ライフサイエンスコーパス: OPSCC

1 s were validated in an independent set of 21 OPSCC patients.

2 -genome patterns of DNA methylation among 24 OPSCC primary tumors and 24 matched normal mucosal sampl

3 Among 240 OPSCCs, 144 (60%) were p16 positive (p16+), 115 (48%) we

4 a good surrogate for ISH+ tumor status among OPSCC, but not a good surrogate for non-OP HNSCC.

5 Among OPSCCs, p16 had high sensitivity (100%), specificity (91

6 resence of lymph node metastases in OSCC and OPSCC, was first re-evaluated and trained on 94 samples

7 HOPX protein expression in these tumours and OPSCCs.

8 nderlying the pathobiology of HPV-associated OPSCC (designated HPV(+) OPSCC) remain unclear.

9 C) could select patients with HPV-associated OPSCC for reduced radiation dose as a means of sparing l

10 favorable-risk patients with HPV-associated OPSCC.

11 -related oropharyngeal squamous cell cancer (OPSCC), leading to calls for a new staging system.

12 lated oropharyngeal squamous cell carcinoma (OPSCC) has been reported predominantly among middle-aged

13 lated oropharyngeal squamous cell carcinoma (OPSCC) has increased more than 200% in the past 20 years

14 ative oropharyngeal squamous cell carcinoma (OPSCC) has shown resistance to conventional concurrent c

15 ce of oropharyngeal squamous cell carcinoma (OPSCC) incidence has occurred throughout the developed w

16 itive oropharyngeal squamous cell carcinoma (OPSCC) is disproportionately high among men, yet empiric

17 nt of oropharyngeal squamous cell carcinoma (OPSCC) is evolving toward risk-based modification of the

18 iated oropharyngeal squamous cell carcinoma (OPSCC) is treatment-responsive.

19 itive oropharyngeal squamous cell carcinoma (OPSCC) represents an emerging disease that differs from

20 HPV+ oropharyngeal squamous cell carcinoma (OPSCC) samples to identify differentially methylated reg

21 py in oropharyngeal squamous cell carcinoma (OPSCC) that was determined to be relevant to the America

22 rozen oropharyngeal squamous cell carcinoma (OPSCC) tissues and normal mucosa samples using microarra

23 er in oropharyngeal squamous cell carcinoma (OPSCC), its prevalence and significance have not been we

24 or in oropharyngeal squamous cell carcinoma (OPSCC).

25 with oropharyngeal squamous cell carcinoma (OPSCC).

26 Oropharyngeal squamous cell carcinomas (OPSCC) that are associated with human papilloma virus (H

27 e of oropharyngeal squamous cell carcinomas (OPSCCs) is attributable to human papillomavirus (HPV) in

28 t of oropharyngeal squamous cell carcinomas (OPSCCs), and current evidence supports these tumors as h

29 n of oropharyngeal squamous cell carcinomas (OPSCCs), particularly in white men.

30 n of oropharyngeal squamous cell carcinomas (OPSCCs), particularly in white men.

31 Comparing OPSCC and non-OPSCC, patients with p16-positive OPSCC ha

32 obal gene promoter methylation in HPV-driven OPSCCs and identifies a signature that predicts the clin

33 ommonly presenting at late stage, HPV-driven OPSCCs are associated with improved prognosis compared w

34 owever, was largely restricted to HPV-driven OPSCCs, which were associated with increased levels of t

35 d clinical behavior compared with HPV-driven OPSCCs.

36 , a weaker inverse association was found for OPSCC that were HPV(+) and p16(INK4a) high (HR = 0.55, 9

37 In this study, we analyzed 199 fresh-frozen OPSCC specimens for HPV DNA, viral load, RNA expression

38 several policy implications to guide future OPSCC prevention efforts to combat this disease.

39 y of HPV-associated OPSCC (designated HPV(+) OPSCC) remain unclear.

40 profile miRNA expression patterns in HPV(+) OPSCC to provide a more detailed understanding of pathol

41 The overall proportion of HPV(+) OPSCC between 2002 and 2011 was 51.8% [95% confidence in

42 from an initial clinical cohort of HPV(+/-) OPSCC tumors by quantitative PCR-based miRNA profiling.

43 nd Measures: The annual percentage change in OPSCC incidence from 2000 to 2012, stratified according

44 ant decrease in expression of these genes in OPSCC primary tumors relative to adjacent mucosa.

45 Objective: To update the trends in OPSCC incidence using US cancer registry data, with an e

46 changes in incidence and survival trends in OPSCC with selected tobacco-related cancers (larynx, ora

47 xpression to identify HPV16-driven tumors in OPSCC patient populations.

48 nature that predicts the clinical outcome in OPSCCs.

49 Similar results were observed for ISH+ OPSCC (P </= .01 for all).

50 with HPV16 and/or p16-positive, stage III-IV OPSCC received three cycles of IC with cisplatin, paclit

51 ), with the majority having stage T1-3N0-N2b OPSCC and a history of </= 10 pack-years of cigarette sm

52 N1-2b pathologically confirmed HPV-negative OPSCC in 2010 to 2012 were identified using the National

53 rging disease that differs from HPV-negative OPSCC in natural history and prognosis.

54 S was similar for patients with HPV-negative OPSCC when treated with primary surgery vs CRT.

55 ith newly diagnosed cT1-2 N1-2b HPV-negative OPSCC when treated with primary surgical resection vs CR

56 proportion of HPV-positive and HPV-negative OPSCC within the United Kingdom.

57 for HPV-positive OPSCC than for HPV-negative OPSCC.

58 ve non-OPSCC, but patients with p16-negative OPSCC and non-OPSCC have similar outcomes.

59 but patients with p16-negative OPSCC and non-OPSCC have similar outcomes.

60 Comparing OPSCC and non-OPSCC, patients with p16-positive OPSCC have better PFS

61 son of HPV transcript-positive OPSCC and non-OPSCC.

62 ynx, or larynx, collectively referred as non-OPSCC, where HPV infection is less common than in the or

63 velopment of a p16 IHC scoring system in non-OPSCC and improvement of HPV detection methods are warra

64 rmine whether HPV plays a causal role in non-OPSCC and to investigate whether HPV confers a survival

65 s with OPSCC, patients with p16-negative non-OPSCC have worse outcomes than patients with p16-positiv

66 is also detectable in nonoropharyngeal (non-OPSCC), but its pathogenic role and clinical significanc

67 so have a role in outcome in a subset of non-OPSCC.

68 outcomes than patients with p16-positive non-OPSCC, and HPV may also have a role in outcome in a subs

69 S and OS than patients with p16-positive non-OPSCC, but patients with p16-negative OPSCC and non-OPSC

70 Notably, however, HPV-driven non-OPSCCs display a distinct immune microenvironment and cl

71 ing lymphocytes compared with HPV-driven non-OPSCCs.

72 6 expression and high-risk HPV status in non-OPSCCs from RTOG 0129, 0234, and 0522 studies were deter

73 (15 of 103), and 6.9% (seven of 101) of non-OPSCCs from RTOG 0129, 0234, and 0522 studies, respectiv

74 HPV-driven tumors accounted for 4.1% of non-OPSCCs.

75 usal role for HPV in transcript-positive non-OPSCCs throughout the head and neck.

76 udy, patients with HPV-related nonmetastatic OPSCC were identified in the National Cancer Database be

77 ropharyngeal squamous cell carcinomas (OCSCC/OPSCC).

78 ation sites may provide biomarkers for OCSCC/OPSCC diagnosis and prognosis as well as novel avenues f

79 for study of their potential role in OCSCCs/OPSCCs.

80 ps of microbial signatures related to OCSCCs/OPSCCs.

81 f 40264 patients who received a diagnosis of OPSCC from 2000 to 2012 were included.

82 40 264 patients who received a diagnosis of OPSCC from 2000 to 2012, 13 313 (33.1%) were aged 65 yea

83 ever, over the same period, the incidence of OPSCC in the broader UK population underwent a 2-fold in

84 gue that the rapidly increasing incidence of OPSCC in the United Kingdom cannot be solely attributabl

85 Conclusions and Relevance: The incidence of OPSCC is increasing among elderly patients in the United

86 t increases in the age-adjusted incidence of OPSCC were observed during the study period for both you

87 est that HPV DNA is found in the majority of OPSCC diagnosed in patients 65 years or older.

88 ystemic therapy following primary surgery of OPSCC, induction chemotherapy in the treatment of OPSCC,

89 without systemic therapy in the treatment of OPSCC are outlined for a variety of disease stages and c

90 , induction chemotherapy in the treatment of OPSCC, and the appropriate dose, fractionation, and volu

91 definitive radiotherapy in the treatment of OPSCC, postoperative radiotherapy with and without syste

92 Although the number of OPSCCs diagnosed within the United Kingdom from 2002 to

93 During 1995 through 2012, the proportion of OPSCCs caused by HPV has increased significantly.

94 During 1995 through 2012, the proportion of OPSCCs caused by HPV has increased significantly.

95 ma of the oral cavity (OSCC) and oropharynx (OPSCC) in a large multicenter cohort, using a diagnostic

96 mours of the oral cavity (OSCC), oropharynx (OPSCC) and nasopharynx (NPC).

97 From 1995 to 2012, the proportion of p16+ OPSCC increased significantly among women (from 29% to 7

98 sequencing was performed on 46 HPV-positive OPSCC and 25 normal tissue samples.

99 Strikingly, patients with HPV-positive OPSCC are highly curable with ionizing radiation and hav

100 Because HPV-positive OPSCC patients have a better clinical outcome, there is

101 better prognosis and outcome of HPV-positive OPSCC patients would warrant imaging follow-up that is l

102 egies for elderly patients with HPV-positive OPSCC should be performed.

103 ase course during follow-up for HPV-positive OPSCC than for HPV-negative OPSCC.

104 CT imaging in the management of HPV-positive OPSCC.

105 CC and non-OPSCC, patients with p16-positive OPSCC have better PFS and OS than patients with p16-posi

106 ensive comparison of HPV transcript-positive OPSCC and non-OPSCC.

107 lation between HPV-negative and HPV-positive OPSCCs and identified a specific pattern of differential

108 Analysis of ASE in HPV-related OPSCC identified multiple alterations likely involved in

109 l objectively derived system for HPV-related OPSCC using a national database of patients primarily tr

110 images of 70 patients with advanced T-stage OPSCC who had completed concurrent chemoradiotherapy, bi

111 al staging in patients with advanced T-stage OPSCC.

112 predictor in patients with advanced T-stage OPSCC.

113 tion of molecular factors that contribute to OPSCC development, progression, and differential respons

114 ch biomarker(s) can reliably determine which OPSCC specimens are truly driven by HPV infection.

115 rom 1,602 patients previously diagnosed with OPSCC (2002-2011) were collated from 11 centers.

116 tumor status among women and nonwhites with OPSCC and patients with nonoropharyngeal head and neck s

117 tumor status among women and nonwhites with OPSCC and patients with nonoropharyngeal head and neck s

118 y validated in a cohort of 153 patients with OPSCC randomly assigned to a third trial, NRG Oncology R

119 l prediction of OS and PFS for patients with OPSCC treated with primary radiation-based therapy.

120 sed a derivation cohort of 493 patients with OPSCC with known p16 tumor status (surrogate of human pa

121 Similar to results in patients with OPSCC, patients with p16-negative non-OPSCC have worse o

122 es related to treating elderly patients with OPSCC, their limited enrollment in clinical trials, and

123 d for both younger and elderly patients with OPSCC.