Related Experiment Video

Updated: Aug 18, 2026

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
10:00

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

Published on: March 24, 2015

Interferon alfa-2b in the treatment of chronic myelogenous leukemia

N Niederle, O Kloke, R Osieka

    Seminars in Oncology
    |June 1, 1987
    PubMed

    Insights

    Interferon alfa-2b showed promise for chronic phase chronic myeloid leukemia (CML), inducing hematologic remission in 58% of patients. However, it was ineffective in acute phase CML patients.

    Area of Science:

    • Hematology
    • Oncology
    • Pharmacology

    Background:

    • Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm.
    • Philadelphia chromosome-positive (Ph+) CML accounts for the majority of cases.
    • Novel therapeutic strategies are continually sought for CML management.

    Purpose of the Study:

    • To evaluate the efficacy and tolerability of interferon alfa-2b in patients with Philadelphia chromosome-positive chronic myeloid leukemia (CML).

    Main Methods:

    • Thirty-six patients with Ph+ CML (32 chronic phase, 4 acute phase) received subcutaneous interferon alfa-2b.
    • Initial dose was 4 megaunits/m2 daily, with subsequent dose adjustments based on blood counts.
    • Treatment duration ranged from 0.5 to 15 months (median 7 months).

    Main Results:

    • Hematologic remission was achieved in 21 patients (58%), with partial hematologic remission in 12 (33%).
    • No complete remission was observed.
    • All four patients with acute phase CML did not respond to treatment.
    • Adverse reactions were transient and did not impede self-administration.

    Conclusions:

    • Interferon alfa-2b demonstrated significant hematologic response rates in chronic phase Ph+ CML.
    • The drug was ineffective in acute phase CML.
    • Interferon alfa-2b may represent a viable alternative treatment for chronic phase CML.

    More Related Videos

    Development and Validation of an Ultrasensitive Single Molecule Array Digital Enzyme-linked Immunosorbent Assay for Human Interferon-α08:26

    Development and Validation of an Ultrasensitive Single Molecule Array Digital Enzyme-linked Immunosorbent Assay for Human Interferon-α

    Published on: June 14, 2018

    Comet Assay to Quantify DNA Damage in FLT3 Mutant-expressing 32D Cells after Exposure to Type I and Type II FLT3 Inhibitors04:36

    Comet Assay to Quantify DNA Damage in FLT3 Mutant-expressing 32D Cells after Exposure to Type I and Type II FLT3 Inhibitors

    Published on: October 17, 2025

    Related Concept Videos

    Targeted Cancer Therapies02:57

    Targeted Cancer Therapies

    The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
    There are several types of targeted therapies against specific...
    Treatment Resistant Cancers02:56

    Treatment Resistant Cancers

    Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
    Combination Therapies and Personalized Medicine02:50

    Combination Therapies and Personalized Medicine

    Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
    The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
    Treatment Resistent Cancers02:56

    Treatment Resistent Cancers

    Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
    Inhibitors of Viral Protein Synthesis01:30

    Inhibitors of Viral Protein Synthesis

    Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...