ライフサイエンスコーパス: amelanotic

1 melanomas, 275 (8%) were histopathologically amelanotic.

2 sence of these proteins as the tumors become amelanotic, a pigmentary change associated with ongoing

3 ID/g and 0.56 +/- 0.13 %ID/g was observed in amelanotic A375M and U87MG tumors, respectively.

4 tissues were observed (melanotic B16F10 and amelanotic A375M).

5 ants, which grow extremely aggressively, are amelanotic and have lost expression of the tyrosinase an

6 Childhood melanoma is often amelanotic and may also appear as raised or ulcerated le

7 e pattern of metabolic intermediates between amelanotic and melanotic cells.

8 Amelanotic and melanotic melanoma cells were labeled wit

9 melanoma-specific survival of histologically amelanotic and pigmented melanoma were compared using ge

10 al between patients with histopathologically amelanotic and those with pigmented melanoma in a large

11 Melanotic PC1A and amelanotic B16 melanoma cells were incubated with increa

12 Standard Amelanotic, Bleeding, Bump, Color uniformity, De novo, a

13 Amelanotic but not melanotic melanoma cells or normal me

14 transcription factor in melanocytes rendered amelanotic by E1A, basic fibroblast growth factor, or th

15 The highly metastatic amelanotic C8161 human melanoma line was found to exhibi

16 ctor, or the oncogenes ras or neu, and in an amelanotic cell variant of Cloudman S91 mouse melanoma.

17 ked through those organelles rapidly, but in amelanotic cells, TYR is retained within the ER and is e

18 ocessing in the ER, is down-regulated in the amelanotic cells; this is analogous to a hypopigmentary

19 al primary tumors, relatively lower in their amelanotic components, and still lower in all-amelanotic

20 and infant globes exhibited myofibroblasts, amelanotic, fibroblastlike cells having SM alpha-actin i

21 of melanoma characterized by the presence of amelanotic fusiform melanocytes dispersed in a prominent

22 ility to distinguish melanin-expressing from amelanotic human melanoma cells, and to specifically loc

23 Nodular melanoma occurred more frequently as amelanotic/hypomelanotic (37.3%) than did invasive non-N

24 A method for diagnosing amelanotic/hypomelanotic malignant lesions (including ba

25 gmented melanoma but a lower sensitivity for amelanotic/hypomelanotic NM (84%).

26 Lesions were separated into amelanotic/hypomelanotic or pigmented to assess outcomes

27 The LM was classified amelanotic in 10 patients, lightly pigmented in 9, and p

28 he tumor was melanotic in 37 cases (74%) and amelanotic in 13 cases (26%); of these, 13 tumors (26%)

29 Expression of msg1 was undetectable in the amelanotic K1735 murine melanoma cells.

30 o melanoma cell lines, one melanotic and one amelanotic lacking the expression of both tyrosinase pro

31 cales, which contain both mature and dormant amelanotic melanocytes.

32 ing nevus were independently associated with amelanotic melanoma (each P < .05).

33 were more likely to have had a prior primary amelanotic melanoma (OR, 4.62; 95% CI, 1.25-14.13) than

34 s, carriage of MC1R variants, and history of amelanotic melanoma are associated with histopathologica

35 tics and underlying genetics associated with amelanotic melanoma are unknown.

36 nvestigation of the biological properties of amelanotic melanoma are warranted.

37 arriage of MC1R variants was associated with amelanotic melanoma but lost statistical significance in

38 nd CAV1 is first presented here in two human amelanotic melanoma cell lines, derived from vertical gr

39 We found that, in amelanotic melanoma cell lines, tyrosinase failed to rea

40 LF inhibited PE binding to C32 amelanotic melanoma cells in a dose-dependent manner.

41 gene in pigmented melanoma cells, but not in amelanotic melanoma cells or nonmelanocytic cells, indic

42 pressing CHO cells, immobilized TSP, and C32 amelanotic melanoma cells, as well as LF itself.

43 In tyrosinase-positive amelanotic melanoma cells, inactive tyrosinase accumulat

44 to the lack of pigmentation in TYR-positive amelanotic melanoma cells.

45 fate for wild type tyrosinase also occurs in amelanotic melanoma cells.

46 ns and more careful examination for signs of amelanotic melanoma during periodic skin examination in

47 immunochemistry demonstrated the presence of amelanotic melanoma in the CNS without evidence of anoth

48 a sun-sensitive phenotypic index, and prior amelanotic melanoma increase odds for development of ame

49 udies have reported that histopathologically amelanotic melanoma is associated with poorer survival t

50 opulation level, survival after diagnosis of amelanotic melanoma is poorer than after pigmented melan

51 Identifying patients at risk of amelanotic melanoma might enable earlier diagnosis and i

52 examination in patients at increased odds of amelanotic melanoma might lead to earlier diagnosis and

53 Primary amelanotic melanoma of the CNS represents a challenge, c

54 Amelanotic melanoma was generally ofa higher American Jo

55 The association of amelanotic melanoma with presence of mitoses independent

56 ucted on mice bearing B16F10 melanoma, A375M amelanotic melanoma, and U87MG tumors, and comparative s

57 In cases of amelanotic melanoma, conjunctival amyloidosis, and prima

58 pic index were independently associated with amelanotic melanoma.

59 noma are associated with histopathologically amelanotic melanoma.

60 y outcome was diagnosis of BCC compared with amelanotic melanoma.

61 ic melanoma increase odds for development of amelanotic melanoma.

62 Both melanotic and amelanotic melanomas (B16F10 and A375M) tested were foun

63 une cell-poor pigmented and immune cell-rich amelanotic melanomas developed simultaneously in Cdk4R24

64 e central nervous system (CNS) are uncommon; amelanotic melanomas in this region are extremely rare.

65 nicopathologic characteristics suggests that amelanotic melanomas might also grow faster than pigment

66 It is probable that amelanotic melanomas present at more advanced tumor stag

67 Interestingly, amelanotic melanomas showed morphologic and molecular fe

68 Importantly, samples from human amelanotic melanomas subjected to CARS imaging exhibited

69 notypic index) and MC1R status with incident amelanotic melanomas were evaluated using logistic regre

70 Further, patients with incident primary amelanotic melanomas were more likely to have had a prio

71 igmented melanoma; however, small numbers of amelanotic melanomas, selected populations, lack of cent

72 ly localized in melanocytes, skin, and human amelanotic melanomas.

73 y tumors, 5 amelanotic primary tumors, and 3 amelanotic metastases.

74 l lower in all-amelanotic primary tumors and amelanotic metastases.

75 21 melanotic nevi (67%) compared with 2 of 9 amelanotic nevi (22%).

76 nificantly (P = .02) more apparent in 7 of 9 amelanotic nevi (78%) compared with 6 of 21 melanotic ne

77 murine and human melanocytes; however, seven amelanotic or very weakly pigmented human melanoma cell

78 95% CI, 1.0-1.9) and presented more often as amelanotic (OR, 1.9; 95% CI, 1.4-2.5) and rapidly growin

79 EZH2 was also identified as regulating the amelanotic phenotype of motile cells in vivo by suppress

80 melanotic components, and still lower in all-amelanotic primary tumors and amelanotic metastases.

81 ed, there were 5 melanotic primary tumors, 5 amelanotic primary tumors, and 3 amelanotic metastases.

82 Hazard of death from melanoma was higher for amelanotic than for pigmented melanoma (hazard ratio [HR

83 survival is poorer from histopathologically amelanotic than pigmented melanoma because of more advan

84 addition of an irradiated GM-CSF-expressing, amelanotic tumor cell vaccine significantly delayed s.c.

85 ee of the proteins, except for an apparently amelanotic tumor sample in which all were expressed, but

86 uman zinc alpha-2-glycoprotein clones formed amelanotic tumors in vivo, despite their melanin product

87 levels in skin; the exceptions were some all-amelanotic tumors in which no tyrosinase transcripts wer

88 In contrast, the amelanotic tumors lacked detectable levels of one, two,

89 In the amelanotic tumors, tyrosinase was most often deficient,

90 Very few cases of amelanotic variation of primary melanoma in the CNS were

91 then established from the melanotic and the amelanotic zones of such a melanoma and were carried in

92 luded some cases with distinct melanotic and amelanotic zones, which were separately analyzed.