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      Obesity, Thrombotic Risk, and Inflammation in Cancer.

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          Abstract

          Neoplasms exhibits a high incidence and mortality rates due to their complex and commonly overlapping clinical, biochemical, and morphologic profiles influenced by acquired or inherited molecular abnormalities, cell of origin, and level of differentiation. Obesity appears related to ~20% of cancers including endometrial, esophageal, colorectal, postmenopausal breast, prostate, and renal. Several factors other than obesity, i.e., insulin, insulin-like growth factor, sexual hormones, and adipokines may play a potential role in neoplasia. Cancer-associated hypercoagulable and thrombotic states are influenced by abnormalities in the vascular wall and susceptibility to invasion, interference in blood flow and increase in circulating tissue factor and thrombin, activation of cell growth factors, the presence of a central catheter, chemotherapies, neoplasm type, and surgery. In cancer, thromboembolic complications are the second most frequent cause of death with pulmonary thromboembolism in ~50% of cases postmortem. Thrombosis worsens prognosis as demonstrated with a survival rate as low as 12% per year vs 36% in nonthrombic patients. Deep vein thrombosis is the most frequent thromboembolic complication in cancer. It is usually detected at diagnosis and within the first 3 months of chemotherapy. The underlining mechanisms of this association should be further studied to identify patients at higher risk and develop adequate prevention, diagnostic, and treatment measures. The D-dimer test can be successfully used to assess the fibrinolytic phase of coagulation and as such is routinely used in suspected cases of deep vein thrombosis and pulmonary thromboembolism. In addition, significant advances have been made in understanding the composition and functional capabilities of the gut microbiota in the inflammatory process, obesity, and its roles in cancer; however, the intricate balance that exists within the microbiota may not only affect the host directly, it can also disrupt the entire microbial community.

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          Author and article information

          Journal
          Adv Clin Chem
          Advances in clinical chemistry
          Elsevier BV
          0065-2423
          0065-2423
          April 16 2018
          : 85
          Affiliations
          [1 ] Onco-Hematology Division, UMAE HE CMNO IMSS, Guadalajara, Jalisco, Mexico; Unidad de Investigación Biomédica 02 (UIEC), UMAE HE CMNO IMSS, Guadalajara, Jalisco, Mexico; Extension, Consulting and Research Division, Universidad de Monterrey, San Pedro Garza García, Nuevo León, Mexico.
          [2 ] Unidad de Investigación Biomédica 02 (UIEC), UMAE HE CMNO IMSS, Guadalajara, Jalisco, Mexico; Basic Sciences Division, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico.
          [3 ] Vicerrectoría Académica Escuela Ciencias de la Salud, Universidad de Monterrey, San Pedro Garza García, Nuevo León, Mexico.
          [4 ] Programa Internacional de Medicina, Universidad Autónoma de Guadalajara, Zapopan, Jalisco, Mexico.
          [5 ] Unidad de Investigación en Epidemiología Clínica, UMAE, Hospital de Pediatría CMNS-XXI, IMSS/UNAM, Mexico City, Mexico.
          [6 ] Division of Research, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.
          [7 ] Unidad de Investigación Biomédica 02 (UIEC), UMAE HE CMNO IMSS, Guadalajara, Jalisco, Mexico; Programa Internacional de Medicina, Universidad Autónoma de Guadalajara, Zapopan, Jalisco, Mexico; División de Medicina Interna, Servicio de Inmunología y Reumatología, Hospital General de Occidente, Secretaria de Salud Jalisco, Zapopan, Jalisco, Mexico. Electronic address: navazava@yahoo.com.mx.
          Article
          S0065-2423(18)30006-4
          10.1016/bs.acc.2018.02.006
          29655462
          d5a0bbe7-be8d-42ee-8ca6-3baec5783a5b
          History

          D-dimer,Obesity,Inflammation,Cancer,Prothrombotic state,Pulmonary thromboembolism

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