Timothy A. Graubert, MD, Massachusetts General
Hospital Cancer Center, Harvard Medical School

Comprehensive studies of the acute myeloid leukemia (AML) genome have revealed new insights into the genetic basis of this disease. Recurrently mutated genes fall into pathways previously implicated in AML pathogenesis (e.g., cytokine signaling, line age specific transcription factors) and novel pathways (e.g., RNA splicing, epigenetic regulation, cohesin biology). This increased knowledge provides opportunities to refine prognostic algorithms and has identified new potential targets for therapy.

Acute Myeloid Leukemia (AML) Pathology: Causes and Side Effects

In today's video, we will be discussing acute myeloid leukemia pathology. Acute myeloid leukemia, also known as AML, is a type of cancer that affects the blood and bone marrow. It is a rapidly progressive disease that requires immediate medical attention. According to the American Cancer Society, approximately 21,400 people in the United States are diagnosed with AML each year.

In this video, we will be discussing the pathology of AML, including its etiology, pathogenesis, and molecular features. We will also discuss the various diagnostic techniques and treatment options available for AML patients.

Acute myeloid leukemia is a type of blood cancer that affects the myeloid cells in the bone marrow. These cells are responsible for producing red blood cells, white blood cells, and platelets. In AML, the myeloid cells grow and divide rapidly, leading to an overproduction of immature cells called blasts.

According to a study published in the Journal of Clinical Oncology, "AML is characterized by the accumulation of immature myeloid blasts in the bone marrow, peripheral blood, and other tissues." These blasts are unable to function properly and can't fight infections like normal white blood cells. They also interfere with the production of normal blood cells, leading to anemia, bleeding, and infections.

The exact cause of AML is not yet known, but research suggests that certain risk factors can increase the likelihood of developing the disease. These risk factors include exposure to radiation, chemotherapy, and certain chemicals such as benzene.

A study published in the Journal of the National Cancer Institute suggests that "AML is a heterogeneous disease with a complex etiology, involving genetic, epigenetic, and environmental factors." Genetic mutations play a significant role in the development of AML. Mutations in genes such as FLT3, NPM1, and IDH1/2 have been linked to AML.

AML can be diagnosed through various techniques, including blood tests, bone marrow biopsy, and imaging tests such as CT scans and X-rays. A blood test can reveal abnormal levels of white blood cells, red blood cells, and platelets. A bone marrow biopsy involves removing a small sample of bone marrow tissue for examination under a microscope.

According to a study published in Blood Advances, "Molecular and cytogenetic testing is critical for the diagnosis, classification, and risk stratification of AML." These tests can detect specific genetic mutations that are associated with AML and help determine the best treatment options.

Treatment options for AML depend on several factors, including the patient's age, overall health, and the specific genetic mutations present. Treatment options may include chemotherapy, radiation therapy, stem cell transplantation, and targeted therapy.

A study published in the Journal of Clinical Oncology suggests that "Combination chemotherapy, usually consisting of cytarabine and an anthracycline, is the standard of care for most AML patients." Targeted therapies, such as tyrosine kinase inhibitors and immune checkpoint inhibitors, are also being developed for AML treatment.

In conclusion, acute myeloid leukemia is a type of blood cancer that affects the myeloid cells in the bone marrow. AML is a rapidly progressive disease that requires immediate medical attention. The exact cause of AML is not yet known, but research suggests that certain risk factors can increase the likelihood of developing the disease.

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Timothy A. Graubert, MD
Comprehensive studies of the acute myeloid leukemia (AML) genome have revealed new insights into the genetic basis of this disease. Recurrently mutated genes fall into pathways previously implicated in AML pathogenesis (e.g., cytokine signaling, line age specific transcription factors) and novel pathways (e.g., RNA splicing, epigenetic regulation, cohesin biology). This increased knowledge provides opportunities to refine prognostic algorithms and has identified new potential targets for therapy.

This presentation provides information to assist clinicians in identifying patients with Acute Myeloid Leukemia and selecting appropriate treatment options based on clinical and genetic variables. The presentation also reviews appropriate criteria for investigational/novel therapies and non-cytotoxic therapies, including stem cell transplantation, using cytogenetics and other variables.

Lecture Objective:
-Differentiate, among patients with Acute Myeloid Leukemia, those with favorable, intermediate, or unfavorable disease biology based on clinical, cytogenetic, and molecular genetic variables.
-Identify patients with Acute Myeloid Leukemia likely to benefit from cytotoxic induction chemotherapy, and those unlikely to benefit from induction chemotherapy who are candidates for investigational or non-cytotoxic therapies.
-Select appropriate patients with Acute Myeloid Leukemia for referral to consider stem cell transplantation.

This lecture was presented as a part of the Medical and Surgical Oncology Lecture Series.

Naval Daver, MD, from the MD Anderson Cancer Center, Houston, TX, discusses clinical trials of immune checkpoint inhibitors in acute myeloid leukemia (AML) at the International Symposium on Acute Leukemias (ISAL) 2017 in Munich, Germany. He explains the background of this work, which was that in AML patients, high expression of a number of immune checkpoints including PD-1, OX40, and CTLA-4 was seen. A dozen different clinical trials are now assessing different combination approaches with immune checkpoint inhibitors. In AML, the focus has been on the drugs nivolumab and ipilimumab. Dr Daver describes a study of nivolumab in combination with azacitidine, which showed a higher response rate than azacitidine alone, with very durable responses seen in around 35% of patients. In addition, immune profiling at baseline and on treatment showed that patients who responded developed an increasing T-cell infiltrate with response to treatment, with T-cells displaying a favorable immune profile high in CD8 and CD4 effectors. On the other hand, patients who did not respond did not show any favorable T-cell infiltrate in the bone marrow. CTLA-4, an immune checkpoint which can be targeted with ipilimumab, was increased in almost all patients, suggesting that by combinint nivolumab with ipilimumab to block both major immune checkpoints, the response rate may be further increased from 35% to as high as 60 or 80% as has been seen in melanoma. Dr Daver speaks about the next step, which is a frontline treatment with azacitidine in combination with nivolumab, as well as a frontline treatment with the combination of azacitidine, nivolumab and ipilimumab.

0:00 Synopsis
2:45 Case Presentation
3:50 Practice Question
6:00 AUER RODS
7:45 Definition of AML
9:30 What Do Myelodysplastic & Myeloproliferative Mean?
11:30 AML Risk Factors
14:10 AML Clinical Presentation
16:40 AML Lab Studies
19:25 Tumor Lysis Syndrome
23:15 Important AML Subtypes
25:25 APL - Acute Promyelocytic Leukemia
30:15 Acute Monocytic Leukemia
31:40 Myeloid Sarcoma
33:40 Myelodysplastic Syndromes
36:15 Pseudo-Pelger-Huet
37:35 Bone Marrow Bx in MDS