#NephMadness #OncoRegion #Bracket Cancer in Tx Patients Studies Abstracts

JAMA. 2011 Nov 2;306(17):1891-901. doi: 10.1001/jama.2011.1592.
Spectrum of cancer risk among US solid organ transplant recipients.

Engels EA(1), Pfeiffer RM, Fraumeni JF Jr, Kasiske BL, Israni AK, Snyder JJ,
Wolfe RA, Goodrich NP, Bayakly AR, Clarke CA, Copeland G, Finch JL, Fleissner ML,
Goodman MT, Kahn A, Koch L, Lynch CF, Madeleine MM, Pawlish K, Rao C, Williams
MA, Castenson D, Curry M, Parsons R, Fant G, Lin M.

Author information:
(1)National Cancer Institute, 6120 Executive Blvd, EPS 7076, Rockville, MD 20892,
USA. engelse@exchange.nih.gov

Comment in
    JAMA. 2012 Feb 15;307(7):663; author reply 663-4.

CONTEXT: Solid organ transplant recipients have elevated cancer risk due to
immunosuppression and oncogenic viral infections. Because most prior research has
concerned kidney recipients, large studies that include recipients of differing
organs can inform cancer etiology.
OBJECTIVE: To describe the overall pattern of cancer following solid organ
transplantation.
DESIGN, SETTING, AND PARTICIPANTS: Cohort study using linked data on solid organ
transplant recipients from the US Scientific Registry of Transplant Recipients
(1987-2008) and 13 state and regional cancer registries.
MAIN OUTCOME MEASURES: Standardized incidence ratios (SIRs) and excess absolute
risks (EARs) assessing relative and absolute cancer risk in transplant recipients
compared with the general population.
RESULTS: The registry linkages yielded data on 175,732 solid organ transplants
(58.4% for kidney, 21.6% for liver, 10.0% for heart, and 4.0% for lung). The
overall cancer risk was elevated with 10,656 cases and an incidence of 1375 per
100,000 person-years (SIR, 2.10 [95% CI, 2.06-2.14]; EAR, 719.3 [95% CI,
693.3-745.6] per 100,000 person-years). Risk was increased for 32 different
malignancies, some related to known infections (eg, anal cancer, Kaposi sarcoma)
and others unrelated (eg, melanoma, thyroid and lip cancers). The most common
malignancies with elevated risk were non-Hodgkin lymphoma (n = 1504; incidence:
194.0 per 100,000 person-years; SIR, 7.54 [95% CI, 7.17-7.93]; EAR, 168.3 [95%
CI, 158.6-178.4] per 100,000 person-years) and cancers of the lung (n = 1344;
incidence: 173.4 per 100,000 person-years; SIR, 1.97 [95% CI, 1.86-2.08]; EAR,
85.3 [95% CI, 76.2-94.8] per 100,000 person-years), liver (n = 930; incidence:
120.0 per 100,000 person-years; SIR, 11.56 [95% CI, 10.83-12.33]; EAR, 109.6 [95%
CI, 102.0-117.6] per 100,000 person-years), and kidney (n = 752; incidence: 97.0
per 100,000 person-years; SIR, 4.65 [95% CI, 4.32-4.99]; EAR, 76.1 [95% CI,
69.3-83.3] per 100,000 person-years). Lung cancer risk was most elevated in lung
recipients (SIR, 6.13 [95% CI, 5.18-7.21]) but also increased among other
recipients (kidney: SIR, 1.46 [95% CI, 1.34-1.59]; liver: SIR, 1.95 [95% CI,
1.74-2.19]; and heart: SIR, 2.67 [95% CI, 2.40-2.95]). Liver cancer risk was
elevated only among liver recipients (SIR, 43.83 [95% CI, 40.90-46.91]), who
manifested exceptional risk in the first 6 months (SIR, 508.97 [95% CI,
474.16-545.66]) and a 2-fold excess risk for 10 to 15 years thereafter (SIR, 2.22
[95% CI, 1.57-3.04]). Among kidney recipients, kidney cancer risk was elevated
(SIR, 6.66 [95% CI, 6.12-7.23]) and bimodal in onset time. Kidney cancer risk
also was increased in liver recipients (SIR, 1.80 [95% CI, 1.40-2.29]) and heart
recipients (SIR, 2.90 [95% CI, 2.32-3.59]).
CONCLUSION: Compared with the general population, recipients of a kidney, liver,
heart, or lung transplant have an increased risk for diverse infection-related
and unrelated cancers.

PMCID: PMC3310893
PMID: 22045767  [PubMed - indexed for MEDLINE]


Nat Immunol. 2002 Nov;3(11):991-8.
Cancer immunoediting: from immunosurveillance to tumor escape.

Dunn GP(1), Bruce AT, Ikeda H, Old LJ, Schreiber RD.

Author information:
(1)Department of Pathology and Immunology, Center for Immunology, Washington
University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA.

Comment in
    Nat Immunol. 2003 Mar;4(3):201.
    Lancet Oncol. 2004 Jul;5(7):397-8.
    Nat Immunol. 2004 Jan;5(1):3-4; author reply 4-5.

The concept that the immune system can recognize and destroy nascent transformed
cells was originally embodied in the cancer immunosurveillance hypothesis of
Burnet and Thomas. This hypothesis was abandoned shortly afterwards because of
the absence of strong experimental evidence supporting the concept. New data,
however, clearly show the existence of cancer immunosurveillance and also
indicate that it may function as a component of a more general process of cancer
immunoediting. This process is responsible for both eliminating tumors and
sculpting the immunogenic phenotypes of tumors that eventually form in
immunocompetent hosts. In this review, we will summarize the historical and
experimental basis of cancer immunoediting and discuss its dual roles in
promoting host protection against cancer and facilitating tumor escape from
immune destruction.

PMID: 12407406  [PubMed - indexed for MEDLINE]