatsuru S, Aoki T, Miki Y, Mori T, Nakamura Y. Somatic mutations of the APC gene in colorectal tumors: mutation cluster region in the APC gene. Hum Mol Genet. 1992 Jul;1(4):229-33. doi: 10.1093/hmg/1.4.229.
- Background: PubMed 20420945Jasperson KW, Tuohy TM, Neklason DW, Burt RW. Hereditary and familial colon cancer. Gastroenterology. 2010 Jun;138(6):2044-58. doi: 10.1053/j.gastro.2010.01.054.
- Background: PubMed 21063417Nieuwenhuis MH, Mathus-Vliegen EM, Baeten CG, Nagengast FM, van der Bijl J, van Dalsen AD, Kleibeuker JH, Dekker E, Langers AM, Vecht J, Peters FT, van Dam R, van Gemert WG, Stuifbergen WN, Schouten WR, Gelderblom H, Vasen HF. Evaluation of management of desmoid tumours associated with familial adenomatous polyposis in Dutch patients. Br J Cancer. 2011 Jan 4;104(1):37-42. doi: 10.1038/sj.bjc.6605997. Epub 2010 Nov 9.
- Background: PubMed 19951906Zilberberg A, Lahav L, Rosin-Arbesfeld R. Restoration of APC gene function in colorectal cancer cells by aminoglycoside- and macrolide-induced read-through of premature termination codons. Gut. 2010 Apr;59(4):496-507. doi: 10.1136/gut.2008.169805. Epub 2009 Dec 1.
- Background: PubMed 15498871Lai CH, Chun HH, Nahas SA, Mitui M, Gamo KM, Du L, Gatti RA. Correction of ATM gene function by aminoglycoside-induced read-through of premature termination codons. Proc Natl Acad Sci U S A. 2004 Nov 2;101(44):15676-81. doi: 10.1073/pnas.0405155101. Epub 2004 Oct 21.
- Background: PubMed 14534336Wilschanski M, Yahav Y, Yaacov Y, Blau H, Bentur L, Rivlin J, Aviram M, Bdolah-Abram T, Bebok Z, Shushi L, Kerem B, Kerem E. Gentamicin-induced correction of CFTR function in patients with cystic fibrosis and CFTR stop mutations. N Engl J Med. 2003 Oct 9;349(15):1433-41. doi: 10.1056/NEJMoa022170.
- Background: PubMed 18722008Kerem E, Hirawat S, Armoni S, Yaakov Y, Shoseyov D, Cohen M, Nissim-Rafinia M, Blau H, Rivlin J, Aviram M, Elfring GL, Northcutt VJ, Miller LL, Kerem B, Wilschanski M. Effectiveness of PTC124 treatment of cystic fibrosis caused by nonsense mutations: a prospective phase II trial. Lancet. 2008 Aug 30;372(9640):719-27. doi: 10.1016/S0140-6736(08)61168-X. Epub 2008 Aug 20.
- Background: PubMed 20348368West NJ, Clark SK, Phillips RK, Hutchinson JM, Leicester RJ, Belluzzi A, Hull MA. Eicosapentaenoic acid reduces rectal polyp number and size in familial adenomatous polyposis. Gut. 2010 Jul;59(7):918-25. doi: 10.1136/gut.2009.200642. Epub 2010 Mar 26.
- Background: PubMed 18722078Lips DJ, Barker N, Clevers H, Hennipman A. The role of APC and beta-catenin in the aetiology of aggressive fibromatosis (desmoid tumors). Eur J Surg Oncol. 2009 Jan;35(1):3-10. doi: 10.1016/j.ejso.2008.07.003. Epub 2008 Aug 21.
- Results publication: PubMed 20018966Markowitz SD, Bertagnolli MM. Molecular origins of cancer: Molecular basis of colorectal cancer. N Engl J Med. 2009 Dec 17;361(25):2449-60. doi: 10.1056/NEJMra0804588. No abstract available.
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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.
Revital Kariv, MD study director
Department of Gastroenterol Tel Aviv Medical Center, Sackler Faculty of Medicine, Tel Aviv University.
Rina Rosin-Arbeseld, Ph.D study director
Department of Anatomy Sackler Faculty of Medicine, Tel Aviv University.
Questions about this trial
What is this clinical trial studying?
A Phase 4 study testing Erythromycin in people with FAP-Familial Adenomatous Polyposis, run by michal roll.
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 7 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: status not confirmed, as of the sponsor's last update on 3 Feb 2015. 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.
What does this phase mean?
Phase 4 studies take place after a treatment is approved, to learn more about its long-term benefits and risks in everyday use.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Reut Elya, Ms.C (03-6974458, reute@tlvmc.gov.il), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Evaluation of changes in number of adenomas measured by upper endoscopy (time frame: After 8,16 weeks and 12 months). The study lists 3 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 NCT02354560, which also lists 11 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 3 Feb 2015.