ライフサイエンスコーパス: benign tumor

1 specific (and may, in fact, also be found in benign tumors).

2 sion in anaplastic meningiomas compared with benign tumors.

3 ned from normal brain tissue or low grade or benign tumors.

4 ment of one of the most common kind of human benign tumors.

5 any of 65 malignant, five borderline or six benign tumors.

6 n uterine leiomyomata and a variety of other benign tumors.

7 l tumors showed LOH in contrast to only 1/25 benign tumors.

8 20 (13.6%) were classified as having unknown benign tumors.

9 ences in contrast to no or low expression in benign tumors.

10 has a role in the genesis and progression of benign tumors.

11 rodevelopmental deficits and the presence of benign tumors.

12 nonneuroendocrine origin, and 7 patients had benign tumors.

13 n the SUVmax of (18)F-FDOPA in malignant and benign tumors.

14 tion analysis helped separate malignant from benign tumors.

15 SM overestimates k(ep), particularly for the benign tumors.

16 uppression that restricts the progression of benign tumors.

17 more strongly expressed in malignant versus benign tumors.

18 imit of mean redistribution rate constant in benign tumors (0.88 minutes(-1)) and the volume of cance

19 patients (38%) had malignant tumors, 42 had benign tumors (37%), and 29 (25%) had nonneoplastic lesi

20 = .022) and abdominal pain in patients with benign tumors (45% vs 25%, respectively, P = .025).

21 as associated with a decreased risk of these benign tumors (age- and hospital-adjusted odds ratio = 0

22 The mean age at detection was 11 years for benign tumors and 14 years for malignant tumors (P = .00

23 ncogenic BRAF(V600E) elicited many more such benign tumors and did so more rapidly than KRAS(G12D).

24 is associated with the development of mostly benign tumors and focal dysplasias.

25 20 are both expressed differentially between benign tumors and invasive EOC, and between borderline/L

26 By comparison, all vascular areas in benign tumors and low-stage cancers were endothelial lin

27 s mutations have been identified in multiple benign tumors and malignant cancers.

28 in malignant tumors and the lowest uptake in benign tumors and normal mammary tissue.

29 vities were also observed in EOC compared to benign tumors and normal tissues.

30 tin than tissue samples from 6 patients with benign tumors and samples of healthy ovarian epithelium

31 hat deregulation of growth control occurs in benign tumors and that subsequent mutations not involved

32 basal craniotomy is well established in both benign tumors and vascular lesions, but has only limited

33 , 6 of 6 low malignant potential, 5 of the 6 benign tumors, and 9 of 10 normal patient samples.

34 ow malignant potential (LMP) tumors, 16 with benign tumors, and a separate validation group of 39 wom

35 opment of multiple mucocutaneous lesions and benign tumors, and enhanced cancer predisposition.

36 sion in malignant human tumors compared with benign tumors, and increased expression correlates stron

37 itical role in many diseases such as cancer, benign tumors, and macular degeneration.

38 Benign tumors are often amenable to surgical excision, w

39 These benign tumors are sensitive to inhibition by ATP-competi

40 These benign tumors are typically composed of adipose cells in

41 Ganglioneuroma (GN) is a rare benign tumor arising from the neural crest cells.

42 of bilateral acoustic schwannomas and other benign tumors associated with the central nervous system

43 l as the differentiation of malignant versus benign tumors based on absolute labeling uptake.

44 as were more often seen in malignant than in benign tumors, but the difference was not statistically

45 (n=38) to potentially reduce the referral of benign tumors by 65% without missing melanoma.

46 Laryngeal papillomas are benign tumors caused by human papillomaviruses types 6 a

47 vated in phenotypically normal or relatively benign tumor cells by experimentally increasing HA produ

48 Uterine leiomyomata are one of several benign tumors characterized by frequent chromosomal rear

49 arcinomas to oncocytomas-rare, predominantly benign tumors characterized by the accumulation of defec

50 acterized by the formation of neurofibromas, benign tumors composed mainly of Schwann cells, which ca

51 Neurofibromas are benign tumors comprised primarily of Schwann cells and f

52 ic value when used to differentiate EOC from benign tumor control samples with an area under the curv

53 ered from that in nontransgenic mice in that benign tumors converted from exophytic to endophytic pap

54 umors (e.g., neurofibrosarcomas) compared to benign tumors (cutaneous neurofibromas).

55 tiation and AP-1 activation while decreasing benign tumor development and malignant progression.

56 Hepatocellular adenomas (HCAs) are rare benign tumors divided into three main subgroups defined

57 ortalization, and metastatic spread, whereas benign tumors do not express gene products that mediate

58 carcinogenesis that lead to the formation of benign tumors, E6 primarily contributes to the late stag

59 mas, 9 follicular thyroid carcinomas, and 26 benign tumors (follicular adenomas and hyperplastic nodu

60 ominant disorder characterized by widespread benign tumor formation in a variety of organs.

61 om our laboratory and others have shown that benign tumor formation in Nf1 genetically engineered mic

62 yte responses to oncogenic ras in culture or benign tumor formation in nude mouse grafts, disruption

63 Twenty-six % of informative benign tumors (four follicular adenomas and three Hurthl

64 What restrains benign tumors from overexpressing tumor-associated prote

65 ncer but not in the VECs (or tumor cells) of benign tumors from ten patients with fibrocystic disease

66 e (83%) of six patients with premalignant or benign tumors had a premalignant condition (cryptochydis

67 None of the benign tumors had CDKN2A/p16 deletions, whereas three of

68 Loss of fak induced once benign tumors had formed inhibited malignant progression

69 l dominant disorder that is characterized by benign tumors (hamartomas and hamartias) involving multi

70 dition in which affected individuals develop benign tumors (hamartomas) in many organs.

71 ous sclerosis (TSC), in which development of benign tumors, hamartomas, occurs via a two-hit mechanis

72 eadily separates malignant from atypical and benign tumors, implicating that DNA methylation patterns

73 Uterine leiomyoma is the most common benign tumor in reproductive-age women.

74 iated with the development of hamartomas and benign tumors in a variety of tissues, including the ski

75 d prostate overexpressed HIF-1alpha, whereas benign tumors in breast and uterus did not.

76 t that in contrast to the narrow spectrum of benign tumors in human NF2 patients, Nf2 heterozygous mi

77 human cancers, we hypothesized that the more benign tumors in mice expressing E7 would be distinct fr

78 d with independently induced SCC relative to benign tumors in mouse skin.

79 d may help explain the diverse nature of the benign tumors in multiple endocrine neoplasia type 1.

80 a tumor suppressor syndrome characterized by benign tumors in multiple organs, including the brain an

81 disorder characterized by the appearance of benign tumors in multiple organs, including the heart.

82 nt disorder that leads to the development of benign tumors in multiple organs.

83 s a rare autosomal dominant disorder causing benign tumors in the brain and other vital organs.

84 fficient to cause oncogenic Ras(V12)-induced benign tumors in the developing eye to exhibit metastati

85 Parathyroid adenomas are benign tumors in the parathyroid glands, whose pathogene

86 ying (TA) cells, are unable to generate even benign tumors in the same genetic context.

87 Activation of mTOR promotes the formation of benign tumors in various organs and the mechanisms under

88 Notably, malignant, but not benign, tumors induce peripheral wasting.

89 er, despite differences in the efficiency of benign tumor induction, only mice with lung epithelium e

90 pigenetic event required for conversion of a benign tumor into a malignant one, thereby explaining wh

91 and familial schwannomatosis, with adulthood benign tumors involving cranial and peripheral nerves.

92 Detection of rare metastatic cells within a benign tumor is a key challenge to diagnose the cancerou

93 ignant tumors, but the role of stem cells in benign tumors is not well understood.

94 asma cell granulomas (pseudotumors) are rare benign, tumor-like proliferations composed chiefly of pl

95 freckles of PJS patients are actually small, benign tumors, LKB1/STK11 mutations must provide these l

96 tases (N = 42), biliary cancer (N = 20), and benign tumors (N = 176).

97 with ovarian cancer (n = 109), patients with benign tumors (n = 19), and healthy donors (n = 56) were

98 Loss of TSC2 results in benign tumors, neurological disorders, and angiomyolipom

99 y, DNA damage in Lisch nodule pathogenesis, "benign tumor of the iris," not "hamartoma," may be a bet

100 Synovial hemangioma is benign tumor of the joints and is seen relatively rare.

101 Infantile hemangiomas are the most common benign tumors of infancy and childhood with a reported i

102 Infantile hemangiomas (IHs) are common benign tumors of infancy that have the potential to inte

103 gene have frequently been detected in human benign tumors of mesenchymal origin, including lipomas.

104 ons in the cylindromatosis (CYLD) gene cause benign tumors of skin appendages, referred to as cylindr

105 Aldosterone-producing adenomas (APAs) are benign tumors of the adrenal gland that constitutively p

106 an include seizures, mental retardation, and benign tumors of the brain, skin, heart, and kidneys.

107 Benign tumors of the breast and uterus, both of which ar

108 Keloids are benign tumors of the dermis that form during a protracte

109 ed autosomal genodermatosis characterized by benign tumors of the hair follicle, has been associated

110 drome, a hamartoma disorder characterized by benign tumors of the hair follicle, lung cysts, and rena

111 Hemangiomas are one of the common primary benign tumors of the intraosseous and soft tissue compar

112 Angiomyolipomas are benign tumors of the kidney derived from putative periva

113 e urogenital system tumors, including mostly benign tumors of the ovary and uterus, and adrenal adeno

114 Neurofibromas are benign tumors of the peripheral nerve sheath, which occu

115 terized by seizures, mental retardation, and benign tumors of the skin, brain, heart, and kidneys.

116 Uterine leiomyomata, or fibroids, are benign tumors of the uterine myometrium that significant

117 Hemangiomas are benign tumors of the vascular endothelium and are the mo

118 Infantile hemangiomas are benign tumors of vascular endothelial cells (ECs), chara

119 significantly associated with female gender, benign tumor on frozen section biopsy, and postoperative

120 found in the cyst fluids of 18 patients with benign tumors or non-neoplastic cysts.

121 neoplasms but not in normal uterine tissue, benign tumors, or most low-grade neoplasms.

122 Cutaneous leiomyomas, rare benign tumors originating from the arrector pili muscle

123 ents after complete and partial resection in benign tumors other than myxomas.

124 fore carcinogen exposure strongly suppressed benign tumor (papilloma) formation, and that the few, sm

125 We now demonstrate that wounding induces benign tumors (papillomas and keratoacanthomas) in InvEE

126 on of TGF-beta signaling in MSCs governs the benign tumor phenotype in OF and highlight TGF-beta sign

127 This benign tumor rarely transforms into conjunctival melanom

128 These benign tumors represent clonal hyperproliferation of mel

129 Initially described for peripheral, benign tumors resected by nonanatomic wedge resections,

130 for ODP were PDAC (OR: 0.45, CI: 0.31-0.64), benign tumor size >5 centimeters (OR: 0.40, CI: 0.23-0.6

131 =0.0003), lipomas (SMR 5.0, P=0.0003), other benign tumors (SMR 4.63, P=0.003), and malignant tumors

132 tion of mitotic APC/C substrates not seen in benign tumors, suggesting that a "mitotic profile" in tu

133 ly increase the malignant conversion rate of benign tumors, suggesting that inhibition of apoptosis c

134 Mdm2 amplification in benign tumors suggests that it is not sufficient for p53

135 TOR signaling and consequently causes TSC, a benign tumor syndrome affecting multiple organs.

136 Tuberous sclerosis is a largely benign tumor syndrome derived from the acquisition of so

137 Our results suggest that PJS and other benign tumor syndromes could be caused by dysregulation

138 hers syndrome (PJS) are dominantly inherited benign tumor syndromes that share striking histopatholog

139 ast two evaluable section cores per case) in benign tumors than in invasive EOC, whereas there were m

140 d Harderian (lachrymal) gland hyperplasia, a benign tumor that does not progress to frank malignancy.

141 Hamartoma of the thoracic wall is a rare benign tumor that occurs in infancy and can be mistaken

142 Plexiform neurofibromas are slow growing benign tumors that are highly vascular and can progress

143 t is characterized by the growth of multiple benign tumors that are often difficult to treat.

144 iated with bilateral vestibular schwannomas, benign tumors that arise from the eighth cranial nerve.

145 on of malignant tissue and suggest that some benign tumors that become cancerous may have genetic abe

146 Uterine leiomyomas are benign tumors that can cause pain, bleeding, and inferti

147 The 2 benign tumors that did not express the VPAC1 receptor we

148 der leading to the widespread development of benign tumors that often contain giant cells.

149 Compared to the benign tumors, the atypical and malignant meningiomas de

150 ch as P27KIP1 for malignant, borderline, and benign tumors, there was a significant difference betwee

151 It takes approximately 17 years for a large benign tumor to evolve into an advanced cancer but <2 ye

152 step involved in the malignant conversion of benign tumors to frank cancer.

153 The mean latency period for benign tumors was longer than that for malignant lesions

154 In benign tumors, we defined three levels of ss-catenin act

155 Hippocampal sclerosis and benign tumors were associated with better outcomes relat

156 ent were broadly overrepresented in the more benign tumors, whereas genes involved in RNA processing

157 crocalcifications are associated mainly with benign tumors, whereas type II microcalcifications are p

158 seen with neurological processes, including benign tumors, which are treatable.

159 events involved in the pathobiology of these benign tumors will provide a basis for understanding the

160 Furthermore, RED differentiated cancers from benign tumors with an overall accuracy of 90% (27 of 30)

161 conjunctival tumors in children by comparing benign tumors with their malignant counterparts.

162 ters that best differentiated malignant from benign tumors, with a typical prolonged washout observed

163 in human neuroblastoma tumors compared with benign tumors, with loss correlating with decreased surv