What is the defect in the cell cycle to cause leukemia?

What is the defect in the cell cycle to cause leukemia?
please in detail and provide the references
also, do you know where i can get information about this in detail
thank you

- Spreedog
There is not just one or "the" defect. There are dozens of different defects that lead to leukemias.
Which leukemia are you asking about? There are dozens of types of leukemia.
Four main general categories :
Acute lymphocytic leukemia (ALL)
Acute myeloid (myelogenous) leukemia (AML)
Chronic lymphocytic leukemia (CLL)
Chronic myelogenous leukemia (CML)

Leukemia subtypes:
Lymphoid leukemia
Acute lymphoblastic leukemia
Chronic lymphocytic leukemia
Subacute lymphocytic leukemia
Prolymphocytic leukemia
Hairy-cell leukemia
Leukemic reticuloendotheliosis
Adult T-cell leukemia
Other lymphoid leukemia
Lymphoid leukemia , unspecified
Myeloid leukemia
Acute myeloid leukemia
Chronic myeloid leukemia
Subacute myeloid leukemia
Acute promyelocytic leukemia
Acute myelomonocytic leukemia
Other myeloid leukemia unspecified
Monocytic leukemia
Acute monocytic leukemia
Chronic monocytic leukemia
Subacute monocytic leukemia
Other monocytic leukemia unspecified
Other leukemias of specified cell type
Acute erythraemia and erythroleukemia
Acute erythraemic myelosis
Di Guglielmo's disease
Chronic erythraemia
Heilmeyer-Schöner disease
Acute megakaryoblastic leukemia
Mast cell leukemia
Acute panmyelosis
Acute myelofibrosis
Lymphosarcoma cell leukemia

Here is the detailed cytogenetic information for the 7 types of AML.
http://atlasgeneticsoncology.org/Anomalies/ClassifAMLID1238.html
You can see there are many different chromosomal translocations leading to various genetic defects which cause different mitotic cell cycle abnormalities.

There are at least five subtypes of ALL with many different cytogenetic aberrations.
Acute lymphoblastic leukemias
Cytogenetic subtypes:
t(12;21)(p12,q22) TEL/AML-1
t(1;19)(q23;p13) PBX/E2A
t(9;22)(q34;q11) ABL/BCR
T(V,11)(V;q23) V/MLL

There is nothing simple about the many different diseases lumped together under the very general term "leukemia." The best way to check for the cytogenetic abnormalities is to look up the specific leukemic type you are asking about.

Added note - Oh, you want to know about CML
Wiki's bit on the Philadelphia Chromosome is quite good for this.
"The exact chromosomal defect in Philadelphia chromosome is a translocation. Parts of two chromosomes, 9 and 22, swap places. The result is that a fusion gene is created by juxtapositioning of a part of the BCR ("breakpoint cluster region") gene from chromosome 22 (region q11) to the Abl1 gene on chromosome 9 (region q34). In agreement with the International System for Human Cytogenetic Nomenclature (ISCN), this chromosomal translocation is designated as t(9;22)(q34;q11).
The result of the translocation is the BCR-Abl gene, which is located on the shorter chromosome 22. BCR-Abl is a chimeric oncogene which encodes the protein p210 or sometimes p185 ("p" stands for protein and the numbers represent the molecular weight of the protein in kDa). Because the Abl gene expresses a membrane-associated protein, a tyrosine kinase, the BCR-Abl transcript is also translated into a tyrosine kinase, adding a phosphate group to tyrosine. Although the BCR region also expresses serine/threonine kinases, the tyrosine kinase function is very relevant for drug therapy. Tyrosine kinase inhibitors (such as imatinib and sunitinib) are important drugs against a variety of cancers including CML, RCC and GISTs. P210 occurs primarily in CML, and sometimes in Ph-positive acute lymphoblastic leukemia (Ph+ALL), for which the P190 protein is more common. For pediatric Ph+ALL, the impact of this type of fusion gene on prognosis after therapy is unknown since Ph+ALL is rare and to populate statistically relevant studies is difficult.
The fused BCR-Abl protein interacts with the interleukin-3 receptor beta(c) subunit. The BCR-Abl transcript is constitutively active, i.e. it does not require activation by other cellular messaging proteins. In turn, BCR-Abl activates a number of cell cycle-controlling proteins and enzymes, speeding up cell division. Moreover, it inhibits DNA repair, causing genomic instability and potentially causing the feared blast crisis in CML."

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