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1 onsequences (accelerated atherosclerosis and second cancer).
2 k of death as a result of cardiac disease or second cancer.
3 p is associated with a substantive risk of a second cancer.
4 second cancer, especially an obesity-related second cancer.
5 second primary cancer or an obesity-related second cancer.
6 diagnosis increases mortality and risk for a second cancer.
7 kely includes recurrences misclassified as a second cancer.
8 s and a predisposition to the development of second cancers.
9 ment of de novo leukaemia or therapy-related second cancers.
10 Two of the 86 (2.3%) patients developed second cancers.
11 We have therefore examined the incidence of second cancers.
12 cessary to reduce the risk of recurrence and second cancers.
13 has been accompanied by an increased risk of second cancers.
14 milar risks of circulatory complications and second cancers.
15 ociated with an increased risk of developing second cancers.
16 nd reduction in numbers of germline mutation second cancers.
17 ure to TKIs increases the risk of developing second cancers.
18 the development of ALL and treatment-related second cancers.
19 er, substantially increase the risk of later second cancers.
20 pse after response, death from any cause, or second cancer, 0.32; 95% CI, 0.15 to 0.66; one-sided P =
21 (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
23 ly. Seven (14%) and 6 (2%) patients reported second cancers after treatment with eBEACOPP and ABVD, r
27 weight management and increase awareness of second cancers among physicians and cancer survivors.
28 ave more than twice the risk of developing a second cancer and an increased frequency of certain canc
29 a on HL relapse, late recurrence, and excess second cancer and cardiac late-effects mortality were es
31 sted that approximately 2% of all the 64 747 second cancers and 7% of the 15 813 excess second cancer
32 significantly associated with mortality from second cancers and other causes, whereas menopausal horm
35 re at high risk of potentially life-limiting second cancers and treatment-associated cardiovascular d
37 noma, nonmelanoma skin cancer, hematological second cancer, and melanoma diagnosed concurrently or af
39 sis and pinealoblastoma, minimizes long-term second cancers, and has few systemic and no ocular toxic
40 (PFS), time to local failure, development of second cancers, and severe grade 3 or higher adverse eve
41 zoxane may reduce treatment efficacy, induce second cancers, and thus compromise overall survival amo
42 ancer; (iv) surveillance for recurrences and second cancers; and (v) cancer prevention and overall he
44 , 3 were treatment-related, and 1 was from a second cancer), as did 20 in the chemotherapy group (17
45 he first cancer sites the RR of developing a second cancer associated with radiotherapy exceeded 1, a
46 fied either the p.His1047Leu alteration or a second cancer-associated alteration, p.His1047Arg, in ni
51 also common after HCT, including infections, second cancers, bone loss, and cardiovascular, pulmonary
52 ation, was associated with more toxicity and second cancers but a significantly longer time to diseas
54 oplasm (MPN) are prone to the development of second cancers, but the factors associated with these ev
57 as a significant excess risk of all types of second cancers combined (SIR, 3.40; 95% CI, 1.55-6.45),
58 survivors had a higher risk of developing a second cancer compared with an age- and sex-matched gene
59 ere associated with earlier age at first and second cancer compared with notDNE_notLOF and DNE_notLOF
61 nt), death (competing event), diagnosis of a second cancer (competing event), emigration (censoring e
62 ciated with increased risk for infection and second cancers, contributing to morbidity and mortality
67 identify the cell cycle-regulated genes in a second cancer-derived cell line and provide a comprehens
68 eservoir from which proliferative lesions or second cancers develop once additional genetic abnormali
69 ival, hematologic toxicity, ocular toxicity, second cancer development and electroretinogram response
71 son comorbidity index, cancer treatment, and second cancer diagnosis before the start of follow-up.
72 f the following events: CBC diagnosis, other second cancer diagnosis, death, last tumor registry foll
73 iagnosis were at higher risk of developing a second cancer, especially an obesity-related second canc
74 as well as the mutually increased risks for second cancer for both organs, grain fiber and whole gra
78 nly orchiectomy, had an increased risk for a second cancer (hazard ratio [HR], 3.2; 95% CI, 1.9 to 5.
80 HCL, there was an increase in the number of second cancers; however, it did not reach statistical si
81 ere diagnosed with prostate cancer without a second cancer in 12 months from January 2011 to December
82 ed the long-term probability of developing a second cancer in a large pooled cohort of patients treat
83 incidence ratios and cumulative incidence of second cancer in HL survivors and compared the standardi
85 n chronic inflammation, atherosclerosis, and second cancer in MPNs favors early intervention at the t
89 8 to 5.4), and the cumulative incidence of a second cancer in the study cohort at 40 years was 48.5%
91 ratios of lung, breast, colorectal, and all second cancers in HL survivors with and without a site-s
93 the literature confirmed some of the common second cancers in retinoblastoma survivors but found lit
95 7 second cancers and 7% of the 15 813 excess second cancers in the cohort may be attributable to adju
97 However, recent studies of radiation-induced second cancers in the lung and breast, covering a very w
98 m diagnosis, 66 patients (4.6%) developed 80 second cancers, including skin (31%), prostate (15%), me
99 derstand the contribution of radiotherapy to second cancer induction and pursue well-coordinated effo
103 Participants were followed until death, second cancer, loss to follow-up, 10 years after diagnos
107 on the different causes of death, including second cancer mortality, noncancer mortality, and cause-
108 cause many acute and late complications (eg, second cancers, neurocognitive deficits, endocrine disor
113 ages (10 to 16 years), the largest number of second cancers occurred in the digestive tract (O/E = 19
118 No patient developed metastatic disease, second cancer, or trilateral retinoblastoma and all eyes
120 sing data from the American Cancer Society's second Cancer Prevention Study (CPS II), a cohort study
126 king before first cancer diagnosis increases second cancer risk among cancer survivors, and elevated
134 d susceptibility, may contribute to elevated second cancer risks in colorectal cancer survivors compa
135 creasing concern regarding radiation-related second-cancer risks in long-term radiotherapy survivors
137 mong both cervical SCC survivors (n = 10,559 second cancers; SIR, 1.31; 95% CI, 1.29 to 1.34) and AC
139 Failures are due to relapse, toxicity, and second cancers such as therapy-related myeloid leukemia
141 BT had no higher probability of developing a second cancer than patients who were treated with surger
142 complex (MHC) loci, confirming that it is a second cancer that can be transmitted between devils as
143 o in the burden of "late effects," including second cancers, that compromise quality of life and limi
144 late relapse of disease, the development of second cancers, the effect of the disease and treatment
145 ge 0 are at increased risk of infections and second cancers, the risk of progression requiring treatm
146 eath has been from HD: five patients died of second cancers, two of cardiac disease, and one of alcoh
159 r Registry, the SIR for risk of all types of second cancers was similar to that in SEER 9 (SIR, 3.45;
160 LFSPRO.MPC model to predict the onset of the second cancer, we obtained an AUC of 0.70 (95% CI, 0.58
161 , local recurrence-free survival and time to second cancer were both: research 96.4%, control 87.8% (
164 With a median follow-up of 19.1 years, 1055 second cancers were diagnosed in 908 patients, resulting
170 The most important cause of death was non-TC second cancer with an overall SMR of 1.53 (95% CI, 1.35
171 1.35) were at increased risk of developing a second cancer with the same aetiology, whereas having ha