This form of cancer originates in lymph nodes, arising when a lymphocyte becomes a malignant cell [19, 97].

HL represents approximately 30 % of all lymphomas in the United States, with an age peak between 15 and 30 years [17, 97]. It is characterized by the proliferation of giant cells, bi- or multinucleated, called Reed-Sternberg cells (RSCs) — or their variants — that characterize 1 % of cells from the lymphoma, while the rest are comprised of inflammatory cells. The RSCs are clonal B-lymphocytes, which do not produce immunoglobulin nor possess functional B-receptors. They can be classified as classical (CHL) or HL with nodular lymphocytic predominance (HLNLP). In HLNLP the predominant cell (LP cell/popcorn cell) is a variant of the RSC, the lymphocyte predominant cell (LP cell/ popcorn cell). The two classifications are differentiated by immunohistochemistry. CHL: CD15+, CD20-, CD30+, CD45-; HLNLP: CD15-, CD20+, CD30-, CD45+ [17].

Hodgkin lymphoma is one of a few neoplasms that are similar in children and adults from a biological standpoint. Children tend to evolve well, but attention must be paid to later complications such as secondary leukemia, pulmonary fibrosis, heart failure, infertility, and secondary neoplasms, features which should, therefore, limit the doses of chemotherapy and radiotherapies [17].

There are strong correlations between Epstein-Barr virus infection and HL [72, 73, 97].

The treatment in childhood usually consists of a combination of chemotherapy and low-dose radiotherapy. In this combined modality treatment, survival is achieved in up to 90 % [97].

Non-Hodgkin lymphoma is a group of diseases that comprise the Burkitt, large-cell, and lymphoblastic subtypes, as classified according to the World Health Organization system. Lymphoblastic lymphoma represents approximately 30 % of all pediatric NHL cases and the vast majority consists of advanced-stage lymphoblastic lymphoma with a precursor T-cell immunophenotype [98].

Non-Hodgkin lymphoma comprises 6 % of the total of childhood cancers, and unlike NHL in adults, childhood NHL is frequently high grade (in adults it is generally low or intermediate grade). It can be divided into three specific categories: mature B-cell (including Burkitt, Burkitt-like lymphoma, and diffuse large B-cell lymphoma); lymphoblastic lymphoma (mostly precursor T-cell); and anaplastic large-cell lymphoma (mature T-cell or null-cell). Currently, the cure rate for childhood NHL is 90 % [99].

Chronic myeloid leukemia is a malignant clonal disease characterized by the excessive proliferation of cells of myeloid lineage, which forms the chronic phase; this is followed by the progressive loss of cellular differentiation, forming the accelerated phase, finally followed by a phase of acute leukemia, which is the blastic phase [42].

Approximately 10 % of cases of this type of leukemia occur in childhood. Characterized by the expansion of hematopoietic stem cells, this is a myeloproliferative disease. CML is associated with the Philadelphia chromosome (Ph), which is the result of a translocation between the long arms of chromosomes 9q34 and 22q11, and the result of this translocation is the hybrid Bcr-abl protein, with increased tyrosine kinase activity. The Bcr-abl protein has the following possible mechanisms in the pathophysiology of CML: activation of mitogenic signaling, apoptosis reduction, and reduction of cell adhesion to the extracellular matrix. The disease is considered to be biphasic or triphasic; one phase is the idle phase (blasts amount to less than 10 %), which is chronic; the other two phases are more aggressive: accelerated (blasts from 10 to 19 %) and blastic (more than 20 % of the leukocytes in peripheral blood are blasts), which is characterized by genomic instability [17].

At present, CML is not curable with drug therapy, and allogeneic bone marrow (family related or not) transplantation is the only curative treatment, to induce molecular remission with the elimination of Bcr-abl [42].

The term AML encompasses a group of leukemias arising in the lineage of myeloid precursor cells, erythroid cells, megakaryocytes, and monocytes, and AML arises originally from the clonal transformation of hematopoietic precursors, acquiring chromosomal rearrangements and multiple gene mutations. Mutated cells have advantages in survival and proliferation; also, their differentiation and apoptosis characteristics are changed [43].

Acute myeloid leukemia is responsible for approximately 20 % of acute leukemias in children and adolescents. Most subtypes of AML are characterized by subpopulations of stem cells, like initiating cells, that have an unlimited self-renewal capacity and an organization similar to that of normal hematopoietic cells [101].

The diagnosis is based on a complete hematological count, to show pancytopenia and blast cells; confirmation is made by bone marrow examination. The diagnosis and classification of the type of AML are based on morphological analysis, cytochemical findings, cytogenetics, fluorescence in situ hybridization, immunophenotyping using flow cytometry, and molecular evidence (such as mutation analysis) [56].

In AML is variable, according to the patient, the stage of maturation arrest of granulopoiesis. The cells are the predominant cells that accumulate at some stage in granulopoiesis and provide morphological characteristics, which are used for classification. Analysis of bone marrow and peripheral blood is done with smears; if hypoplastic marrow puncture reveals material with few cells, bone marrow biopsy is needed. Classification after the bone marrow analysis is done according to the French-American-British (FAB) classification (a universal standard). In this classification created by a French-American-British group of morphologists, the diagnosis of AML is given based on the high number of erythroblasts in the bone marrow, associated with a high percentage of myeloid blasts. The FAB classification is based on morphological and cytochemical characteristics; from it the morphological, immunological, and cytogenetic (MIC) of AML classification was created [36].

The clinical manifestation of ALL is the result of direct invasion to the bone marrow, causing cytopenias, such as anemia, leukopenia, and thrombocytopenia; also there is rare extramedullary involvement, such as fever, bleeding, and pain in the bones. Children with ALL usually have non-specific symptoms reported: anemia and fatigue, as well as irritability and anorexia [26].

The mononuclear cells affected are those of lymphoid lineage; approximately 65 % of infant acute leukemias are of B cell precursors, 15 % are T cell precursors, and 20 % of infant acute leukemias are myeloid. ALL can be divided according to the stage where the arrest of cell maturation has occurred: pro-B ALL, ALL-c (common), and pre-B ALL. The divisions are due to phenotypic expressions; thus: pro-B ALL = HLA-DR+/TdT+/CD19+/cCD79+/CD10-; ALL common = HLA-DR+/TdT+/CD19+/CD10+; pre-B ALL = HLA-DR+/TdT+/CD19+/CD10+/CD20+/μ+; ALL-B = HLA-DR+/TdT-/CD19+/CD10+-/CD20+/SmIg + [18].