According to the original EGIL scoring system BAL is defined when scores  are over two points for both myeloid and T- or B- lymphoid lineages. In 2008, WHO established a new and strict criteria standard for diagnosis of BAL. The presence of specific T-lymphoid antigens, cytoplasmic CD3 (cCD3), MPO and CD 19 became the most important standard for recognizing the lineage. Other B-lineage markers (CD22, CD79a, CD 10) and monocytic markers are also needed. Table 2 shows the method. Compared with the EGIL scoring system, the current  2008 WHO criteria applied less but more specific markers to define the lineage of the blasts,  and incorporated the intensity of markers expression into the diagnostic algorithm. The diagnosis of BAL is so difficult that sometimes is misdiagnosed with AML or ALL because the morphology thus the therapy would not have a good effect. Treatment
BAL is difficult to treat, most patients receive treatment based on the morphology of blasts and get AML or ALL induction chemotherapy. The induction drug for AML such as cytarabine and anthracycline, drug for ALL such as prednisolone, dexamethasone, vincristine, asparaginase or daunorubicin is common for BAL remission induction therapy. Recently, researches showed that using both myeloid and lymphoid induction therapy may be better for prognosis.Chemotherapy has strong side effects such as typhlitis, gastrointestinal distress, anemia, fatigue, hair loss, nausea and vomiting, etc. Thus, the different dose and times of chemotherapy for different individuals is important. If the patients enter fully remission, the consolidation with stem cell transplantation is highly recommended.
In less severe cases where small digits are amputated, the sensation can be described as a tingling feeling as opposed to a painful sensation. Pathophysiology
The neurological basis and mechanisms for phantom limb pain are all derived from experimental theories and observations. Little is known about the true mechanism causing phantom pains, and many theories highly overlap. Historically, phantom pains were thought to originate from neuromas located at the stump tip. Traumatic neuromas, or non-tumor nerve injuries, often arise from surgeries and result from the abnormal growth of injured nerve fibers. Although stump neuromas contribute to phantom pains, they are not the sole cause. This is because patients with congenital limb deficiency can sometimes, although rarely, experience phantom pains. This suggests that there is a central representation of the limb responsible for painful sensations. Currently, theories are based on altered neurological pathways and cortical reorganization. Peripheral mechanisms
Neuromas formed from injured nerve endings at the stump site are able to fire abnormal action potentials, and were historically thought to be the main cause of phantom limb pain. Although neuromas are able to contribute to phantom pain, pain is not completely eliminated when peripheral nerves are treated with conduction blocking agents. Physical stimulation of neuromas can increase C fiber activity, thus increasing phantom pain, but pain still persists once the neuromas have ceased firing action potentials. The peripheral nervous system is thought to have at most a modulation effect on phantom limb pain.