Acute Leukalmias – Bone Marrow Structure in Acute Leukalmias

Acute Leukalmias  – Bone Marrow Structure in Acute Leukalmias

Acute leukaemias generally pursue an aggressive clnical  course which, unless modified by treatment which rapidly result in death in so many patients. The dominant cells is usually an immature blast cell. acute leukaemias are classified into two categories namely,

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{a} acute myeloid leukaemia {AML} or non-lymphoblastic leukaemia {ANLL}

{b} acute lymphoblastic leukaemia {ALL} the above classification which has achieved a high degree of acceptance and is based one blood and bone marrow morphological features defined by romansky and cytochemical staining.

{A} Bone Marrow Structure On Acute Myeloid Leukaemias {AML} Acute myeloid leukalmia {AML} also known as acute myelogenous leukaemia is a cancer of the myeloid line of blood cells, characterized by the rapid growth of abnormal white blood cells that accumulate in the bone marrow and interfere with the production of the normal cells. AML is the most common acute leukaemia affecting adults, and its incidence increases with age.

  • The symptoms of AML are caused by replacement of normal cells, which causes a drop in red blood cells platelets and normal which blood cells.

The symptoms include fatigue, shortness of breath, easy brushing and bleaching and increased risk of infection.

 Clinicial Conditions

Myelodysplastic Symdrome {MDS} formerly known as preleukaemia are a diverse collection of hacmstological condition that involve ineffective production of the myeloid class of blood cells. Patient with MDS often develop severe anaemia and require frequent blood transfusions. In most cases, the disease worsens and the patient develops cytopenias  {low blood counts} due to progressive bone marrows failure


Acute myeloid leukaemia {AML} or acute non-lymphoblastic leukaemia {ANLL} are classified into seven {7) sub types which are donated as M1 M2 M3 M4 M5 M6 M7 respectively.

M1: myeloblastic  leukaemia  with out maturation.

Features:  myelobastic   with non granular  cytoplasm  or rare azurophil granules;

  • More mature myeloid cells not present;
  • Some blast cells myelopexroxidase positive

M2: myeloblastic leukaemia with maturation.

Features:  prmyelocytes and more mature myeloid cells in addition to myeloblasts, Myeloid cells myeloperoxidase positive.

M3: Hypergranular promyelocytic leukaemia

Features:  most cells are mycloperoxidase- positive promyelocytes with heavy cytoplasmic  granulation and reniform nuclei,

v Multiple Auer rods,

v Often in parallel bundles (faggots)

v Also are hypogranular  type.

M4: myelomonocytic leukaemia

Features:  immature andmature cells of myecoid are myeloperoxidase positive;

v Monocytic (non-specific esterase positive) Lineage.

M5:  monocytic leukaemia

Feature: poorly differentiated type (M5a): non-specific esterase-positive monoblasts with non-granular cytoplasm or rare azurophil granules/Auer rods.

v Differentiatyed type (M5b): promocytes and monocytes in addition to monoblasts.

M6: Erythroleukaemia

v Erythroblasts > 50 percent of marrow nucleated cells;

v Mryeloblasts and promyelocytes increased.

v Erythroblasts often strongly periodic Acid-schiff stain positive and posses morphological abnormalities.

M7: megakaryoblastic   leukaemia

Features: megakaryoblasts, some with

v Cytoplasmic budding

v Positive platelet pixilated reaction on election microscopy and reactivity to monoclonal antibodies specific for platelet-specific surface antigens.


Bone Marrow Structure in Actute Lymphoblastic Leukaemia (ALL)

Acute lymphoblastis leukaemia (ALL)  are classified into three subgroups and are donated as follows:-L1, L2, L3 respectively.

L1: Homogeneous small Lymphoblasts

Features:  scanty cytoplasm;

v Regular round nuclei;

v Inconspicuous nucleoli .

L2: Heterogeneous lymphoblasts

Features: variable amounts of cytoplasm;

v Irregular or cleft nuclei,

v Large nucleoli.

L3:  Large homogeneous Lymphoblasts

Features: basophilic  cytoplasm,

v Round nuclei;

v Prominent nucleoli

v Cytoplasmic vacuolation


Morphology: The aspirated marrow fragments in acute Lenkaemia are characteristically numerous are fleshy.

However.  because of  hyper cellulanty  or  associated fibrosis in the marrow, a ‘blood tap’ is not uncommon and occasionally a dry tap ‘ occurs.


Chromosomes: Examination of bone marrow chromosomes reveals abnormalities in up to 75 per cent cases,  and it has been postulated that improvements in technique which result in greater resolution of chromosomes five structure will enable an even higher proportion of chronic  bone abnormalities  to  be detected in acute leukaemia.


Bone Marrow Structure or Chronic Leukaemins

Chronic leukaemias   are divided basically into lymphoid and myeloid categories, and tend to be more indolent in behavour.


Morphology: the characteristic cell in chronic lymphocyte leukaemia is the mature lymphocyte and in chronic granulocyte leukaemia and the myelocyte.


Bone Marrow Structure in Chronic Lymphocytic Leukaemia (CLL)

Chronic lymphoid leukaemia also known as B-cell  chronic lymphocytic  leukaemia (B-Cell), is the most common type of leukaemia.

Leukaemias are cancers of the white blood cells. CLL effects B cell   lymphocytes. Cell effects B cell lymphocytes. B cells originate in the bone marrow, develop in the lymph nodes, and normally fight  infection by producing antibodies. In CLL, the DNA of a B-cell is damaged, so that it cannot produce.

Additionally, B-cells grow out of control and  accumulate in the bone marrow and blood, where they crowd out healthy blood cells.

Most people are diagnosed without symptoms as the result of a  routine blood test that returns a high white blood cell count but as it advances,  CLL results  in swollen  Lymph nodes, spleen, and liver and eventually anemia and infection.

The disease  is easily diagnosed. CLL is usually first suspected by the presence of a Lymphocytosis. Most often the Lymphocyte count is greater than 4000 cells per microliter (ul) of blood, but can be much higher.

The   diagnosis of CLL   is based on the demonstration of an abnormal population of B-lymphocytes in the blood bone marrow, or tissues that displays an unusual characteristic  pattern of molecules on the cell surface.

The combination of the microscopic examination of the peripheral blood and analysis of the lymphocyte by flow cytomety to confirm clonality and marker molecule expression is needed to establish the diagnosis of CLL.


Morphology:  all the B cell  malignancies of the blood and  bone marrow can be differentiated from one another by the combination of cellular microscopic morphology, maker molecule expression, and specific tumor–associated gene defects.   This is accomplished by evaluation of the patients blood, bone marrow and occasionally lymph node cells.


Bone Marrow Structure In Chromic Myeloid Leukaemia  

Chromic myelogenous (or myeloid) leukaemia (CML) also  known as chromic granulocytic leukaemia (CGL) is a cancer of the while blood cells. It is a form of  leukaemia characterized by increased and unregulated growth of predominantly myeloid cells in the bone marrow and the accumulation of these cells in  blood.

CML is a colonal bone marrow stem cell disorder in which proliferation of mature granulocytes ( neutrophils, eosinophils, and basophil) and  their precursors is the main finding.

It is a type of myeloproliferative disease associated with a characteristic chromosomal translocation called the Philadelphia chromosome.

CML is now largely treated with tyrosine kinas inhibitors.


Microscopic Examination: 

CML is often suspected on the basis on the complete blood count which shows increased  granulocytes of all types, including mature myeloid cells. Basophils and eosinophils are almost  universally  increased; this feature may help differentiate CML  from a leukemoid reaction.    


Bone Marrow Structure In Multiple Myeloma

syndecan  I  is up regulated in multiple myeloima.

High levels of shed syndecan  I in a patients serum typically in correlated with poor prognosis.  many studies have shown that syndecan l  plays an important role in cancer progression, and also can be used as a cancer biomarker. For example, syndecan I expression is higher in the bone marrow patients suffering from the multiple myeloma.

In one published study the cells expressing the soluble syndecan 1 ectodomain   promoted  the growth  metastasis of B-Lymphoid tumors more extensively than cells bearing surface syndecan 1 or lacking syndecan 1 expression.

Similarly syndecan 1 expression has been linked with low differentiation in squanmous cell carcinoma of the head and neck. Syndecan 1 also has been  linked with cancer progression by mediating the effects of growth factors in the cells.



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