Seminoma metastásico de primario gonadal / Metastatic seminoma of primary gonadal

El seminoma es la neoplasia testicular más frecuente alcanzando hasta el 50% de todos los casos de cancer del testículo. Dependiendo de su naturaleza, seminomatoso o no seminomatoso, las conductas de manejo y tratamiento médico quirúrgicas varían según los centros, los protocolos de manejo y la experiencia de los equipos de atención. Objetivos. Promover la discusión de adyuvancia o neoadyuvancia en caso de seminoma clásico. Paciente y Método. Presentar un caso de seminoma clásico tratado quirúrgicamente con orquidectomía y una década después se presenta con extensión metastásica mediastinal y retroperitoneal. Conclusiones. Para la etiología no seminomatosa, se establece la orquidectomía seguida de vigilancia; mientras que en caso de origen seminomatoso la discusión se basa en el momento del rol de la cirugía, radiación y quimioterapia, por lo tanto, se debe individualizar cada paciente según las características clínicas manifestadas. (AU)

Seminoma is the most common testicular neoplasm, reaching up to 50% of all cases of testicular cancer. Depending on its nature, seminomatous or non-seminomatous, the management behaviors and surgical medical treatment vary according to the centers, the management protocols and the experience of the care teams. Objective. Promote the discussion of adjuvant or neoadjuvant in case of classic seminoma. Patient and Method. To present a case of classic seminoma treated surgically with orchidectomy and a decade later it presents with mediastinal and retroperitoneal metastatic extension. Conclusions. For non-seminomatous etiology, orchidectomy followed by surveillance is established; while in the case of seminomatous origin, the discussion is based on the time of the role of surgery, radiation and chemotherapy, therefore, each patient must be individualized according to the clinical characteristics manifested. (AU)

Medicina de precisión: aspectos prácticos para el cirujano moderno / Precision medicine: practical aspects for the modern surgeon

Los contenidos de este capítulo se basan en la 3a edición de las Clínicas Quirúrgicas de Cáncer Colorrectal. C. Vaccaro y N. Peralta. del hospital ediciones 2020 (en prensa)

Clinical Significance of Aberrant Wnt7a Promoter Methylation in Human Non-Small Cell Lung Cancer in Koreans

The Wnt signaling pathway has regulatory roles in cell proliferation, differentiation, and polarity. Aberrant Wnt pathway regulation can lead to abnormal cell proliferation and cancer, and loss of Wnt7a expression has been demonstrated in lung cancer cell lines. E-cadherin keeps intercellular integrity and prevents metastasis. Therefore, E-cadherin has been known as a prognostic factor in cancer. In the present study, we investigated the E-cadherin expression status by immunohistochemical stain and the Wnt7a promoter methylation status in human non-small cell lung carcinoma (NSCLC) by methylation-specific PCR. We also analyzed their correlations with clinicopathological factors. Methylation of the Wnt7a gene promoter was detected in the lung tissues of 32 of 121 (26.4%) patients with NSCLC. Wnt7a promoter methylation was correlated with advanced tumor stage (P = 0.036) and distant metastasis (P = 0.037). In addition, Wnt7a promoter methylation showed correlation with loss of E-cadherin expression (P < 0.001). However, Wnt7a promoter methylation was not closely related with gender, age, histological type, or smoking habit. Even though Wnt7a methylation could not show significant correlation with the long term survival of the patients with limited follow up data, these findings suggest that loss of the Wnt7a gene induced by promoter methylation might be another prognostic factor for NSCLC and that restoration of Wnt7a may be a promising treatment for NSCLC.

Clinical Significance of Aberrant Wnt7a Promoter Methylation in Human Non-Small Cell Lung Cancer in Koreans

The Wnt signaling pathway has regulatory roles in cell proliferation, differentiation, and polarity. Aberrant Wnt pathway regulation can lead to abnormal cell proliferation and cancer, and loss of Wnt7a expression has been demonstrated in lung cancer cell lines. E-cadherin keeps intercellular integrity and prevents metastasis. Therefore, E-cadherin has been known as a prognostic factor in cancer. In the present study, we investigated the E-cadherin expression status by immunohistochemical stain and the Wnt7a promoter methylation status in human non-small cell lung carcinoma (NSCLC) by methylation-specific PCR. We also analyzed their correlations with clinicopathological factors. Methylation of the Wnt7a gene promoter was detected in the lung tissues of 32 of 121 (26.4%) patients with NSCLC. Wnt7a promoter methylation was correlated with advanced tumor stage (P = 0.036) and distant metastasis (P = 0.037). In addition, Wnt7a promoter methylation showed correlation with loss of E-cadherin expression (P < 0.001). However, Wnt7a promoter methylation was not closely related with gender, age, histological type, or smoking habit. Even though Wnt7a methylation could not show significant correlation with the long term survival of the patients with limited follow up data, these findings suggest that loss of the Wnt7a gene induced by promoter methylation might be another prognostic factor for NSCLC and that restoration of Wnt7a may be a promising treatment for NSCLC.

Pautas de género en el desarrollo del habitus médico: los años de formación en la escuela de medicina y la residencia médica / Gender norms and the development of the medical habitus: in the years of medical schooling and residency

Se documenta el maltrato de género que enfrentan los estudiantes de medicina en México. Se analiza el concepto de socialización médica, con énfasis en el problema del maltrato a las y los estudiantes de medicina. En el marco teórico se articulan conceptos de Foucault y Goffman, con los conceptos nodales de Bourdieu bajo un enfoque de género. Se ilustra mediante diversos ejemplos la manera en que el espacio de aprendizaje del currículum formal lo es también de reproducción de las jerarquías de género, a través del currículum oculto. Las mujeres enfrentan diversas formas de desmotivación socialmente inducida para optar y mantenerse en la carrera de medicina, particularmente en algunas de sus especialidades. La discriminación se presenta igual bajo interacciones afectivizadas que bajo formas muy autoritarias. Enfrentan acoso sexual en clase y en los años de especialización, y no dejan de ser construidas como sujetos subordinados. Al final se discute la importancia de estos hallazgos en la constitución del habitus médico.

This article documents the gender abuse that Mexican medical students face. The concept of medical socialization is analyzed, with emphasis on the problem of the mistreatment of medical students. The theoretical framework articulates ideas from Foucault and Goffman with the nodal points of Bourdieu using a gender focus. Numerous examples are employed to show that the formal program of study also contains a hidden curriculum which serves to reproduce gender hierarchies. Women face numerous types of socially induced discouragement in choosing and completing their course of study, particularly in certain specialties. Discrimination is present in affectivized as well as in authoritarian interactions. They face sexual harassment in the classroom and in their years of specialization, and are constantly constructed as subordinated subjects. The importance of these findings in the constitution of a medical habitus is discussed.

Changes in biologic features between primary and recurrent or relapsed breast cancers

Changes in ER, PR and Her2 receptor status between primary and metastatic cancer tissue have been suggested in breast cancer. The frequencies of these changes are still not fully understood. The purpose of this study was to evaluate these changes in breast cancer population of Kuwait. Changes in the biological features between primary and recurrent disease in 70 patients who presented between 2009 and 2012 was studied. Statistical comparisons between groups was done using chi square test while Kaplan Meier method was used to perform analysis of survival after relapse. All analysis was carried out using the IBM-SPSS statistical software. There was a decrease in ER and PR positivity from 61.4% to 58.6% and 61.4% to 44.3% respectively. The overall change in ER and PR status was 28.5% and 25.7% respectively. There was an increase in the Her2 positivity as the tumor relapsed and overall changes were seen in 5.7% of cases. Patients with breast cancer experience change in biological markers through the course of their disease. The changes are more with hormone receptors compared to Her2. Re-biopsy should be considered at relapse if feasible

miR-98 suppresses melanoma metastasis through a negative feedback loop with its target gene IL-6

Dysregulated microRNA (miRNA) expression has a critical role in tumor development and metastasis. However, the mechanism by which miRNAs control melanoma metastasis is unknown. Here, we report reduced miR-98 expression in melanoma tissues with increasing tumor stage as well as metastasis; its expression is also negatively associated with melanoma patient survival. Furthermore, we demonstrate that miR-98 inhibits melanoma cell migration in vitro as well as metastatic tumor size in vivo. We also found that IL-6 is a target gene of miR-98, and IL-6 represses miR-98 levels via the Stat3-NF-kappaB-lin28B pathway. In an in vivo melanoma model, we demonstrate that miR-98 reduces melanoma metastasis and increases survival in part by reducing IL-6 levels; it also decreases Stat3 and p65 phosphorylation as well as lin28B mRNA levels. These results suggest that miR-98 inhibits melanoma metastasis in part through a novel miR-98-IL-6-negative feedback loop.

Growth hormone receptor inhibition decreases the growth and metastasis of pancreatic ductal adenocarcinoma

Pancreatic cancer is the only major cancer with very low survival rates (1%). It is the fourth leading cause of cancer-related death. Hyperactivated growth hormone receptor (GHR) levels have been shown to increase the risk of cancer in general and this pathway is a master regulator of key cellular functions like proliferation, apoptosis, differentiation, metastasis, etc. However, to date there is no available data on how GHR promotes pancreatic cancer pathogenesis. Here, we used an RNA interference approach targeted to GHR to determine whether targeting GHR is an effective method for controlling pancreatic cancer growth and metastasis. For this, we used an in vitro model system consisting of HPAC and PANC-1 pancreatic cancer cells lines. GHR is upregulated in both of these cell lines and silencing GHR significantly reduced cell proliferation and viability. Inhibition of GHR also reduced the metastatic potential of pancreatic cancer cells, which was aided through decreased colony-forming ability and reduced invasiveness. Flow cytometric and western blot analyses revealed the induction of apoptosis in GHR silenced cells. GHR silencing affected phosphatidylinositol 3 kinase/AKT, mitogen extracellular signal-regulated kinase/extracellular signal-regulated kinase, Janus kinase/signal transducers and activators of transcription and mammalian target of rapamycin signaling, as well as, epithelial to mesenchymal transition. Interestingly, silencing GHR also suppressed the expression of insulin receptor-beta and cyclo-oxygenease-2. Altogether, GHR silencing controls the growth and metastasis of pancreatic cancer and reveals its importance in pancreatic cancer pathogenesis.

DNA Hypomethylation-Mediated Overexpression of Carbonic Anhydrase 9 Induces an Aggressive Phenotype in Ovarian Cancer Cells

PURPOSE: Both genetic and epigenetic alterations can lead to abnormal expression of metastasis-regulating genes in tumor cells. Recent studies suggest that aberrant epigenetic alterations, followed by differential gene expression, leads to an aggressive cancer cell phenotype. We examined epigenetically regulated genes that are involved in ovarian cancer metastasis. MATERIALS AND METHODS: We developed SK-OV-3 human ovarian carcinoma cell xenografts in mice. We compared the mRNA expression and DNA methylation profiles of metastatic tissues to those of the original SK-OV-3 cell line. RESULTS: Metastatic implants showed increased mRNA expression of the carbonic anhydrase 9 (CA9) gene and hypomethylation at CpG sites in the CA9 promoter. Treatment of wild-type SK-OV-3 cells with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine reduced methylation of the CA9 promoter and increased CA9 mRNA expression. Eight CpGs, which were located at positions -197, -74, -19, -6, +4, +13, +40, and +86, relative to the transcription start site, were hypomethylated in metastatic tumor implants, compared to that of wild-type SK-OV-3. Overexpression of CA9 induced an aggressive phenotype, including increased invasiveness and migration, in SK-OV-3 cells. CONCLUSION: Alterations in the DNA methylation profile of the CA9 promoter were correlated with a more aggressive phenotype in ovarian cancer cells.

Experiencia en la utilización del mammaprint en la Clínica de Mamas de Barquisimeto / Experience in the utilization of mamma print: in the breast clinic of Barquisimeto

El objetivo del presente trabajo es reportar nuestra experiencia con la utilización del Mammaprint. Analizando los resultados de 16 pacientes, los cuales cumplieron con los criterios de selección establecidos. En 56,25 por ciento la prueba fue reportada como insuficiente, 25 por ciento como de alto riesgo y 18,75 por ciento bajo riesgo. 75 por ciento de las pacientes fueron mayores de 50 años. En estas pacientes no se identificaron tumores de alto riesgo, mientras que en menores de 50 años el 50 por ciento de los tumores correspondían al grupo de alto riesgo. En 62,5 por ciento de las pacientes la lesión era menor de 10 mm (T1b), mientras en 37,5 por ciento correspondían al grupo T1c. En el grupo de pacientes de bajo riesgo, no se identificaron ganglios axilares, por el contrario en 50 por ciento de las pacientes con alto riesgo si se identificaron y en consecuencia se realizó una punción con aguja fina, con resultado negativo para metástasis. En ninguna de las 3 pacientes del grupo de bajo riesgo se identificaron metástasis en la evaluación histológica posoperatoria, sin embargo, en 75 por ciento del grupo de pacientes de alto riesgo si se identificaron metástasis a los ganglios axilares. La determinación de las características genéticas y sus alteraciones en un cáncer de mama, es de fundamental importancia para una mejor identificación de los grupos de bajo y de alto riesgo y para determinar los mejores tratamientos

The objective of this work was information of genetic characteristics of tumor, determined by methods such as mamma print identifies more adequately the risks and treatments for patients. In this work we report our experience with the use of mamma print. Analyzing the results of 16 patients whom met the selection criteria. 56.2 5 percent of the cases were in the test reported insufficient, 25 percent high risk and 18.75 percent low risk. 75 percent of patients were older than 50 years. In these patients were not identified high-risk tumors, mean while in patients less than 50 years 50 percent of the tumors corresponded to the high risk group. In 62.5 percent of patients the lesion was less than 10 mm (T1b), while 37.5 percent were T1c group. In the group of low risk patients, axillaries nodes were not identified to the US, by contrast 50 percent of patients at high risk were identified and accordingly a fine needle punting was performed, with results negative for metastases. In none of the patients in low-risk & group metastases was identified in the postoperative histological evaluation, however in 75 percent of the group of at high risk patients was identified axillaries node metastases. Determining of the characteristics and genetic alterations in breast cancer has fundamental importance for a better identification of groups of low and high risk and to determine the best treatments

Análise da expressão de RNAs não-codificadores intrônicos em tumores de mama / Gene expression analysis of intronic non-coding RNAs in breast tumors

O câncer de mama é o carcinoma que mais acomete mulheres no Brasil. Os tratamentos disponíveis são recomendados a partir da análise de fatores de prognóstico como a classificação pelo sistema TNM, tipo histológico, status de receptores hormonais e marcadores de proliferação tumoral. No entanto, a classificação dos tumores de mama é muito variável e o poder prognóstico dos marcadores tumorais atuais ainda é limitado, levando muitas pacientes à terapia adjuvante desnecessária. Portanto, novos métodos de prognóstico mais sensíveis são necessários para melhorar a tomada de decisão na clínica oncológica de pacientes com câncer de mama. Do ponto de vista de ciência básica, as modificações transcricionais associadas à oncogênese e progressão do câncer de mama ainda são pouco conhecidas. Além da alteração na expressão de genes codificadores para proteínas, evidências recentes sugerem que RNAs não-codificadores (ncRNAs) podem ter um papel importante na transformação maligna. Este projeto teve como principais objetivos: i) investigar a expressão de ncRNAs intrônicos em amostras de adenocarcinoma de mama e ii) identificar assinaturas de expressão gênica associadas a características anatomo-patológicas e clínicas de tumores de mama com potencial aplicação clínica. Para isso, foram comparados os perfis de expressão gênica de 58 amostras de tecido tumoral de mama, com seguimento clinico conhecido, utilizando uma plataforma de microarranjos de cDNA, enriqueci da em ncRNAs provenientes de regiões intronicas de genes humanos conhecidos...

role of matrix metalloproteinase-3 functional 5A/6A promoter polymorphism in tumor cell progression and metastasis of breast cancer

In the human genome, chromosome 11 contains a cluster of matrix metalloproteinase [MMP] genes. Single nucleotide polymorphisms in the promoter region of MMP genes are important for MMP expression. A common adenine deletion polymorphism [5A] at position -1171 of the MMP-3 gene promoter [5-AAAAAACCAT-3 change to 5-AAAAACCAT-3] facilitates transcriptional factor binding and MMP-3 promoter activity. A case-control study was performed including 120 breast cancer patients [60 patients with metastatic activity and 60 patients without metastatic activity]; and 60 healthy controls. Whole blood samples were obtained from patients and healthy controls. Genomic DNA was extracted from samples and the MMP-3 5A/6A genotypes were determined using PCR-RFLP. MMP-3 genotype distributions between patients and controls were similar [OR= 0.89, 95%CI, 0.43-1.84, P= 0.047]. It was observed that the 5A allele was more frequent among patients with metastatic activity than controls [OR= 2.9, 95%CI, 0.94-8.9, P= 0.074]. Therefore, the 5A polymorphism in the MMP-3 promoter showed correlation with the metastasis group than patients without metastasis; both at the time of diagnosis. However our results do not show evidence for correlation between 5A/6A polymorphism and breast cancer susceptibility

Screening of differently expressed genes in human prostate cancer cell lines with different metastasis potentials / 华中科技大学学报（医学）（英德文版）

In order to screen the genes differentially expressed in two human prostate cancer cells with different metastasis potentials, suppression subtractive hybridization (SSH) was done twice on human prostate cancer cell line with high potential of metastasis PC3M-1E8 and its synogenetic cell line PC3M-2B4 with low metastasis potential. In the first subtraction PC3M-2B4 was used as tester and PC3M-1E8 as driver and the forward subtractive library was constructed. In the second on the tester and driver were interchanged and the reverse subtractive library was constructed. The screened clones of both libraries were sequenced and Gene Bank homology search was performed. Some clones were confirmed by quantitative real-time PCR. The results showed that two subtractive libraries containing 238 positive clones were constructed. Analysis of 16 sequenced clones randomly picked from two libraries showed that 4 differentially expressed gene fragments were identified as new EST with unknown functions. It was concluded that two subtractive libraries of human prostate cancer cell lines with different metastasis potentials were constructed successfully.

História natural do câncer de mama / Natural history of the breast cancer

Ao que tudo indica, a lesão genética iniciadora do câncer de mama ocorre em tecidos precursores da neoplasia. Formando-se o tumor, seu ritmo de crescimento é determinado basicamente pela função de proliferação celular, com desenvolvimento lento. A principal via de disseminação das células neoplásicas da mama é linfática e, após os êmbolos neoplásicos atingirem a circulação sistêmica, podem ser neutralizados pelo sistema de defesa do hospedeiro (resposta imune inata ou adaptativa) ou se multiplicar a distãncia. As assinaturas genéticas de cada tumor relacionam-se com o seu potencial metastatizante e a predileção por certos órgãos-alvo.

Apparently, the genetic lesion initiator of breast cancer occurs in tissues precursors of neoplasia. Forming the tumor, its growth rate is basically determined by the function of cell proliferation, with slow development. The major route of spread of breast cancer cells is lymphatic and after neoplastic emboli reach the systemic circulation, can be neutralized by the system of host defense (innate or adaptive immune response) or multiply the distance. Genetic signatures of each tumor are related to their potential metastasizing and the preference for certain target organs.

Cancer Metastasis and Metastasis Suppressors / 대한소화기학회지

Cancer metastasis, a complex and sequential network of cellular events involved in the migration and establishment of malignant cells from original site to distant foci, is an important and significant contributor to morbidity and mortality of cancer patients. Despite the clinical importance of cancer metastasis, its molecular and biochemical mechanism remains unclear. The identification of tumor suppressor gene confirmed that metastasis might involve the functional loss of genes that maintain the cellular differentiation optimally. Metastasis suppressor is defined by the ability to reduce the metastatic property of cancer cells without affecting its tumorigenesis. Since NM23 was first identified in 1988 as a metastasis suppressor, several metastasis suppressor genes have been identified and characterized. In this article, we review the complex and multi-step process of cancer metastasis and describe the recent progress of metastasis suppressors in the studies of identified. Consequently, we hope to introduce the new therapeutic target for the metastasis suppressors in cancer patients.

Perfil de expressão gênica em carcinoma neuroendócrino produtos de insulina: avaliação da agressividade tumoral / Gene expression profiling in insulin-producing neuroendocrine carcinom: tumor aggressiveness evaluation

Insulinomas malignos correspondem entre 5-10per cent de todos os tumores de ilhota. O diagnóstico histopatológico não identifica a malignidade, somente a presença de metástase. Neste estudo foi realizada análise de expressão gênica diferencial em insulinomas com o intuito de identificar genes associados a malignidade. Foram estudados 25 pacientes com insulinoma (2 metástases). Análise de agrupamento hierárquico de alguns genes isolados reuniu os pacientes em grupos com diferentes potenciais malignos, contribuindo para melhor compreensão dos processos carcinogênicos em insulinomas / The gene expression profile associated with benign and malignant insulinomas.Five to 10 per cent insulinomas are malignant, associated with distant metastases or local invasion and histopathological diagnosis cannot identify these tumors as malignant at all. In this study differential gene expression analysis was performed in order to identify genes linked to different aggressive potentials of benign in comparison to malignant insulinomas. Twenty-five patients were studied (two metastases). Hierarchical cluster analysis of expression patterns of some isolated genes put the patients into different groups with progressive malignant potential and that may add new insights into carcinogenesis...

Study of the difference of high and low metastasis cell line's gene expression map and metastasis-related genes of adenoid cystic carcinoma

We searched for metastasis-related genes in adenoid cystic carcinoma by suppression subtractive hybridization analysis of high and low metastasis cell lines. Twelve genes (ten previously identified and two novel sequences) were identified as being expressed at lower levels in high metastasis cell line Acc-M when compared to low metastasis cell line Acc-2. The known sequences corresponded to the genes for cysteine-rich angiogenesis induction factor (cyr61), chromosome 7 RP11-52501 clone, G-protein, WAS familial ferritin I heavy chain, jumping translocation breakpoint, eukaryotic translation elongation, folate receptor and three ribosomal proteins. Among them, the G protein and ferritin I heavy chain genes contained mutations in the high metastasis cell line. The two novel gene sequences have been named ACC metastasis-associated RNH and ACC metastasis-associated suspected protein (GenBank # AF522024 and AF522025, respectively). Taken together, these results suggest that reduced expression and/or mutation of several genes in the tumor cell line Acc-M are associated with high tumor metastasis, providing important molecular biological materials for further study of metastasis control and possible targets for cancer gene therapy.

Oncogene-mediated downregulation of RECK, a novel transformation suppressor gene

The RECK gene was initially isolated as a transformation suppressor gene encoding a novel membrane-anchored glycoprotein and later found to suppress tumor invasion and metastasis by regulating matrix metalloproteinase-9. Its expression is ubiquitous in normal tissues, but undetectable in many tumor cell lines and in fibroblastic lines transformed by various oncogenes. The RECK gene promoter has been cloned and characterized. One of the elements responsible for the oncogene-mediated downregulation of mouse RECK gene is the Sp1 site, where the Sp1 and Sp3 factors bind. Sp1 transcription factor family is involved in the basal level of promoter activity of many genes, as well as in dynamic regulation of gene expression; in a majority of cases as a positive regulator, or, as exemplified by the oncogene-mediated suppression of RECK gene expression, as a negative transcription regulator. The molecular mechanisms of the downregulation of mouse RECK gene and other tumor suppressor genes are just beginning to be uncovered. Understanding the regulation of these genes may help to develop strategies to restore their expression in tumor cells and, hence, suppress the cells' malignant behavior

Study on the metastatic mechanisms of human giant-cell lung carcinoma comparison between the strains C and D.

The biologic characteristics of the two human giant-cell lung carcinoma strains with high (strain D) and low metastatic potential (strain C) were studied, including karyotype of chromosome, intracellular free calcium ([Ca2+]i), morphologic changes of cell surface and the expression of nm23-H1, p53, ras, c-myc, c-erbB2, bcl-2 genes and PCNA. The correlation between different biologic features and the metastatic potential of the two strains was analyzed. We found: 1) Both strains had the karyotypic abnormality of -13, -14, -15, +20, +21 with seven same marker chromosomes. Only strain D had the karyotypic abnormality of +7, -17, -18, +X, 7p+; 2) [Ca2+]i of the strain C (984.7 +/- 573.8) and D (517.6 +/- 216.6) was significantly different (p < 0.05). The amplitude of intracellular calcium oscillations of strain C was lower than the one of strain D; 3) strain C had more villous-like protrusions on the cell surface, whereas strain D had more bubble-like protrusions; 4) The expression of nm23-H1 and p53 protein of strain C was all higher than that of strain D. The expression of PCNA of strain C was lower than strain D; 5) nm23-H1 mRNA levels of strain C was lower than that of strain D. We consider that the karyotype of chromosomes, intracellular free calcium, the structure of cell membrane and the expression of nm23-H1 gene, p53 gene, PCNA could be closely related to the metastatic potential of human giant-cell lung carcinoma. They could be used as the sign for judging whether the tumor will metastasize in clinical practice as well as in judging the prognoses of patients.