title: Status of leptin in MBCR-ABL p210 positive chronic myeloid leukemia patients before and after imatinib therapy: a conflicting scenario.
abstract: BACKGROUND
  Chronic myelogenous leukemia (CML), a myeoloproliferative disorder, is characterized by the presence of the fusion gene BCR-ABL in hematopoietic cells. Leptin, considered a link between cancer and obesity, has been reported to be actively involved in hemopoiesis and pathophysiology of CML. There are few and conflicting reports about the status of serum leptin levels and recently alteration in leptin has been reported due to imatinib mesylate.
  
  
  METHODS
  Leptin and CRP were estimated in 30 (male: 20; female: 10) newly diagnosed and confirmed MBCR- ABL p210 positive CML patients before and after 3 months of therapy by commercial enzyme linked immunosorbent assays. Leptin levels were compared with 30 (male: 20; female: 10) age matched healthy controls accounting for the differences due BMI and gender.
  
  
  RESULTS
  Leptin/BMI ratio was significantly raised in both male and female chronic phase patients as compared to controls (p < 0.001, p = 0.048) and accelerated phase patients as compared to controls (males, p < 0.001; females, p < 0.001). The normal gender difference and dependence on BMI was lost in patients. In patients, who failed to achieve hematological baseline, leptin/BMI was higher only in male patients (p = 0.012). Leptin/BMI also correlat- ed with TLC and blast percentage (TLC, R2 = 0.412, p = 0.001; Blast %, R2 = 0.408, p < 0.001). There was no correlation between leptin and CRP levels. Levels decreased significantly after complete hematological remission in both males and females (p = 0.001, p = 0.028). Levels after 3 months of imatinib therapy were significantly higher than controls in all patients not in remission (males, p < 0.001; females, p = 0.018) but only in male patients in re- mission (p = 0.002).
  
  
  CONCLUSIONS
  Leptin levels were increased in CML patients. The findings suggest a possible role of leptin in patho- genesis of CML or disease progression independent of inflammatory state or reactionary rise. Imatinib itself may increase leptin levels, and, as leptin plays an active role in the pathophysiology of CML, this conflicting scenario needs further investigation. Alterations in leptin need to be investigated cautiously accounting for confounding and differences due to BMI and gender.
authors: Piyush
authors: P
authors: Bansal
authors: Veena S
authors: VS
authors: Ghalaut
authors: Tarun K
authors: TK
authors: Sharma
authors: Pratap S
authors: PS
authors: Ghalaut
authors: Sumit
authors: S
authors: Dokwal
authors: Ragini
authors: R
authors: Ghalaut
authors: Manish
authors: M
authors: Kulshrestha
authors: Kiran
authors: K
authors: Dahiya
mesh_terms: D000328:Adult; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001549:Benzamides / Q000627:therapeutic use*; D014408:Biomarkers, Tumor / Q000097:blood*; D015992:Body Mass Index; D016022:Case-Control Studies; D015986:Confounding Factors, Epidemiologic; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D016044:Fusion Proteins, bcr-abl / Q000235:genetics*; D020022:Genetic Predisposition to Disease; D006801:Humans; D000068877:Imatinib Mesylate; D020738:Leptin / Q000097:blood*; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000097:blood* / Q000188:drug therapy* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D010879:Piperazines / Q000627:therapeutic use*; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*; D011743:Pyrimidines / Q000627:therapeutic use*; D012737:Sex Factors; D013997:Time Factors; D016896:Treatment Outcome; D015854:Up-Regulation
chemical_list: D000970:Antineoplastic Agents; C581634:BCR-ABL1 fusion protein, human; D001549:Benzamides; D014408:Biomarkers, Tumor; D020738:Leptin; D010879:Piperazines; D047428:Protein Kinase Inhibitors; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D016044:Fusion Proteins, bcr-abl