| 1. |
|
|
| 2. |
- Hemminki, Kari, et al.
(författare)
-
Concordance of survival in family members with prostate cancer
- 2008
-
Ingår i: Journal of Clinical Oncology. - : American Society of Clinical Oncology. - 0732-183X .- 1527-7755. ; 26:10, s. 1705-1709
-
Tidskriftsartikel (refereegranskat)abstract
- PURPOSE: Several earlier studies have assessed survival in prostate cancer based on familial risk of this disease. As a novel concept, we posit that factors governing survival in prostate cancer are likely to be different from those governing risk of prostate cancer. To prove this, we searched for familial clustering of survival (ie, concordance of survival among family members).PATIENTS AND METHODS: We used the nationwide Swedish Family-Cancer Database to estimate hazard rates (HRs) for cause-specific and overall survival in invasive prostate cancer. HRs show the probability of death in the study group compared with the reference group. The study covered 610 sons of affected fathers with median follow-up times for survival ranging from 34 to 76 months.RESULTS: When the survival in sons was analyzed according to the fathers' length of survival, there was a concordance of prognosis; the HR was 0.62 for sons whose fathers had survived longer than 59 months, compared with sons whose fathers had survived fewer than 24 months (P for trend, .02). On a continuous scale, the sons' survival increased almost linearly with the fathers' survival time. When the analysis was reversed and HRs were derived for fathers, the concordance of good and poor survival remained.CONCLUSION: The results are consistent in showing that both good and poor survival in prostate cancer aggregate in families. Genetic factors are likely to contribute to the results, which provide the first challenging population-level evidence on heritability in prognosis of prostate cancer.
|
|
| 3. |
- Hemminki, Kari, et al.
(författare)
-
Familial Mortality and Familial Incidence in Cancer.
- 2011
-
Ingår i: Journal of Clinical Oncology. - 1527-7755. ; 29, s. 712-718
-
Tidskriftsartikel (refereegranskat)abstract
- PURPOSE An overwhelming majority of data on familial risk in cancer is based on incident cancer, whereas familiality in cancer mortality is largely unknown. If fatal form of cancer was a highly familial subtype, then familial risk for mortality may exceed that of incidence, which would be particularly relevant for clinical decision making and counseling. PATIENTS AND METHODS The individuals in the nationwide Swedish Family-Cancer Database were classified according to family history of fatal and nonfatal cancer. Familial risks of incident and fatal concordant cancer were calculated for offspring based on their parental family history using a Cox model with hazard ratio (HR); offspring without family history were the reference. Results Most HRs for offspring incident cancers were somewhat higher for fatal compared with nonfatal parental family history. For breast (HR, 1.87 fatal v 1.66 nonfatal; P < .001) and prostate (HR, 2.30 fatal v 1.84 nonfatal; P < .001) cancers, 51.0% of patients with familial breast cancer and 56.6% of patients with prostate cancer had fatal family history. HRs for death in offspring according to a fatal compared with nonfatal family history were significantly increased for colorectal (HR, 1.76 v 1.47, respectively; P = .02), breast (HR, 1.97 v 1.51, respectively; P = .002), and prostate (HR, 2.03 v 1.59, respectively; P = .002) cancers. TNM classification did not seem to differ between the family histories. We showed also that an overwhelming proportion of offspring were diagnosed after the parental death. CONCLUSION Familial breast, prostate, and colorectal cancers might have a yet unidentified genetic component associated with poorer survival. It may be useful to record survival data in family history records.
|
|
| 4. |
- Hemminki, Kari, et al.
(författare)
-
Familial risks in cancer of unknown primary: tracking the primary sites.
- 2011
-
Ingår i: Journal of Clinical Oncology. - 1527-7755. ; 29:4, s. 435-440
-
Tidskriftsartikel (refereegranskat)abstract
- PURPOSE Cancer of unknown primary (CUP) is diagnosed at the metastatic stage, and despite extensive diagnostic work-up, the primary tumor often remains unidentified. No data are available on familial clustering of CUP. We hypothesize that familial clustering of CUP with other cancers may be informative of the primary sites. PATIENTS AND METHODS A total of 35,168 patients with CUP were identified in the Swedish Family-Cancer Database, and risks between family members were calculated for concordant (CUP-CUP) and discordant (CUP-any other cancer) cancers using standardized incidence ratio (SIR). Results Familial cases of CUP accounted for 2.8% of all CUP cases in the offspring generation. Familial SIR for CUP was 1.69 when a sibling was diagnosed with CUP. As to discordant associations between siblings, CUP was associated with lung (SIR, 1.87), kidney (SIR, 1.82), liver (SIR, 1.67), ovarian (SIR, 1.45), colorectal (SIR, 1.26), and breast (SIR, 1.15) cancers and melanoma (SIR, 1.26). Upper aerodigestive tract, bladder, pancreatic, and prostate cancers were additionally associated with CUP. Notably, CUP was associated with families of kidney, lung, and colorectal cancers. CONCLUSION The present data show that CUP is not a disease of random metastatic cancers but, instead, a disease of a defined set of cancers. The association of CUP with families of kidney, lung, and colorectal cancers suggests a marked genetic basis and shared metastatic mechanisms by many cancer types. Familial sites shared by CUP generally match those arising in tissue-of-origin determinations and, hence, suggest sites of origin for CUP. Mechanistic exploration of CUP may provide insight into defense against primary tumors and the metastatic process.
|
|
| 5. |
|
|
| 6. |
- Hemminki, Kari, et al.
(författare)
-
Risk of subsequent solid tumors after non-Hodgkin's lymphoma : effect of diagnostic age and time since diagnosis.
- 2008
-
Ingår i: J Clin Oncol. - 1527-7755. ; 26:11, s. 1850-1857
-
Tidskriftsartikel (refereegranskat)abstract
- PURPOSE: Quantitative data on subsequent cancers after primary cancers provide information on treatment-related risks on second cancers, with implications for therapeutic adverse effects and human susceptibility in general. Quantitative data on solid tumors are limited. We focus on survivors of non-Hodgkin's lymphoma (NHL) because the disease is diagnosed at a wide range of ages and treated uniformly primarily with chemotherapy. PATIENTS AND METHODS: The nationwide Swedish Family-Cancer Database included 11.5 million individuals whose cancers were retrieved from the Swedish Cancer Registry. Standardized incidence ratios (SIRs) were calculated for subsequent neoplasms among 28,131 patients with NHL. RESULTS: The SIR for solid tumors after NHL was 1.65 (2,290 patients) and that for lymphohematopoietic neoplasms was 5.36 (369 patients). Among the 25 most common solid tumors, the SIRs were increased for all but nine sites; the highest SIR (40.8) was observed for spinal meningioma. The SIRs for solid tumors declined in an age-dependent manner from 4.52 in diagnostic age younger than 20 years to 1.12 in diagnostic age 70+ years. In the most common patient groups, the SIRs for solid tumors increased up to 30 years after NHL diagnosis. Because of the high incidence of solid tumors in these age groups, they contributed the largest numbers of therapy-related cases. CONCLUSION: These data indicate that age at treatment determines both the magnitude of the initial relative risk and the time-dependent modulation of the response. Therapy-related damage persists at least 30 years and its toll of solid tumors is largest 21 to 30 years after diagnosis.
|
|
