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Cytogenetic Marker May Predict Second Cancer After Hodgkin's Disease

Cytogenetic Marker May Predict Second Cancer After Hodgkin's Disease

NEW ORLEANS--A cytogenetic biomarker may be able to predict second cancers in patients with Hodgkin's disease, Sara Strom, PhD, of M.D. Anderson Cancer Center, reported at the American Society of Preventive Oncology (ASPO) annual meeting.

She presented data showing a high relative risk of second cancers (11.6) associated with high levels of sister chromatid exchanges (SCEs).

Sister chromatid exchanges are the cytological manifestation of DNA double-strand breakage and rejoining between two chromatids, Dr. Strom said.

They are possibly induced by agents that form DNA adducts or interfere with DNA replication. The association between the initial events in cell transformation and induction of DNA alterations makes SCEs a relevant indicator of carcinogenesis.

The researchers evaluated SCEs and clinical and demographic characteristics in 105 adult Hodgkin's disease patients treated from 1988 to 1992.

Sister chromatid exchanges were measured in 50 metaphases from pretreatment blood samples. Patients with a break frequency in the highest quartile were considered at high risk. Kaplan-Meier survival analysis was used to predict second cancer risk.

During the follow-up period (mean of seven years), seven second cancers occurred, including one case each of leukemia, non-Hodgkin's lymphoma, breast cancer, metastatic tongue cancer, and melanoma, and two cases of nonmela-noma skin cancer. The mean time between the primary cancer and diagnosis of the second cancer was 4.6 years.

For patients with high SCEs, there was a significant difference in the cumulative probability of developing a second cancer in the high-risk group, compared with the low-risk group.

Among all the variables analyzed, only older age at diagnosis was associated with increased risk, Dr. Strom said. Histology, stage, and treatment were not associated with elevated risk. Two other cytogenetic biomarkers that measure chromosome breaks, spontaneous and bleomycin-induced, were also evaluated, but, she said, they did not seem to be useful in identifying patients at high risk of developing secondary cancers.

"These findings suggest that an increased genetic susceptibility may explain the occurrence of second cancers in some Hodgkin's disease patients," she said.

 
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