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The link between obesity and renal cell carcinoma (RCC) appears to be complex and may provide insight into differing etiologies for various histologic subtypes of this cancer, according to a nested case-control study and subsequent meta-analysis.

Investigators led by Catherine L. Callahan, PhD, a postdoctoral fellow with the Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Md., first analyzed data from the Kaiser Permanente Northern California health care network. They matched 685 patients with RCC (421 clear cell, 65 papillary, 24 chromophobe, 35 other, and 140 not otherwise specified) with 4,266 unaffected control patients on age, sex, race/ethnicity, duration of network membership, and medical center of diagnosis.

Compared with normal-weight counterparts (body mass index less than 25 kg/m2), obese patients (body mass index of at least 30 kg/m2), had a significantly elevated risk of clear cell RCC (odds ratio, 1.5) and a nonsignificantly elevated risk of chromophobe RCC (2.5), but a similar risk of papillary RCC (1.0), according to results reported in Cancer Epidemiology. Associations weakened when cases were restricted to stage II or higher RCC, suggesting potential bias from incidental diagnoses related to abdominal imaging. Patients who were overweight (body mass index of 25 to 29.9 kg/m2) did not have significantly elevated risks of any subtype of RCC.

The investigators next conducted a meta-analysis, including this new study and three others. Results showed a significant link between obesity and clear cell RCC (summary relative risk, 1.8) and chromophobe RCC (2.2), but not papillary RCC (1.2). Here, however, patients who were overweight also had elevated risks of clear cell RCC (1.3) and chromophobe RCC (1.9).

“Our results provide support for the hypothesis that histologic subtypes of RCC represent distinct etiologic pathways, and that obesity is more strongly associated with risk of clear cell RCC. Additional research to elucidate the underlying biology of specific subtypes of RCC is warranted,” wrote Dr. Callahan and her coinvestigators. “More generally, our findings underscore the importance of accounting for histologic subtype in investigations of RCC etiology.”

The investigators disclosed that they had no conflicts of interest. The research was supported by the Intramural Research Program of the NIH and the National Cancer Institute.

SOURCE: Callahan CL et al. Cancer Epidemiol. 2018 Jul 18, doi: 10.1016/j.canep.2018.07.002.

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The link between obesity and renal cell carcinoma (RCC) appears to be complex and may provide insight into differing etiologies for various histologic subtypes of this cancer, according to a nested case-control study and subsequent meta-analysis.

Investigators led by Catherine L. Callahan, PhD, a postdoctoral fellow with the Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Md., first analyzed data from the Kaiser Permanente Northern California health care network. They matched 685 patients with RCC (421 clear cell, 65 papillary, 24 chromophobe, 35 other, and 140 not otherwise specified) with 4,266 unaffected control patients on age, sex, race/ethnicity, duration of network membership, and medical center of diagnosis.

Compared with normal-weight counterparts (body mass index less than 25 kg/m2), obese patients (body mass index of at least 30 kg/m2), had a significantly elevated risk of clear cell RCC (odds ratio, 1.5) and a nonsignificantly elevated risk of chromophobe RCC (2.5), but a similar risk of papillary RCC (1.0), according to results reported in Cancer Epidemiology. Associations weakened when cases were restricted to stage II or higher RCC, suggesting potential bias from incidental diagnoses related to abdominal imaging. Patients who were overweight (body mass index of 25 to 29.9 kg/m2) did not have significantly elevated risks of any subtype of RCC.

The investigators next conducted a meta-analysis, including this new study and three others. Results showed a significant link between obesity and clear cell RCC (summary relative risk, 1.8) and chromophobe RCC (2.2), but not papillary RCC (1.2). Here, however, patients who were overweight also had elevated risks of clear cell RCC (1.3) and chromophobe RCC (1.9).

“Our results provide support for the hypothesis that histologic subtypes of RCC represent distinct etiologic pathways, and that obesity is more strongly associated with risk of clear cell RCC. Additional research to elucidate the underlying biology of specific subtypes of RCC is warranted,” wrote Dr. Callahan and her coinvestigators. “More generally, our findings underscore the importance of accounting for histologic subtype in investigations of RCC etiology.”

The investigators disclosed that they had no conflicts of interest. The research was supported by the Intramural Research Program of the NIH and the National Cancer Institute.

SOURCE: Callahan CL et al. Cancer Epidemiol. 2018 Jul 18, doi: 10.1016/j.canep.2018.07.002.

The link between obesity and renal cell carcinoma (RCC) appears to be complex and may provide insight into differing etiologies for various histologic subtypes of this cancer, according to a nested case-control study and subsequent meta-analysis.

Investigators led by Catherine L. Callahan, PhD, a postdoctoral fellow with the Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Md., first analyzed data from the Kaiser Permanente Northern California health care network. They matched 685 patients with RCC (421 clear cell, 65 papillary, 24 chromophobe, 35 other, and 140 not otherwise specified) with 4,266 unaffected control patients on age, sex, race/ethnicity, duration of network membership, and medical center of diagnosis.

Compared with normal-weight counterparts (body mass index less than 25 kg/m2), obese patients (body mass index of at least 30 kg/m2), had a significantly elevated risk of clear cell RCC (odds ratio, 1.5) and a nonsignificantly elevated risk of chromophobe RCC (2.5), but a similar risk of papillary RCC (1.0), according to results reported in Cancer Epidemiology. Associations weakened when cases were restricted to stage II or higher RCC, suggesting potential bias from incidental diagnoses related to abdominal imaging. Patients who were overweight (body mass index of 25 to 29.9 kg/m2) did not have significantly elevated risks of any subtype of RCC.

The investigators next conducted a meta-analysis, including this new study and three others. Results showed a significant link between obesity and clear cell RCC (summary relative risk, 1.8) and chromophobe RCC (2.2), but not papillary RCC (1.2). Here, however, patients who were overweight also had elevated risks of clear cell RCC (1.3) and chromophobe RCC (1.9).

“Our results provide support for the hypothesis that histologic subtypes of RCC represent distinct etiologic pathways, and that obesity is more strongly associated with risk of clear cell RCC. Additional research to elucidate the underlying biology of specific subtypes of RCC is warranted,” wrote Dr. Callahan and her coinvestigators. “More generally, our findings underscore the importance of accounting for histologic subtype in investigations of RCC etiology.”

The investigators disclosed that they had no conflicts of interest. The research was supported by the Intramural Research Program of the NIH and the National Cancer Institute.

SOURCE: Callahan CL et al. Cancer Epidemiol. 2018 Jul 18, doi: 10.1016/j.canep.2018.07.002.

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Key clinical point: Obesity is a risk factor for only certain histologic subtypes of RCC.

Major finding: Obese individuals had a significantly elevated risk of clear cell RCC (odds ratio, 1.5) and a nonsignificantly elevated risk of chromophobe RCC (OR, 2.5), but a similar risk of papillary RCC (OR, 1.0).

Study details: A nested case-control study of 685 patients with RCC and 4,266 unaffected matched control patients.

Disclosures: The investigators disclosed that they had no conflicts of interest. The research was supported by the Intramural Research Program of the NIH and the National Cancer Institute.

Source: Callahan CL et al. Cancer Epidemiol. 2018 Jul 18. doi: 10.1016/j.canep.2018.07.002.

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