Gastrointestinal (GI) cancer

In a French and British cohort-nested, case-control study of childhood solid tumor survivors diagnosed before age 17 years, the risk of developing a digestive organ SN varied with therapy.[93]

In a French and British cohort-nested, case-control study of childhood solid tumor survivors diagnosed before age 17 years, the risk of developing a digestive organ SN varied with therapy.[93]

The risk of GI cancer was 9.7-fold higher than in population controls.

In a French and British cohort-nested, case-control study of childhood solid tumor survivors diagnosed before age 17 years, the risk of developing a digestive organ SN varied with therapy.[93]

The SNs most often involved the colon/rectum (42%), liver (24%), and stomach (19%).

In a French and British cohort-nested, case-control study of childhood solid tumor survivors diagnosed before age 17 years, the risk of developing a digestive organ SN varied with therapy.[93]

A strong radiation dose-response relationship was observed, with an OR of 5.2 (95% CI, 1.7–16.0) for local radiation doses between 10 Gy to 29 Gy and 9.6 (95% CI, 2.6–35.2) for doses of 30 Gy and above, compared with survivors who had not received radiation therapy.

In a French and British cohort-nested, case-control study of childhood solid tumor survivors diagnosed before age 17 years, the risk of developing a digestive organ SN varied with therapy.[93]

Chemotherapy alone and combined-modality therapy were associated with a significantly increased risk of developing a GI SN (SIR, 9.1; 95% CI, 2.3–23.6; SIR 29.0; 95% CI, 20.5–39.8, respectively).

The PanCare Childhood and Adolescent Cancer Survivor Care and Follow-Up Studies (PanCareSurFup) consortium quantified the absolute risks by radiation therapy treatment characteristics in a cohort of 69,450 5-year childhood cancer survivors in Europe. ORs were calculated from a case-control study comprising 143 subsequent colorectal cancers within the cohort of childhood cancer survivors.[92]

The PanCare Childhood and Adolescent Cancer Survivor Care and Follow-Up Studies (PanCareSurFup) consortium quantified the absolute risks by radiation therapy treatment characteristics in a cohort of 69,450 5-year childhood cancer survivors in Europe. ORs were calculated from a case-control study comprising 143 subsequent colorectal cancers within the cohort of childhood cancer survivors.[92]

Survivors treated with any abdominopelvic radiation therapy were three times more likely to develop a subsequent colorectal cancer than those who did not receive radiation therapy (OR, 3.1; 95% CI, 1.4–6.6).

The PanCare Childhood and Adolescent Cancer Survivor Care and Follow-Up Studies (PanCareSurFup) consortium quantified the absolute risks by radiation therapy treatment characteristics in a cohort of 69,450 5-year childhood cancer survivors in Europe. ORs were calculated from a case-control study comprising 143 subsequent colorectal cancers within the cohort of childhood cancer survivors.[92]

By age 40 years, survivors who were treated with abdominopelvic radiation therapy already have a similar risk of colorectal cancer as individuals aged 50 years in the general population when population-based colorectal cancer screening begins.

The PanCare Childhood and Adolescent Cancer Survivor Care and Follow-Up Studies (PanCareSurFup) consortium quantified the absolute risks by radiation therapy treatment characteristics in a cohort of 69,450 5-year childhood cancer survivors in Europe. ORs were calculated from a case-control study comprising 143 subsequent colorectal cancers within the cohort of childhood cancer survivors.[92]

The risk of colorectal cancer increases with abdominopelvic radiation therapy dose. Survivors treated with spinal or whole-abdomen radiation therapy are at higher risk than those treated with radiation to other abdominopelvic fields.

CCSS investigators reported a 4.6-fold higher risk of GI SNs among their study participants than in the general population (95% CI, 3.4–6.1).[90]

CCSS investigators reported a 4.6-fold higher risk of GI SNs among their study participants than in the general population (95% CI, 3.4–6.1).[90]

The SNs most often involved the colon (39%), rectum/anus (16%), liver (18%), and stomach (13%).

CCSS investigators reported a 4.6-fold higher risk of GI SNs among their study participants than in the general population (95% CI, 3.4–6.1).[90]

The SIR for colorectal cancer was 4.2 (CI, 2.8–6.3).

CCSS investigators reported a 4.6-fold higher risk of GI SNs among their study participants than in the general population (95% CI, 3.4–6.1).[90]

The most prevalent GI SN histology was adenocarcinoma (56%).

CCSS investigators reported a 4.6-fold higher risk of GI SNs among their study participants than in the general population (95% CI, 3.4–6.1).[90]

The highest risk of GI SNs was associated with abdominal irradiation (SIR, 11.2; CI, 7.6–16.4), but survivors not exposed to radiation also had a significantly increased risk (SIR, 2.4; CI, 1.4–3.9).

CCSS investigators reported a 4.6-fold higher risk of GI SNs among their study participants than in the general population (95% CI, 3.4–6.1).[90]

High-dose procarbazine (RR, 3.2; CI, 1.1–9.4) and platinum drugs (RR, 7.6; CI, 2.3–25.5) independently increased the risk of GI SNs.

St. Jude Children's Research Hospital investigators observed that the SIR for subsequent colorectal carcinoma was 10.9 (95% CI, 6.6–17.0) compared with U.S. population controls. Investigators also observed the following:[91]

St. Jude Children's Research Hospital investigators observed that the SIR for subsequent colorectal carcinoma was 10.9 (95% CI, 6.6–17.0) compared with U.S. population controls. Investigators also observed the following:[91]

Incidence of a subsequent colorectal carcinoma increased steeply with advancing attained age, with a 40-year cumulative incidence of 1.4% ± 0.53% among the entire cohort (N = 13,048) and 2.3% ± 0.83% for 5-year survivors.

St. Jude Children's Research Hospital investigators observed that the SIR for subsequent colorectal carcinoma was 10.9 (95% CI, 6.6–17.0) compared with U.S. population controls. Investigators also observed the following:[91]

Colorectal carcinoma risk increased by 70% with each 10 Gy increase in radiation dose. Increasing radiation volume also increased the risk.

St. Jude Children's Research Hospital investigators observed that the SIR for subsequent colorectal carcinoma was 10.9 (95% CI, 6.6–17.0) compared with U.S. population controls. Investigators also observed the following:[91]

Treatment with alkylating agent chemotherapy was also associated with an 8.8-fold excess risk of subsequent colorectal carcinoma.

A multi-institutional prospective study observed that potentially precancerous neoplastic polyps were found in 27.8% of childhood cancer survivors who received radiation to the abdomen/pelvis at least 10 years earlier and who had colonoscopic screening between age 35 and 49 years.[94]

A multi-institutional prospective study observed that potentially precancerous neoplastic polyps were found in 27.8% of childhood cancer survivors who received radiation to the abdomen/pelvis at least 10 years earlier and who had colonoscopic screening between age 35 and 49 years.[94]

This polyp prevalence is at least as high as that previously reported for the average-risk population older than 50 years and is similar to the 24% incidence rate for patients with hereditary nonpolyposis colon cancer. Polyp prevalence rates in the general population for people aged 35 to 49 years are unclear.

A DCOG-LATER record linkage study evaluated the risk of histologically confirmed colorectal adenomas among 5,843 5-year childhood cancer survivors followed for a median of 24.9 years.[95]

A DCOG-LATER record linkage study evaluated the risk of histologically confirmed colorectal adenomas among 5,843 5-year childhood cancer survivors followed for a median of 24.9 years.[95]

The cumulative incidence of colorectal adenoma by age 45 years was 3.6% among survivors who received abdominal pelvic radiation versus 2.0% for survivors who did not receive abdominal pelvic radiation, versus 1.0% among siblings.

A DCOG-LATER record linkage study evaluated the risk of histologically confirmed colorectal adenomas among 5,843 5-year childhood cancer survivors followed for a median of 24.9 years.[95]

Factors associated with adenoma risk were abdominal pelvic radiation (HR, 2.1), TBI (HR, 10.6), cisplatin (HR, 2.1 for <480 mg/m2; HR, 3.8 for ≥480 mg/m2), diagnosis of hepatoblastoma (HR, 27.1), and family history of early-onset colorectal cancer (HR, 20.5).

A DCOG-LATER record linkage study evaluated the risk of histologically confirmed colorectal adenomas among 5,843 5-year childhood cancer survivors followed for a median of 24.9 years.[95]

Procarbazine exposure was also associated with an increased risk among survivors not exposed to abdominal pelvic radiation or TBI (HR, 2.7).

The PanCareSurFup consortium reported on digestive cancers in a cohort of 69,460 5-year childhood cancer survivors in Europe.[96]

The PanCareSurFup consortium reported on digestive cancers in a cohort of 69,460 5-year childhood cancer survivors in Europe.[96]

Survivors of Wilms tumor (SIR, 12.1; 95% CI, 9.6–15.1) and Hodgkin lymphoma (SIR, 7.3; 95% CI, 5.9–9.0) were at the highest risk for GI SMNs.

The PanCareSurFup consortium reported on digestive cancers in a cohort of 69,460 5-year childhood cancer survivors in Europe.[96]

By age 55 years, 2.3% of survivors of Wilms tumor and Hodgkin lymphoma developed a secondary colorectal cancer, a rate that is comparable to that of the general population with two or more first-degree relatives affected by GI cancer.

A nested case-control study examined the rate of colorectal cancer according to large bowel radiation therapy dose and procarbazine dose among 5-year Hodgkin lymphoma survivors who were diagnosed between age 15 and 50 years (only 27% of cases were 15 to 24 years old) at five hospital centers in the Netherlands (diagnosed between 1964 to 2000; median follow-up, 26 years).[97]

A nested case-control study examined the rate of colorectal cancer according to large bowel radiation therapy dose and procarbazine dose among 5-year Hodgkin lymphoma survivors who were diagnosed between age 15 and 50 years (only 27% of cases were 15 to 24 years old) at five hospital centers in the Netherlands (diagnosed between 1964 to 2000; median follow-up, 26 years).[97]

The median interval between Hodgkin lymphoma diagnosis and subsequent colorectal cancer was 25.7 years (range, 18.2–31.6 years).

A nested case-control study examined the rate of colorectal cancer according to large bowel radiation therapy dose and procarbazine dose among 5-year Hodgkin lymphoma survivors who were diagnosed between age 15 and 50 years (only 27% of cases were 15 to 24 years old) at five hospital centers in the Netherlands (diagnosed between 1964 to 2000; median follow-up, 26 years).[97]

Treatment with subdiaphragmatic radiation therapy (RR, 2.4; 95% CI, 1.4–4.1) and more than 8.4 g/m2 of procarbazine (RR, 2.5; 95% CI, 1.3–5.0) were associated with increased rates of colorectal cancer on univariable analysis.

A nested case-control study examined the rate of colorectal cancer according to large bowel radiation therapy dose and procarbazine dose among 5-year Hodgkin lymphoma survivors who were diagnosed between age 15 and 50 years (only 27% of cases were 15 to 24 years old) at five hospital centers in the Netherlands (diagnosed between 1964 to 2000; median follow-up, 26 years).[97]

Colorectal cancer rate increased linearly with mean radiation therapy dose to the whole large bowel and dose to the affected bowel segment. The dose response became steeper with higher doses of procarbazine and increased 1.2-fold (95% CI, 1.1–1.3) for each 1 g/m2 increase in procarbazine.