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VDJ-Seq: Deep Sequencing Analysis of Rearranged Immunoglobulin Heavy Chain Gene to Reveal Clonal Evolution Patterns of B Cell Lymphoma

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Published on: December 28, 2015

Immune-Genomic Evolution in AML Spontaneous Remission: A 66-Patient Pooled Analysis and Longitudinal Clonal Tracking.

Yanping Sun^1,2, Mengyuan Chang^1,2, Jinlin Chen^1,2

¹Department of Hematology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250012, China.

|May 13, 2026

Summary

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Spontaneous remission (SR) in acute myeloid leukemia (AML) is often triggered by infection. Understanding the immune and genetic factors driving AML SR and relapse is crucial for improving patient outcomes.

Area of Science:

Hematology
Immunology
Oncology

Background:

Spontaneous remission (SR) in acute myeloid leukemia (AML) provides critical insights into anti-tumor immunity.
The clinical and molecular mechanisms underlying blast clearance and subsequent relapse in AML SR are not fully understood.

Purpose of the Study:

To define the clinical triggers and outcomes associated with AML SR.
To elucidate the molecular dynamics, including clonal shifts and immune responses, during AML SR and relapse.

Main Methods:

A systematic pooled analysis of 66 adult AML SR cases (1990-2024).
Longitudinal molecular tracking and immune profiling of two institutional AML SR cases.

Main Results:

Infection was the primary trigger for SR in 78.6% of cases, with a predominance of males and monocytic leukemia.

Keywords:

acute myeloid leukemia clonal evolution cytokine storm infection-associated immunity interleukin-8 spontaneous remission tumor microenvironment

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VDJ-Seq: Deep Sequencing Analysis of Rearranged Immunoglobulin Heavy Chain Gene to Reveal Clonal Evolution Patterns of B Cell Lymphoma

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Immunoglobulin Gene Sequence Analysis In Chronic Lymphocytic Leukemia: From Patient Material To Sequence Interpretation

Immunoglobulin Gene Sequence Analysis In Chronic Lymphocytic Leukemia: From Patient Material To Sequence Interpretation

Published on: November 26, 2018

SR duration and relapse risk were not dependent on the trigger, AML subtype, or patient age.

Immune profiling revealed an acute IL-8 surge with NKT and CD4+ T cell activation during blast clearance, followed by relapse associated with TP53 or NRAS mutations in DNMT3A-mutated clones.

Conclusions:

A clinical-evolutionary framework for AML SR is proposed, emphasizing the balance between acute immune activation and clonal stability for remission durability.
Complex immune-genomic crosstalk is implicated in AML SR and relapse, suggesting potential selective pressure from chronic inflammation on resistant subclones.
Findings generate hypotheses for future prospective studies on AML SR mechanisms and therapeutic strategies.