Immunophenotypic Evaluation of IL-7R α in Acute Leukaemia

• ClinicalTrials.gov Identifier: NCT05643547
• Recruitment Status: Not yet recruiting
• First Posted: December 8, 2022
• Last Update Posted: December 8, 2022
• Sponsor: Rania Abdeltwab Abdelazeim
• Information provided by (Responsible Party): Rania Abdeltwab Abdelazeim, Assiut University

Study Description

Brief Summary:

Acute leukemia is generally understood to be a neoplastic process that exerts a maturational block at a hematopoietic precursor cell level, accompanied by a proliferative drive of varying degree. The resulting accumulation of cells, most frequently in the marrow, causes the typical clinical picture, which includes marrow failure, tissue infiltration, organomegaly and on occasion, tumor masses. AL is broadly classified as acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL) (1).

Acute lymphoblastic leukemia is frequently diagnosed in children and young adults, with incidence peaks between 2 and 5 years of age (2), whereas AML is the most common acute type in adults (3).

In addition to leukemia cells themselves, cells of the immune system are a fundamental component of the tumor microenvironment (TME), which often modify the TME to be more favorable to tumor development and progression through producing cytokines and mediators (4,5) . Interleukins / interleukin receptors interaction plays important roles in the antitumor immune response through mediating cell-cell communication in TME and is reported to be relevant to patient prognosis (6,7). As a member of the Interleukin family, Interleukin 7 (IL7) play vital roles in hematopoiesis and the development of T lymphocytes, as well as the inflammation, autoimmune diseases and hematological cancers. Its function is mediated by the IL7 R, which is a membrane receptor consisted of the specific IL7Ra chain (CD127) and IL-7Rγ chain (common gamma chain shared by the receptors for IL-2,-4,-9,-15, and-21) (8). It is thus not surprising that activation of IL-7 signalling is seen in the majority of T-ALLs and in some of the B cell precursor ALL (9,10).

Consistent with the absolute requirement of IL-7 to human T cell development, most T-ALLs have been shown to respond to IL-7. Thus targeting IL-7 signaling might be a reasonable general approach for treatment of T-ALL, regardless the presence of activating mutations. (10)

Condition or disease
Benefit: To Patient Have Investigation for Diagnosis and Follow up for His Disease and Reach to New Method Help in Early Diagnosis of Lymphoid Disorder

Detailed Description:

Acute leukemia is generally understood to be a neoplastic process that exerts a maturational block at a hematopoietic precursor cell level, accompanied by a proliferative drive of varying degree. The resulting accumulation of cells, most frequently in the marrow, causes the typical clinical picture, which includes marrow failure, tissue infiltration, organomegaly and on occasion, tumor masses. AL is broadly classified as acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL) (1).

Acute lymphoblastic leukemia is frequently diagnosed in children and young adults, with incidence peaks between 2 and 5 years of age (2), whereas AML is the most common acute type in adults (3).

In addition to leukemia cells themselves, cells of the immune system are a fundamental component of the tumor microenvironment (TME), which often modify the TME to be more favorable to tumor development and progression through producing cytokines and mediators (4,5) . Interleukins / interleukin receptors interaction plays important roles in the antitumor immune response through mediating cell-cell communication in TME and is reported to be relevant to patient prognosis (6,7). As a member of the Interleukin family, Interleukin 7 (IL7) play vital roles in hematopoiesis and the development of T lymphocytes, as well as the inflammation, autoimmune diseases and hematological cancers. Its function is mediated by the IL7 R, which is a membrane receptor consisted of the specific IL7Ra chain (CD127) and IL-7Rγ chain (common gamma chain shared by the receptors for IL-2,-4,-9,-15, and-21) (8). It is thus not surprising that activation of IL-7 signalling is seen in the majority of T-ALLs and in some of the B cell precursor ALL (9,10).

Consistent with the absolute requirement of IL-7 to human T cell development, most T-ALLs have been shown to respond to IL-7. Thus targeting IL-7 signaling might be a reasonable general approach for treatment of T-ALL, regardless the presence of activating mutations. (10).

Study Design

• Study Type: Observational
• Estimated Enrollment: 83 participants
• Observational Model: Case-Crossover
• Time Perspective: Cross-Sectional
• Official Title: Immunophenotypic Evaluation of IL-7R α in Acute Leukaemia
• Estimated Study Start Date: March 1, 2023
• Estimated Primary Completion Date: December 30, 2023
• Estimated Study Completion Date: October 30, 2024

Groups and Cohorts

Outcome Measures

Primary Outcome Measures :

1. Immunophenotypic expression of IL7R α in acute leukemia cases. [ Time Frame: 2022-2024 ]
   Immunophenotypic expression of IL7R α in acute leukemia cases.

Eligibility Criteria

• Ages Eligible for Study: Child, Adult, Older Adult
• Sexes Eligible for Study: All
• Sampling Method: Probability Sample

Study Population

- Newly diagnosed patients with Acute leukemia (ALL, AML), male or female at any age will be investigated for Immunophenotypic expression of IL7R α and its diagnostic value.

Criteria

Inclusion Criteria:

• Newly diagnosed patients with Acute leukemia (ALL, AML), male or female at any age.

Exclusion Criteria:

• Patients diagnosed with hematological malignancy other than acute leukemias
• Patients receiving chemo and/or radiotherapy
• Patients on steroid therapy for any other reason
• Patients receiving any immunosuppressive drug

Contacts and Locations

No Contacts or Locations Provided

More Information

• Responsible Party: Rania Abdeltwab Abdelazeim, Immunophenotypic evaluation of IL-7R α in Acute leukaemia, Assiut University
• ClinicalTrials.gov Identifier: NCT05643547
• Other Study ID Numbers: 159159
• First Posted: December 8, 2022
• Last Update Posted: December 8, 2022
• Last Verified: November 2022

Additional relevant MeSH terms:

Disease; Pathologic Processes