人乳头状瘤病毒感染与食管癌的关系

人类乳头状瘤病毒（ＨＰＶ）的感染是上皮性肿瘤发生的一个重要原因。特别是ＨＰＶ１６和ＨＰＶ１８型感染与宫颈癌的发生。但ＨＰＶ的感染与食管癌的关系仍不清楚。我们采用免疫组织化学和敏感的ＨＰＶ共同引物、ＨＰＶ１６和ＨＰＶ１８型特异性引物的ＰＣＲ方法及３２Ｐ标记特异性探针Ｓｏｕｒｈｅｒｎ杂交检测食管癌中的ＨＰＶ及其亚型。结果显示，１２７例食管鳞癌标本免疫组化方法检测，ＢＰＶ阳性者占６０．６（７７／１２７），ＨＰＶＥ６蛋白抗原阳性者占４３％（５４／１２７）。其阳性染色明确定位于鳞癌组织内，并与肿瘤的分化有着密切的关系。经β球蛋白引物扩增证实不含ＰＣＲ抑制标本共１０３例，其中ＨＰＶ共同引物ＰＣＲ扩增阳性者为３７例，占３５．９％，经型特异ＰＣＲ及Ｓｏｕｔｈｅｒｎ杂交证实其中ＨＰＶ１６阳性者２１例，占２０．４％；ＨＰＶ１８阳性者８例，占７．８％。仅一例为ＨＰＶ１６和１８均阳性。以上结果显示ＨＰＶ感染的确存在于食管癌中，并可能在食管癌发生中起一定的作用。     

尖锐湿疣组织中人乳头状瘤病毒的检测

用免疫组织化学、ＤＮＡ原位杂交和聚合酶链反应技术，检测人生殖器尖锐湿疣和女阴假性湿疣组织中人乳头状瘤病毒衣壳抗原（ＨＰＶ－Ａｇ）和病毒核酸序列（ＨＰＶ－ＤＮＡ），并观察了ＨＰＶ在尖锐湿疣组织中的分布特点与病变组织学改变的关系。结果显示尖锐湿疣中ＨＰＶ－Ａｇ阳性率为７１．４％（３５／４９）；原位杂交ＨＰＶ６／１１ＤＮＡ阳性率为９６．５％（２８／２９）；ＰＣＲ扩增后尖锐湿疣ＨＰＶ６／１１／１６／１８ＤＮＡ阳性率为１００％（５３／５３）；假性湿疣ＨＰＶ６／１１／１６／１８ＤＮＡ阳性率为２１．４％（３／１４）。观察ＨＰＶ－Ａｇ和ＨＰＶ－ＤＮＡ分布，表明ＨＰＶ增殖性感染和尖锐湿疣特异的病理改变密切相关。     

人乳头状瘤病毒不同型别与宫颈病变的相关性研究

目的探讨人乳头状瘤病毒（ＨＰＶ）不同型别与宫颈病变性质的关系。方法应用ＰＣＲ技术和原位杂交方法对６１例宫颈上皮内瘤（ＣｅｒｖｉｃａｌｉｎｔｒａｅｐｉｔｈｅｌｉａｌＮｅｏｐｌａｓｉａＣＩＮ）和１２例宫颈鳞癌（ＳＣＣ）进行ＨＰＶ６Ｂ／１１、１６、１８ＤＮＡ检测。结果ＰＣＲ检测结果显示ＨＰＶ６、１１主要分布于低度鳞状上皮内病变（６１９％）和一部分ＣＩＮⅡ中（２０％），而在ＣＩＮⅢ和ＳＣＣ中检测不到；ＨＰＶ１６、１８的检出率随ＣＩＮ级别增高而增加，在ＳＣＣ中高达８３３％。原位杂交结果显示在低度鳞状上皮内病变中，地高辛（Ｄｉｇ）标记的ＨＰＶ６Ｂ／１１、１６、１８ＤＮＡ杂交物质在核中均呈细颗粒状，为“游离型”。上述杂交阳性信号形态亦出现于ＣＩＮⅡ的所有ＨＰＶ６Ｂ／１１及部分ＨＰＶ１６、１８型感染中，而ＣＩＮⅢ和宫颈鳞癌及部分ＣＩＮⅡ中，其杂交阳性信号均为非颗粒状的“整合型”。结论低度鳞状上皮内病变是以ＨＰＶ６、１１低危型为主的多型别病毒的繁殖性感染，ＣＩＮⅢ和宫颈鳞癌为ＨＰＶ１６、１８高危型病毒的整合型感染，而在ＣＩＮⅡ中存在着ＨＰＶ６，１１和ＨＰＶ１６，１８的繁殖性感染及ＨＰＶ１６，１８的整合型感染     

人乳头瘤病毒与P 53协同致膀胱移行细胞癌关系的研究

目的 研究人类乳头瘤病毒（ＨＰＶ）６、１１、１６和１８型及Ｐ５３与膀胱移行细胞癌的关系。方法 采用聚合酶链反应（ＰＣＲ）方法检测了７５例膀胱移行细胞癌组织中ＨＰＶ的感染,免疫组化ＳＰ法检测Ｐ５３蛋白表达情况。结果 膀胱移行细胞癌组织中ＨＰＶ６、１１、１６和１８的阳性率分别为６．７％（５／７５）,５．３％（４／７５）,３３．３％（２５／７５）和６．７％（５／７５）。低危型ＨＰＶ（６或１１）阳性率为９．３％（７／７５）,高危型ＨＰＶ（１６或１８）阳性率为３４．７％（２６／７５）。同一膀胱癌组织中两种以上（包括两种）ＨＰＶ亚型感染８例,占１０．６％。ＨＰＶ６、１６和１８型之间感染阳性率在肿瘤有无转移组中差异显著（Ｐ〈０．０５）,ＨＰＶ１６、１８的阳性率在肿瘤病理分级中差异有极显著性（Ｐ〈０．０１）。ＨＰＶ ＤＮＡ型别     

应用通用引物聚合酶链反应技术检测结肠癌组织中人乳头瘤病毒DNA

应用人乳头瘤病毒（ＨＰＶ）通用引物介导的聚合酶链反应（ＰＣＲ）技术检测了１５例结肠癌石蜡包埋病理组织切片中ＨＰＶＤＮＡ，其中１０例呈阳性扩增（阳性率为６６．７％）。１２例正常结肠组织经上述ＰＣＲ检测均呈阴性反应。阳性扩增产物经核酸斑点杂交进行ＨＰＶ型别分析，ＨＰＶ１６型占４例（４０．０％），１８型１例（１０．０％），１６／１８型５例（５０．０％），未检出其他ＨＰＶ型别。表明ＨＰＶ可能对结肠癌的发生具有病原相关性。     

多重聚合酶链反应在人乳头瘤病毒检测和分型中的应用

采用多重聚合酶反庆技术，在一个反应中同时加入３对人乳头瘤病毒型特异性引物，１次可完成３个型别ＨＰＶＤＮＡ扩增。其结果显示，在有ＨＰＶ感染的样品中，ＨＰＶ１６占７２．７％，ＨＰＶ１８占１６．４％，其他型占１０．９％，从正常宫颈上皮细胞到宫颈癌变细胞，ＨＰＶ１６ＤＮＡ检出率随病变程度的加重而增加（８．８％－２２．２％－６０．％），反了宫颈癌与ＨＰＶ１６感染关系密切；在正常宫颈和良性病变宫颈上皮细胞中未     

食管鳞癌HPV感染与病毒致癌基因E6的关系

目的：探讨人乳头瘤病毒（ＨＰＶ）与食管鳞状细胞癌的关系。方法：采用多重引物多聚酶链反应（ＰＣＲ）的免疫组化技术、对１０４例食管鳞癌进行ＨＰＶ ＤＮＡ和病毒癌基因Ｅ６蛋白检测。结果：ＨＰＶ ＤＮＡ阳性者占５０．９６％（５３／１０４），其中ＨＰＶ１６型ＤＮＡ４９．０６％（２６／５３），ＨＰＶ１８型 ＤＮＡ５．６％（３／５３），ＨＰＶ６／１１ ＤＮＡ７．５％（４／５３）；两上或三个类型的混合感染占３７．     

人宫颈癌中C—myc,H—ras和HPV基因的检测和分析

收集６０例宫颈癌活检组织，对同一病例同时进行ＨＰＶ、Ｃ－ｍｙｃ，Ｈ－ｒａｓ对比研究。采用ＨＰＶ高保守序列区一对共有引物检测多型ＨＰＶ基因型的存在，发现８５％（５１／６０％的组织中存在ＰＨＶ，经限制性片段长度多态性分析，ＨＰＶ１６占７８．４３％（４０／５１），ＨＰＶ１８占２１．６５％（１１／５１）。     

宫颈癌组织中HPV16,18E6蛋白表达的观察

目的观察ＨＰＶ１６、１８早期蛋白Ｅ６在人宫颈鳞状细胞癌中的表达并评价Ｅ６单抗的应用价值。方法采用ＳＰ免疫组化染色法,检测４０例宫颈鳞状细胞癌,３０例慢性宫颈炎及３０例正常宫颈组织中ＨＰＶ１６、１８Ｅ６蛋白的表达。结果癌组中Ｅ６的阳性率为６７．５％（２７／４０）,慢性宫颈炎中为３．３％（１／３０）,正常宫颈组织中均为阴性,良、恶组ＨＰＶ１６、１８Ｅ６的阳性率差异有显著意义（Ｐ＜０．０１）。结论ＨＰＶ１６、１８感染与本地区宫颈癌病因学密切相关,Ｅ６单抗可作为预测ＨＰＶ１６、１８感染及宫颈癌早期诊断的标记之一。     

卵巢上皮性肿瘤p16抑癌基因突变与HPV感染的研究

采用聚合酶链反应－单链构象多态性分析（ＰＣＲ－ＳＳＣＰ）技术，对同一卵巢上皮性肿瘤石蜡包埋组织中ｐ１６基因（第二外显子）突变及人乳头状瘤病毒（ＨＰＶ）感染进行相关性研究。并与正常卵巢组织进行对照。结果，２８例卵巢上皮性肿瘤组织中ｐ１６基因突变１５例，突变率为５３．６％（１５／２８），其中７例伴有ＨＰＶ１６型或ＨＰＶ１８型感染，占突变率的４６．７％。在卵巢上皮性肿瘤组ＨＰＶ１６、１８ＤＮＡ阳性率为５３．６％（１５／２８），对照组ＨＰＶ１６、１８ＤＮＡ阳性率为５．６（１／１８），二者比较有显著性差异。提示：卵巢上皮性肿瘤中ｐ１６基因突变与ＨＰＶ１６、１８型感染有关。ＨＰＶ１６、１８型感染与卵巢上皮肿瘤密切相关     

Human papillomavirus infection and anal carcinoma. Retrospective analysis by in situ hybridization and the polymerase chain reaction.

To examine the association of human papillomavirus (HPV) infection with anal squamous cell carcinoma, the authors applied the highly sensitive polymerase chain reaction (PCR) and in situ hybridization (ISH) techniques to detect HPV DNA in formalin-fixed, paraffin-embedded tissues from 18 patients. The presence of HPV types 16/18 in 3 (16.7%) of 18 patients with anal carcinoma was found, using a colorimetric ISH technique for HPV types 6, 11, 16, 18, 31, 35, and 51. Results from one of these three patients were also positive for HPV 31, 35, 51 by ISH techniques. When the same series was analyzed using the PCR and consensus primers to the L1 open reading frame of the HPV genomes, the frequency of positive patients rose to 14 (77.8%) of 18. PCR analysis of the 14 lesions containing HPV DNA, using type-specific primers and probes for HPV 6, 11, 16, 18, and 33, showed that 1 contained HPV 6, 1 contained HPV 11, 4 contained HPV 16, 1 contained HPV 18, 1 contained HPV 33, 5 contained HPV of unclassified type(s), and 1 contained a mixture of three HPV types. There was concordance between typing of cases that were positive by ISH and PCR methods. These data agree with the concept that HPV, in particular type 16, is implicated in the pathogenesis of anal cancer.     

The t(14;18) and bcl-2 expression are present in a subset of primary cutaneous follicular lymphoma: association with lower grade

According to the European Organization for Research and Treatment of Cancer classification, primary cutaneous follicle center cell lymphoma is not associated with the t(14;18)(q32;q21) and only rarely expresses bcl-2 protein. To further investigate this issue, we evaluated a series of 20 patients (14 men, 6 women) with primary cutaneous follicular lymphoma (PCFL). The presenting skin lesion was located in the head and neck region in 16 of 20 patients. Most cases were grade 2 (6/20) or grade 3 (13/20), and all had a follicular architecture. Immunohistochemical analysis demonstrated bcl-2 expression in 8 cases (40%), and expression was inversely related to the grade. Of 7 grade 1 or 2 cases, 5 (71%) were positive, whereas only 3 (23%) of 13 grade 3 cases were positive for bcl-2. Clonal immunoglobulin heavy chain gene rearrangements were detected in 9 (45%) of 20 cases. In 4 (20%) of 20 cases, we identified the major breakpoint of the t(14;18) by polymerase chain reaction, 3 of which were grade 1 or 2. We conclude that bcl-2 protein expression and the t(14;18) are present in a subset of PCFL, particularly in lower grade cases.     

Sequential analysis of the thymocyte differentiation in fully allogeneic bone marrow chimera in mice. II. Further characterization of the CD4+ or CD8+ single positive thymocytes

Differentiation of CD4+8- and CD4-8+ single-positive (SP) thymocytes in fully allogeneic bone marrow chimeras were investigated using multicolor cytometric analysis. The proportion of CD3+ cells in CD4+ SP population derived from donor mice considerably increased between day 12 and 14 after bone marrow transplantation (BMT), and gradually increased thereafter. The proportion of V beta 8+ cells in the CD3+CD4+ population remained constant (around 20%) at each period, suggesting that alpha and beta chains were used as TCR. The proportion of J11d+ cells in the CD4+ SP thymocytes transiently increased from day 12 to 14 and decreased thereafter, even though almost half of CD4+ SP cells were still dull J11d+ at day 35 after BMT. When CD8+ SP populations were analyzed, the proportion of CD3+ cells was very small until day 18. Thereafter, the proportion considerably increased and reached a maximum (83.2%) at day 21. The proportion of V beta 8+ cells in the CD3+ CD8+ SP population fell within range between 20 and 30%. However, before day 18, most of the V beta 8+ cells were dull positive, while after day 21 the majority were bright V beta 8+. Further, CD8+ SP cells at day 12, 14 and 18 were largely bright J11d+. After day 21, however, the proportion of bright J11d+ cells rapidly decreased. Similar results were obtained when the sequence of appearance of CD4+ and CD8+ SP cells was compared among bright CD3+, bright V beta 8+ or J11d- mature populations. The CD4+ SP cells regularly appeared earlier than CD8+ SP cells in the mature populations. These findings indicate that a considerable heterogeneity exists within both CD4+ and CD8+ SP populations and that the differentiation process for CD4+ SP cells precedes that for CD8+ SP cells.     

Analysis of genetic alterations in primary nasopharyngeal carcinoma by comparative genomic hybridization

To identify genetic alterations associated with the development and progression of human nasopharyngeal carcinoma (NPC), 57 tumors were analyzed by comparative genomic hybridization (CGH). In 47 cases, chromosomal imbalances were found. Several recurrent chromosomal abnormalities were identified in the present study. The most frequently detected chromosomal gains involved chromosome arms 12q (24 cases, 51%), 4q (17 cases, 36%), 3q (16 cases, 34%), 1q (15 cases, 32%), and 18q (15 cases, 32%). Common regions of gain involved 12q13--q15, 4q12--q21, and 3q21--q26. High-copy-number increases of chromosomal materials were detected in four chromosomal regions, 3q21--q26.2, 4p12--q21, 8p, and 12q14--q15. The most frequently detected loss of chromosomal materials involved chromosome arms 16q (26 cases, 55%), 14q (21 cases, 45%), 1p (20 cases, 43%), 3p (20 cases, 43%), 16p (19 cases, 40%), 11q (17 cases, 36%), and 19p (16 cases, 34%). The most common regions of loss involved 14q24--qter, 1pter--p36.1, 3p22--p21.3, 11q21--qter, and the distal region of 19p. Genomic alterations detected by CGH were compared and found to be largely consistent with those identified in banding analysis and loss of heterozygosity studies. However, several previously unrecognized recurrent alterations were also identified in the present study, including gain of 4q and 18q, and loss of 16q, 14q, and 19p. In addition, gain of 1q, 8q, 18q, and loss of 9q showed a statistically significant association with advanced clinical stages (P < 0.05). Identification of recurrent sites of chromosomal gain and loss identify regions of the genome that may contain oncogenes or tumor suppressor genes, respectively, which may be involved in the tumorigenesis of NPC. Published 2000 Wiley-Liss, Inc.     

Cytogenetic abnormalities in 106 oral squamous cell carcinomas

We report karyotypic features of 106 short-term cultured oral squamous cell carcinomas (SCC), 51 new and 55 previously reported cases, with clonal chromosome aberrations. The major cytogenetic findings were as follows: simple karyotypic changes were present in 38 cases (36%) and 68 tumors (64%) displayed complex karyotypes. The most common numerical changes were +7, +8, +9, +16, +18, +20, and -4, -10, -13, -14, -18, -19, -21, -22, and -Y. Structural rearrangements frequently (43% of the breaks) affected the centromeric regions, resulting in the formation of isochromosomes and whole-arm translocations. Among the recurrent structural aberrations identified, the most common were i(1q), i(3q), i(5p), i(8q), del(16)(q22), and hsr. With the exception of chromosomal band 11q13, which was involved in 25 tumors, only centromeric or near-centromeric bands were commonly involved: 3p11 approximately q11 (59 cases), 8p11 approximately q11 (57), 1p11 approximately q11 (48), 13p11 approximately q11 (46), 5p11 approximately q11 (41), 14p11 approximately q11 (41), and 15p11 approximately q11 (37). Losses of genetic material dominated over gains. The most frequent imbalances included loss of 2q33 approximately qter, 3p, 4p, 6q, 8p, 10p, 11q, 13p, 14p, and 15p, and chromosomes 18, 21, 22, and Y, and gain of chromosomes 7 and 20, 8q, and 11q13. No major karyotypic differences could be discerned between the present series of oral SCC and a previously reported series of laryngeal SCC, indicating that common genetic pathways are involved in the initiation and progression of SCC irrespective of site of origin.     

PCR-based analysis of PD-L1 RNA expression in lung cancer: comparison with commonly used immunohistochemical assays

BackgroundPD-L1 testing is currently performed by immunohistochemistry (IHC). We questioned whether the results of PCR-based measurement of PD-L1 RNA expression correlate with IHC scores obtained by different commercial assays.Materials and methods167 consecutive non-squamous non-small cell lung carcinomas (NSCLCs) were analyzed for PD-L1 RNA expression and 22C3, SP263, and SP142 IHC scoring using recommended cut-offs. RNA expression was divided into low, moderate, and high categories.ResultsRNA and protein expression demonstrated moderate correlation as continuous variables. Using prespecified RNA cut-offs, PCR testing showed a high negative predictive value towards the IHC analysis: the share of PD-L1 protein-negative tumors among cases classified as PD-L1-low by the PCR test reached 92–99% for all three antibodies. Meanwhile, about half of cases with moderate to high PD-L1 RNA expression had IHC staining in less than 1% tumor cells as determined by 22C3 or SP263 antibodies. Among the 51 discordant cases, which had <1% tumor staining by both 22C3 and SP263 clones but high RNA level, 29 (57%) showed ≥1% positive immune cells by SP263 and/or 22C3, 14 cases (27%) had detectable IHC expression in 0.1–0.9% tumor or immune cells by SP263 and/or 22C3, and 8 (16%) were entirely negative by IHC.ConclusionSome NSCLCs demonstrate readily detectable PD-L1 expression on the level of RNA, but fall below commonly accepted cut-offs by IHC. It remains to be studied whether these discrepancies are attributed to technical or biological reasons. Clinical sensitivity of these tumors to immune therapy deserves additional investigations.     

Comparative genomic hybridization analysis of nasopharygeal carcinoma: consistent patterns of genetic aberrations and clinicopathological correlations

To define the patterns of genetic imbalances in nasopharyngeal carcinoma (NPC), we studied 30 primary NPC tumors with comparative genomic hybridization (CGH). The common sites of chromosomal gains were found in descending order of frequency in 12p11.2-p12 (36%), 12q14-q21 (33%), 2q24-q31 (23%), 1q31-qter (20%), 3q13 (20%), 1q13.3 (20%), 5q21 (17%), 6q14-q22 (13%), 7q21 (13%), 8q11.2-q23 (13%) and 18q12-qter (13%). The common sites of chromosomal loss were at 3p14-p21 (20%), 11q23-qter (20%), 16q21-qter (17%) and 14q24-qter (13%). Correlation with clinicopathologic features showed that 3p loss was associated with a significantly higher risk of death related to recurrence as compared with patients without 3p loss (50% vs. 9%, P=.029). The presence of 16q loss was associated with more advanced stage tumors (stages I & II: 6% vs. stages III & IV: 33%, P=.046). We conclude that consistent patterns of genetic imbalances can be observed in NPC. Deletion of 3p and 16q were associated with higher risk of tumor recurrence and advanced stage cancer.     

Substance P receptors in the rat spinal cord: the effect of GTP and of chronic antidepressant treatment

Substance P receptors were examined in crude synaptosomal fraction preparations of the rat spinal cord using [125I]Bolton Hunter Substance P ([125I]BHSP) which binds with an affinity of 0.043 +/- 0.015 nM. The concentration of binding sites in the dorsal and in the ventral part was 4.55 +/- 0.86 and 2.35 +/- 0.35 fmol mg-1, respectively. GTP inhibited the specific binding of [125I]BHSP in a concentration dependent manner, with 10(-3) mol l-1 GTP yielding 89-90% inhibition and 10(-5) mol l-1 GTP producing 50% inhibition. This value was similar in dorsal and ventral spinal cord. The effects on SP receptors of chronic treatment with the tricyclic antidepressant imipramine (2 x 10 mumol kg-1 day-1 p.o. 14 days) and the specific 5-HT (serotonin) uptake blockers alaproclate (2 x 20 mumol kg-1 day-1 p.o. 14 days) and zimelidine (2 x 10 mumol kg-1 day-1 p.o. 14 days) were examined in the ventral spinal cord, where SP and 5-HT coexist in the terminals of descending neurons from the raphe nucleus. Zimelidine treatment was found to cause a significant reduction in the number of substance P binding sites in the rat ventral spinal cord as compared to saline treated controls. These findings are discussed in light of the previous observation (Brodin et al. 1984) that SP levels are significantly elevated after treatment with antidepressant drugs especially with zimelidine, which alters the firing rates of 5-HT and 5-HT/SP neurons.     

Brief communication HLA class II antigens DR4 and DQ8 are associated with allergy to hevein, a major allergen of Hevea latex

In this study we investigated the relationship between HLA class II alleles and the IgE-specific immune response to the 4.7 kDa polypeptide hevein of Hevea brasiliensis , a major latex allergen. 51 individuals with immediate-type latex allergy and 90 controls were examined for the polymorphisms in exon 2 of HLA-DRB1, 3, 4, 5 and DQB1 by sequence-specific oligonucleotide probe typing. 35 (69%) out of 51 latex-sensitized subjects showed positive hevein-specific IgE values. Analysis of the HLA data among these 35 subjects revealed increased phenotype frequencies for DR4 (22/35, 63%) and DQ8 (18/35, 51%) when compared with those in the 16 hevein-negative but latex-positive subjects (DR4: 2/16, 13%, p=0.0009, p_c=0.047; DQ8: 0/16, p=0.0003, p_c=0.018) and with healthy controls (DR4: 22/90, 24%, p=0.00012, p_c=0.013; DQ8: 16/89, 18%, p=0.0003, p_c=0.036). Finally the DR4-DQ8 haplotype frequency was significantly elevated in hevein-positives when compared with hevein-negatives (51% vs. 0, p=0.0003, p_c=0.034) or controls (51% vs. 18%, p=0.0002, p_c=0.045) The present data suggest DR4 and DQ8 to be operating jointly as susceptibility factor for the allergy to hevein.     

Immunohistochemical study of cytokeratins in amyloid deposits associated with squamous cell carcinoma and dysplasia in the oral cavity,pharynx and larynx

The frequency of amyloid deposits associated with squamous cell carcinoma (SCC) and dysplasia in the oral cavity, pharynx and larynx was examined. In addition, the origin of amyloid proteins by immunohistochemical staining with a panel of anticytokeratin monoclonal antibodies was investigated. Amyloid deposits were found in eight of 73 (11.0%) SCC and one of seven (14.3%) dysplasias in the oral cavity, in eight of 22 (36.4%) SCC and zero of two (0%) dysplasias in the pharynx, and in 22 of 37 (59.5%) SCC and four of 10 (40.0%) dysplasias in the larynx. Eight of 12 different cytokeratin (CK) antibodies reacted with these deposits: 34 beta E12 (CK1, -5, -10, -14) reacted with amyloid deposits in 19 of 19 cases (100%), LL002 (CK14) in eight of 18 cases (44.4%), MNF116 (CK5, -6, -8, -17) in eight of 19 cases (42.1%), D5/16B4 (CK5, -6) in five of 18 cases (27.8%), DE-K10 (CK10) in four of 17 cases (23.5%), RCK108 (CK19) in three of 18 cases (16.7%), 34 beta B4 (CK1) in three of 19 cases (15.8%) and AE8 (CK13) in two of 17 cases (11.8%). These antibodies always reacted with the cytoplasm of squamous cell lesions. Amyloid deposits in two cases contained a CK5 and CK14 pair, and in another two cases they contained both a CK5 and CK14 pair, and a CK1 and CK10 pair. Anti-CK antibodies, including OV-TL12/30 (CK7), c-51 (CK8), DC10 (CK18) and IT-Ks20.8 (CK20) did not react with the amyloid deposits. We conclude that the amyloid deposits associated with SCC or dysplasia in the oral cavity, pharynx or larynx were derived from CK of cancer cells and that some amyloid deposits might be assembled by two or more different CK.