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1 onsequences (accelerated atherosclerosis and second cancer).
2 p is associated with a substantive risk of a second cancer.
3 kely includes recurrences misclassified as a second cancer.
4 k of death as a result of cardiac disease or second cancer.
5 ment of de novo leukaemia or therapy-related second cancers.
6 Two of the 86 (2.3%) patients developed second cancers.
7 We have therefore examined the incidence of second cancers.
8 ociated with an increased risk of developing second cancers.
9 nd reduction in numbers of germline mutation second cancers.
10 has been accompanied by an increased risk of second cancers.
11 ure to TKIs increases the risk of developing second cancers.
12 milar risks of circulatory complications and second cancers.
13 er, substantially increase the risk of later second cancers.
14 s and a predisposition to the development of second cancers.
15 (HR, 0.90; 95% CI, 0.61 to 1.32) followed by second cancers (13.6% of deaths; HR, 1.24; 95% CI, 0.49
20 ave more than twice the risk of developing a second cancer and an increased frequency of certain canc
21 a on HL relapse, late recurrence, and excess second cancer and cardiac late-effects mortality were es
22 significantly associated with mortality from second cancers and other causes, whereas menopausal horm
24 re at high risk of potentially life-limiting second cancers and treatment-associated cardiovascular d
26 sis and pinealoblastoma, minimizes long-term second cancers, and has few systemic and no ocular toxic
27 zoxane may reduce treatment efficacy, induce second cancers, and thus compromise overall survival amo
29 he first cancer sites the RR of developing a second cancer associated with radiotherapy exceeded 1, a
30 fied either the p.His1047Leu alteration or a second cancer-associated alteration, p.His1047Arg, in ni
35 also common after HCT, including infections, second cancers, bone loss, and cardiovascular, pulmonary
36 ation, was associated with more toxicity and second cancers but a significantly longer time to diseas
39 as a significant excess risk of all types of second cancers combined (SIR, 3.40; 95% CI, 1.55-6.45),
40 survivors had a higher risk of developing a second cancer compared with an age- and sex-matched gene
44 identify the cell cycle-regulated genes in a second cancer-derived cell line and provide a comprehens
45 eservoir from which proliferative lesions or second cancers develop once additional genetic abnormali
46 ival, hematologic toxicity, ocular toxicity, second cancer development and electroretinogram response
48 f the following events: CBC diagnosis, other second cancer diagnosis, death, last tumor registry foll
49 as well as the mutually increased risks for second cancer for both organs, grain fiber and whole gra
53 nly orchiectomy, had an increased risk for a second cancer (hazard ratio [HR], 3.2; 95% CI, 1.9 to 5.
55 HCL, there was an increase in the number of second cancers; however, it did not reach statistical si
56 ed the long-term probability of developing a second cancer in a large pooled cohort of patients treat
57 incidence ratios and cumulative incidence of second cancer in HL survivors and compared the standardi
59 n chronic inflammation, atherosclerosis, and second cancer in MPNs favors early intervention at the t
63 8 to 5.4), and the cumulative incidence of a second cancer in the study cohort at 40 years was 48.5%
65 ratios of lung, breast, colorectal, and all second cancers in HL survivors with and without a site-s
69 However, recent studies of radiation-induced second cancers in the lung and breast, covering a very w
70 m diagnosis, 66 patients (4.6%) developed 80 second cancers, including skin (31%), prostate (15%), me
71 derstand the contribution of radiotherapy to second cancer induction and pursue well-coordinated effo
77 on the different causes of death, including second cancer mortality, noncancer mortality, and cause-
78 cause many acute and late complications (eg, second cancers, neurocognitive deficits, endocrine disor
83 ages (10 to 16 years), the largest number of second cancers occurred in the digestive tract (O/E = 19
89 sing data from the American Cancer Society's second Cancer Prevention Study (CPS II), a cohort study
95 king before first cancer diagnosis increases second cancer risk among cancer survivors, and elevated
102 d susceptibility, may contribute to elevated second cancer risks in colorectal cancer survivors compa
103 creasing concern regarding radiation-related second-cancer risks in long-term radiotherapy survivors
105 mong both cervical SCC survivors (n = 10,559 second cancers; SIR, 1.31; 95% CI, 1.29 to 1.34) and AC
107 Failures are due to relapse, toxicity, and second cancers such as therapy-related myeloid leukemia
109 BT had no higher probability of developing a second cancer than patients who were treated with surger
110 complex (MHC) loci, confirming that it is a second cancer that can be transmitted between devils as
111 o in the burden of "late effects," including second cancers, that compromise quality of life and limi
112 late relapse of disease, the development of second cancers, the effect of the disease and treatment
113 ge 0 are at increased risk of infections and second cancers, the risk of progression requiring treatm
114 eath has been from HD: five patients died of second cancers, two of cardiac disease, and one of alcoh
125 r Registry, the SIR for risk of all types of second cancers was similar to that in SEER 9 (SIR, 3.45;
126 With a median follow-up of 19.1 years, 1055 second cancers were diagnosed in 908 patients, resulting
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