Associations between the Two Serum Proteins Haptoglobin and Transferrin and Leukaemia

Abstract

Haptoglobin and transferrin (TF) types were determined for 134 patients with leukaemia of the four most common types: acute lymphocytic (ALL), chronic lymphocytic (CLL), acute myelocytic (AML) and chronic myelocytic leukaemia (CML). The phenotype HPl was found to have an increased incidence in the total patient group due to an increased incidence in those with AML, ALL and CML compared with controls, but not in those with CLL. Although tests of association applied to each of the samples of the four common types of leukaemia produced no significant χ2 values, they did indicate that the relative incidence (RI) was just under 2 for the groupings of the acute forms ALL and AML, the myelocytic forms AML and CML and for the combination of ALL, AML and CML, respectively. All these associations were statistically significant (p < 0.05). Analysis of TF subtypes and leukaemia indicated a significantly increased frequency of TF C1C1 among leukaemia patients compared with controls (p < 0.005). Analysis of the samples of each of the four common types suggested that while the RI was raised in all but ALL patients, the association was significant only in AML patients (p < 0.05). However, when the two myelocytic types were combined the RI was 2.3 and the association was highly significant (p < 0.005). No such association could be detected in the lymphocytic forms.

Association between methylene tetrahydrofolate reductase and glutathione S-transferase M1 gene polymorphisms and chronic myeloid leukemia in a Brazilian population

“…Because the expression of BCR/ABL stimulates ROS production, which may contribute to increased DNA damage in CML cells (Sattler et al, 2000;Nowicki et al, 2004), the Hp polymorphism has been investigated in leukemias, and the Hp1-1 phenotype has been associated with increased risk (Nevo and Tatarsky, 1986;Mitchell et al, 1988;Campregher et al, 2004). Despite the small sample size and large confidence interval, results indicated increased CML risk for Hp1F-1S individuals of black skin color and decreased risk for the same group carrying the Hp1S-2 genotype.…”

“…It is known that the BCR/ABL expression stimulates ROS production in hematopoietic progenitor cells (Sattler et al, 2000) and studies have suggested that ROS may contribute to increased DNA damage in CML cells (Nowicki et al, 2004). Because the ability of Hp to block hemoglobin-induced oxidative stress and damage is phenotype dependent (Carter and Worwood, 2007), Hp polymorphism has been investigated in association with leukemia, and the Hp1-1 phenotype has been associated with CML, acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) (Nevo and Tatarsky, 1986;Mitchell et al, 1988). However, the frequency distributions of Hp phenotypes and alleles vary among populations worldwide (Carter and Worwood, 2007), so it is important to run further association studies with CML in different ethnic groups to better evaluate these risks.…”

Under Increased Hydrogen Peroxide conditions, the Antioxidant Effects of Pequi Oil (Caryocar brasiliense Camb.) to Decrease DNA Damage in Runners are Influenced by Sex, Age and oxidative Stress-related Genetic Polymorphisms

“…[58] It has also been investigated with leukemia, and the Hp1-1 phenotype associated with CML, acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL). [58,59] Recently, Hp polymorphism has also been suggested as a determining factor in runners' performance. [44] In our previous studies, deviation from HWE was mainly due to higher than expected frequency of Hp1F-1F and 1S-1S contrasting with lower frequency of Hp1F-1S.…”

Elevated Serum Haptoglobin is Associated with Clinical Outcome in Triple-Negative Breast Cancer Patients

“…In humans, the HP locus is polymorphic, with two codominant alleles (HP1 and HP2) that yield three distinct genotypes/phenotypes (Hp1-1, Hp2-1 and Hp2-2) (Sadrzadeh and Bozorgmehr, 2004). Elevated levels of haptoglobin have been demonstrated in lung cancer (Beckman et al, 1986), bladder cancer (Benkmann et al, 1987), leukemia (Mitchell et al, 1988), breast cancer (Awadallah and Atoum, 2004), malignant lymphoma (Epelbaum et al, 1998), urogenital tumors (Dunzendorfer et al, 1980), esophageal squamous cell carcinoma , ovarian cancer (Zhao et al, 2007) and gliomas (Kumar et al, 2010).…”