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PubMed1985

[Analysis of Epstein-Barr virus transformation of human lymphocytes: susceptibility of B lymphocyte subpopulations and differentiation stage of the transformed cells].

The subpopulations of B lymphocytes in human adult peripheral blood which are susceptible to infection and transformation by Epstein-Barr virus (EBV), and also the stage of EBV-transformed cells in B cell differentiation lineage were identified. The EBV susceptibility were analyzed by two-color immunofluorescence and colony formation in semisolid agar. Surface Ig-bearing lymphocytes of 3 major Ig classes, IgM, IgG, and IgA, in peripheral blood expressed viral nuclear antigen (EBNA) after exposure to the virus, indicating that all these subpopulations are susceptible to EBV infection. In contrast, cytoplasmic Ig-positive lymphocytes were totally resistant to infection. The Ig-positive cells of either Ig class proliferated equally after EBV infection and formed colonies in semisolid agar, thereby showing that these subpopulations are also susceptible to transformation by EBV. Analysis of clonally transformed cells originating from each target cell by using a series of newly developed monoclonal antibodies to B cell differentiation antigens showed that EBV-transformed cells corresponded to the immunoblast stage of B cell differentiation. These data suggest that EBV infects and transforms mature B lymphocytes, and makes them differentiated to the more advanced immunoblast stage within the terminal B cell differentiation process.

Antibodies, Monoclonal↗
PubMed1987

Characterization of the blast cells in acute leukemia with translocation (4;11): report of eight additional cases and of one case with a variant translocation.

Eight new cases (five adults and three children) of acute leukemia characterized by the presence in bone marrow cells of a t(4;11)(q21;q23)and one similar case, a child, with a t(1;11)(p32;q23) are reported. All patients were diagnosed as having acute lymphoblastic leukemia (ALL) with high-risk features. Immunologically the blast cells of the nine cases showed a strikingly consistent immature lymphoid phenotype, i.e., TdT+, HLA-DR+, B4(CD19)+, CALLA(CD10)-, Smlg-, cmu-, BA-2(CD9)+ corresponding to a "null ALL." In addition, six of nine cases expressed the myeloid marker VIM-D5(CD15). By double immunofluorescence staining it was determined that the VIM-D5(CD15) antigen was expressed by terminal deoxynucleotidyl transferase-positive blast cells, excluding the possibility of double leukemia. In five cases investigation of the Ig heavy chain genes by Southern blot analysis showed clonal rearrangement of both Ig heavy chain gene alleles. These data suggest that the blast cells involved in t(4;11) leukemia represent early B-cell progenitors with "aberrant" expression of myelomonocytic features, possibly related to the 11q23 breakpoint.

Adolescent↗
PubMed1985

Cytoplasmic localization and chordamesoderm induction in the frog embryo.

The experiments described here were designed to reveal the distribution in the frog early embryo of components which are sufficient for specification of the dorsal structures of the embryonic body axis. The approach was to allow cleavage planes to divide the embryo into various well-defined regions and to transplant cells from each region into recipient embryos which would otherwise fail to form axial structures. Partial or complete body axis development could then be scored by the use of external criteria or histological methods. Recipients were embryos which had been irradiated before first cleavage with ultraviolet light on the vegetal surface. Irradiated embryos display a well-characterized set of deficiencies in the dorsal structures of the body axis, but their development can be 'rescued' toward normalcy in several ways. In particular, transplantation of certain small groups of blastomeres from the normal 32- to 64-cell embryo into irradiated recipients was sufficient to cause partial or complete axis development. Cell groups which could cause rescue were located in the vegetal and equatorial levels of one quadrant of the normal embryo--the quadrant centered on the future dorsal midline. Clonal marking analysis showed that the vegetal-most cells of this quadrant contribute primarily to endodermal structures in normal development. In rescued recipient embryos, these cells also contributed only to the endoderm; the dorsal mesoderm and central nervous system were formed exclusively by host cells which originated near the transplant. Rescue could also result from transplantation of equatorial cells from the dorsal quadrant of the normal embryo. As in normal development, these cells formed primarily the chordamesoderm of the rescued embryo. Host cells were induced to contribute the somitic mesoderm, central nervous system, and other structures which would have been missing but for the presence of the transplanted cells. The frequency and degree of rescue caused by equatorial and vegetal transplants is variable. This was explained by the discovery that the location of components needed for rescue varies among individual embryos without regard to the positions of cleavage planes. This was true even when donor embryos were selected on the basis of a precisely regular pattern of cleavage. In such selected embryos, particular blastomeres make a predictable contribution of progeny to the body axis. Thus it may be that the positions of components which can cause axis formation vary without exact regard to the fate map of prospective areas. The implications of this for the study of cytoplasmic localization in the early embryo are discussed.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Primary melanoma cells of the vertical growth phase: similarities to metastatic cells.

Three primary and 16 metastatic melanoma cell lines were established from primary and metastatic lesions of 4 patients with malignant melanoma. Comparison of metastatic melanoma cells with cells of the vertical growth phase (VGP) or late primary melanoma from the same individual revealed, generally, a shorter population-doubling time, growth to a higher cell density, higher tyrosinase activity, and more pigmentation in metastatic cells. Conversely, primary and metastatic melanoma cells had similar morphology, plating efficiency, and tumorigenicity in nude mice. Karyotypic analysis revealed clonality and nonrandom abnormalities in chromosomes 1, 6, and 7 in cells of the primary and metastatic lesions of the 3 patients studied. Few differences were found in the expression of melanoma-associated antigens on short-term and long-term cultured cells by tests with monoclonal antibodies in mixed hemadsorption assays, flow cytometry, and radioimmunoassays. Our results indicate that cells cultured from the VGP but not from the radial growth phase of primary melanoma are similar to metastatic melanoma cells.

Antigens, Neoplasm↗
PubMedDate not supplied

Some insights into X chromosome inactivation from studies of human cells.

The inactivation of all but one X chromosome in the somatic cells of mammalian females in an important mechanism for regulating X chromosomal genes. Although the molecular basis for the single active X remains to be elucidated, recent studies have provided some insights. Inactivation occurs about the time of implantation, at least in mouse embryos. On the other hand, germ cells from human embryos have two active X chromosomes and may never be subjected to inactivation. As a consequence of X inactivation, one X chromosome becomes the sole determinant of X specified characteristics of the cell, resulting in cellular mosaicism. Transfer of gene products between cells occurs via gap junctions and by pinocytosis so that in heterozygotes carrying X linked mutations, the mutant phenotype may be masked by the presence of cells or normal type. There is considerable evidence that inactivation in the embryo is random with respect to parental origin of the X chromosome, but that selection occurs subsequently, and may lead to elimination of a whole population of cells in the female. Although there is evidence for preferential inactivation of the paternal X in extra-embryonic membranes of rodents, studies in human embryos have not been confirmatory. Analysis of clonal populations from heterozygotes for X chromosome mutations have been used to determine whether a whole X chromosome is inactive or only parts thereof. Individuals with multiple X chromosomes often manifest somatic abnormalities as well as gonadal ones. There is recent evidence that some loci on the short arm may escape inactivation. X inactivation in diploid human cells has been shown to be a very stable process. The silent X, once inactivated, maintains inactivity despite attempts to turn it on. Our recent studies of enzyme activity in cells from a human triploid abortus (69, XXY) with two active chromosomes indicates that the "active chromosomes" are also stably maintained. The presence of two active chromosomes in triploid cells implicates the autosomes in the regulation of X chromosome activity.

Animals↗
PubMed1995

Presence of host-specific interleukin 2-secreting T helper cell precursors correlates closely with active primary and secondary chronic graft-versus-host disease.

We investigated the role of interleukin 2 (IL-2)-secreting T helper cell precursors (Th-p) in primary and secondary chronic graft-versus-host disease (GVHD). Twelve patients with chronic GVHD (8 primary and 4 secondary chronic GVHD) and 8 patients without chronic GVHD were investigated using a sensitive limiting dilution assay. High frequencies of host-reactive interleukin 2-secreting T helper cell precursors were detectable in all patients with chronic GVHD irrespective of the mode of onset. Host-reactive IL-2-secreting T helper cell precursors disappeared in patients whose GVHD resolved. Host-reactive IL-2-secreting T helper cell precursors were never found in the control patients without chronic GVHD. Host-reactive cytotoxic T cell precursors (CTL-p) were not consistently detectable in patients with chronic GVHD and were occasionally found in patients without GVHD. No autoreactive IL-2-secreting T helper cell precursors or cytotoxic T cell precursors were detectable in either group. The absence of autoreactive IL-2-secreting T helper cell precursors in patients was confirmed by clonal specificity analysis in 4 patients. These data suggest a role for host-reactive IL-2-secreting T helper cell precursors in the initiation and maintenance of chronic GVHD as previously shown for acute GVHD.

Adolescent↗
PubMed1995

Clonality studies in patients undergoing allogeneic and autologous bone marrow transplantation for haematological malignancies.

Twenty three allogeneic bone marrow transplant (BMT) patients with female donors and 23 female autologous transplant patients were assessed for clonality status after transplant to determine the nature of haemopoietic reconstitution. The X chromosome probes PGK, HPRT and M27 beta were used to assess clonality by analysis of X chromosome inactivation. Results were obtained for 15 allogeneic patients, 14 of whom gave polyclonal results after transplantation. One patient gave a skewed pattern of X chromosome inactivation after transplant due to extreme Lyonisation of the donor cells. Results were obtained from 19 autologous transplant patients, 17 of whom gave polyclonal results after transplant. Two patients gave patterns of skewed X chromosome inactivation in post-transplant samples, reflected in their constitutive DNA, due to extreme Lyonisation. The remaining patients could not be assessed because of hypermethylation of HpaII sites or indistinguishable digested and undigested alleles using M27 beta probe analysis. Haemopoietic reconstitution after allogeneic and autologous BMT, in our patients, was found to be polyclonal. Skewed patterns of X chromosome inactivation seen after transplant were due to extreme Lyonisation of the infused haemopoietic cells.

Bone Marrow Transplantation↗
PubMed1994

[B-lymphoma arising in the temporal muscle].

B cell lymphoma arising in skeletal muscle is described with the review of literature. A 72-year-old man visited our hospital on September 21st 1992, because of a right temporal mass which had grown gradually since one year previously. A CT scan and MRI showed a soft tissue mass adjacent to the temporal muscle expanding from the right temporal to infratemporal fossa. Physical examination on admission revealed that the mass at the right temporal region, was non-tender, elastic soft, and 5 x 2 cm in diameter. Some elastic hard masses at the right infraauricular region, approximately 1.5 x 1.2 cm in diameter, were also found. Histological examination of a biopsied specimen obtained from the temporal mass revealed B cell lymphoma, diffuse medium-sized cell type. Tests for surface markers using tumor cell suspension showed positive results for CD5, CD19, CD20, SmIg mu, delta, lambda, but negative for CD10. Chromosomal analysis revealed clonal aberrations, and the defining karyotype as 51, X, +X, -Y, +2, +3, +4, +8, +12. The patient achieved a complete remission after treatment with combination chemotherapy including doxorubicin, cyclophosphamide, vincristine, etoposide, vindesine, procarbazine, and prednisolone.

Aged↗
PubMed1993

Association of Epstein-Barr virus with gastric carcinoma with lymphoid stroma.

Epstein-Barr virus (EBV) has been detected in lymphoepithelioma of nasopharynx and lymphoepitheliomalike carcinomas in various organs. To clarify the association of EBV with gastric carcinoma with lymphoid stroma, which often resembles lymphoepithelioma, the authors examined 22 such cases by polymerase chain reaction and in situ hybridization techniques. In 18 informative cases, EBV DNA was detected by polymerase chain reaction in 14 (77.8%) cases, including lymph node metastases. EBV RNA was detected within the nuclei of carcinoma cells by in situ hybridization in all cases that were positive by polymerase chain reaction. Infiltrating lymphocytes and normal epithelia adjacent to carcinoma were EBV-negative. Southern blot analysis indicated clonal proliferation of tumor cells and episomal form of EBV. These findings suggest that EBV infection occurs before transformation and may be related to oncogenesis of EBV-associated gastric carcinoma.

Adult↗
PubMed1996

Characterization of postcardiac transplant lymphomas. Histology, immunophenotyping, immunohistochemistry, and gene rearrangement.

OBJECTIVE: Between 2% and 9% of cardiac transplant recipients develop posttransplant lymphoproliferative disease, which includes lymphomas. These are usually aggressive Epstein-Barr virus-associated B-cell proliferations similar to those seen in other immunodeficiency states. A retrospective pathologic study of the tumor tissue from 21 cardiac transplant recipients with posttransplant lymphoproliferative disease was undertaken. DESIGN: Tumor histology, immunohistochemistry, immunophenotyping, and DNA analysis for clonal gene rearrangement and the presence of Epstein-Barr virus DNA were performed. PATIENTS: The mean patient age was 53.4 +/- 10.2 years (range 33-67 years); 33% of the patients were alive at the time of study. RESULTS: Histologically, the samples comprised one Burkitt's lymphoma, three diffuse mixed lymphomas, eight diffuse large-cell lymphomas, and nine immunoblastic lymphomas. Thirteen (93%) of 14 samples were infiltrated by small reactive T cells; five of the lymphomas qualified as T-cell rich. Of 14 cases studied, 12 had clonal immunoglobulin gene rearrangements, 1 had oligoclonal bands, and 1 exhibited only a germline pattern. The B cells were CD10+, CD19+, and CD20+, and the reactive T cells were CD2+, CD3+, CD5+, CD7+, CD8+, and CD57+ by immunophenotyping. CONCLUSIONS: In this patient series, morphologically aggressive lymphomas and disseminated disease occurred early as well as late after transplantation. Most of the tumors showed a reactive T-cell component, which may represent a host attempt at controlling the B-cell proliferation.

Adult↗
PubMed1997

Molecular analysis of T-cell clonality in ulcerative jejunitis and enteropathy-associated T-cell lymphoma.

Ulcerative jejunitis (UJ) and enteropathy-associated T-cell lymphoma (EATL) are closely related conditions both associated with celiac disease. Benign-appearing inflammatory ulcers are seen in both, which has led to the suggestion that UJ is a manifestation of EATL. The aim of this study was to investigate this relationship using the polymerase chain reaction (PCR) to detect T-cell gene rearrangement. PCR amplification of the T-cell receptor gamma-chain gene was performed on DNA extracted from lymphoma, associated inflammatory ulcers, and intervening mucosa in six EATL cases and from ulcers and intervening mucosa of seven cases of UJ. In two of these cases, DNA from a subsequent lymphoma was also studied. The PCR products from the tumor and an ulcer from one EATL case, two ulcers from one case of UJ, and one ulcer and subsequent cutaneous lymphoma from one UJ case were sequenced. Twenty-five ulcers from twelve cases of Crohn's disease, twenty sections of normal bowel, and nine celiac biopsies were included as controls. A monoclonal T-cell population defined by a dominant band equal in size to that amplified from the lymphoma was identified in at least one ulcer from four informative EATL cases and from intervening mucosa in three. Monoclonality was demonstrated in at least one, and up to thirteen, ulcers from all seven cases of UJ, in intervening mucosa in five, and in the two subsequent lymphomas. Sequencing showed the same clone was present in the tumor and the ulcer in the EATL case, in two of three ulcers from the UJ case, and in an ulcer and subsequent cutaneous lymphoma in one UJ case. All Crohn's disease ulcers and all sections of normal bowel were polyclonal. One of nine celiac biopsies showed a dominant band. In conclusion, we have shown that T-cell monoclonality is a feature of the ulcers in both UJ and EATL and that the same clone is present in EATL and its associated inflammatory ulcers and in UJ and subsequently developing lymphoma.

Celiac Disease↗
PubMed1998

[A case of marginal zone B-cell lymphoma].

A 60-year-old woman had an abnormal shadow in the right lower lung field on chest roentgenogram. Transbronchial lung biopsy revealed findings consistent with malignant lymphoma, and a right middle lobectomy was performed. Pathological findings showed that tumor cells had infiltrated the epithelium, forming so-called lymphoepithelial lesions. Flow cytometric analysis of the resected specimen revealed that B-cell associated antigens (CD 19, 20) were expressed, and that the tumor cells were CD 5-, CD 10-. A marked increase in the number of lymphocytes with an IgM kappa component suggested monoclonal origin for the tumor cells in the resected specimen. Southern blot analysis showed clonal rearrangement of the heavy chain of the immunoglobulin gene. A diagnosis of malignant lymphoma of bronchus-associated lymphoid tissue was made. This tumor was defined according to the revised European. American classification of lymphoid neoplasms as a marginal zone B-cell lymphoma.

Antigens, CD19↗
PubMed2004

Detection of clonality with kappa and lambda immunohistochemical analysis in cutaneous plasmacytomas.

CONTEXT: Cutaneous plasmacytomas rarely occur in the setting of multiple myeloma. However, since poorly differentiated lesions may resemble other neoplasms, such as carcinoma, melanoma, and lymphoma, the diagnosis of cutaneous plasmacytoma may be difficult. OBJECTIVE: To demonstrate clonality using kappa and lambda immunohistochemical analysis in cutaneous plasmacytomas and to ascertain whether or not interpretation is hindered by background staining. DESIGN: Pathology reports of all patients with the diagnosis of multiple myeloma were reviewed. Twelve patients had cutaneous lesions diagnosed as plasmacytoma, and these lesions were analyzed for light chain restriction with kappa and lambda immunohistochemical analysis. RESULTS: In most cases (11 of 12), monoclonality was demonstrated. In the remaining case, monoclonality could not be established because most cells did not stain for either kappa or lambda. CONCLUSIONS: Light chain restriction can be demonstrated in most multiple myeloma-related cutaneous plasmacytomas, establishing the neoplastic nature of the infiltrate.

Clone Cells↗
PubMed2000

Molecular analysis reveals somatically mutated and unmutated clonal and oligoclonal B cells in T-cell-rich B-cell lymphoma.

This paper describes the immunohistology and molecular genetics of 18 cases of T-cell-rich B-cell lymphoma (TCRBL). In all cases, the large B cells stained strongly for CD20, with more variable expression of CD79a, and were negative for CD30 and CD15. The majority of T cells were predominantly positive for TIA-1 and negative for CD57; a large population of histiocytes was present in all cases. Epstein-Barr virus (EBV)-coded RNA (EBER) was found in B blasts from four cases and in one case was present among the background lymphoid cells. IgH PCR products were generated in 16/18 cases and revealed clonal, oligoclonal and polyclonal PCR products in 12, two and two cases, respectively. In addition, TCRG clonal gene rearrangements were identified in two cases. TCRB gene rearrangements were polyclonal. Sequence analysis of seven cases with clonal/oligoclonal IgH gene rearrangements revealed functional sequences with predominant V(H)3 gene usage associated with various D genes and J(H)4 or J(H)6 gene segments. Four cases displayed varying degrees of replacement and silent mutations (1.8-21%), with one case exhibiting intraclonal heterogeneity; the distribution of mutations was indicative of antigen selection in three cases. The remaining three cases, including two cases with functional oligoclonal IgH rearrangements, harboured unmutated V region genes. The EBV-positive cases were associated with clonal, oligoclonal and polyclonal PCR products and with mutated and germline clonal sequences. These data indicate that TCRBL may be a heterogeneous entity associated with clonal and oligoclonal B cells derived from both germinal centre and naïve B cells.

Adult↗
PubMed2002

Angio-immunoblastic T cell lymphoma (AILD-TL) rich in large B cells and associated with Epstein-Barr virus infection. A different subtype of AILD-TL?

We studied eight patients with characteristic features of angio-immunoblastic T cell lymphoma (AILD-TL) associated with more than 25% of large B cells. Polymerase chain reaction (PCR) analysis showed a clonal rearrangement of the T cell receptor (TCR)-gamma chain gene in all cases. One additional case showed a clonal rearrangement of the TCR-beta chain gene by Southern blot hybridization. PCR analysis showed a clonal immunoglobulin rearrangement in three cases presenting with more than 50% of large B cells whereas the other cases had a germline configuration. In 6/8 cases, double-labeling immunohistochemistry and in situ hybridization demonstrated that Epstein-Barr virus (EBV) was mostly present in the large B cells but also detected in some T cells. We further evaluated the frequency of AILD-TL with more than 25% of large B cells in the 106 cases collected by the French GELA group and found an incidence of 18%. The outcome of these patients did not differ significantly from those with less than 25% of B cells. With this approach we confirm the heterogeneity of AILD-TL features and the possible association with a substantial numbers of CD20(+), EBV(+) large B cells. We propose to denominate these cases as 'AILD-TL rich in large B cells' and to consider them as a different entity which can be misdiagnosed as a reactive process or as T cell rich B cell lymphoma.

Aged↗
PubMed2000

Peripheral T-cell lymphoma complicated by a proliferation of large B cells.

We studied 14 cases that showed a morphologic appearance of peripheral T-cell lymphoma and contained substantial numbers of CD20+ large B cells. In all but 2 cases, the CD20+ large cells showed a mix of kappa and lambda light chain expression. Two cases showed a focal predominance of kappa expression. In situ hybridization using the EBER1 probe for detection of Epstein-Barr virus (EBV) RNA was performed on every case. EBV RNA was present in 10 cases. Of 8 cases with EBV RNA stained by immunohistochemistry for the latent membrane protein of EBV, 6 were positive. Double-labeling immunohistochemistry and in situ hybridization confirmed that EBV was present in the large B cells. Polymerase chain reaction (PCR) analysis showed a clonal rearrangement of the T-cell receptor (TCR)-gamma chain gene in 12 of 13 cases tested. One additional case showed a clonal rearrangement of the TCR-beta chain gene by Southern blot hybridization. PCR analysis showed a clonal immunoglobulin gene rearrangement in 5 cases, a suggestion of a clonal rearrangement in 1, an oligoclonal pattern in 4, and a polyclonal pattern in 4. The finding of large B and T cells may result in a misdiagnosis of a reactive process or of T-cell-rich B-cell lymphoma. The presence of EBV in some cases could cause further confusion with the reactive T- and B-immunoblastic proliferation of infectious mononucleosis.

Adult↗
PubMed1994

Clonality studies and N-ras and p53 mutation analysis of hematopoietic cells in Fanconi anemia.

Patients with Fanconi anemia (FA) have an extraordinary predisposition to acute myelogenous leukemia (AML). The genetic mechanisms underlying the neoplastic transformation of FA hematopoietic cells are unknown. In this study, we have investigated the molecular features of hematopoiesis in the course of FA at different stages of the disease, including aplastic anemia, myelodysplastic syndrome (MDS), and AML. The analysis focused on defining the clonality status of FA hematopoiesis as well as the putative involvement of N-ras, a dominantly acting oncogene, and p53, a tumor suppressor gene, which are known to play a role in human hematopoietic tumors. Clonality of hematopoiesis was assessed by testing X-chromosome inactivation at the DXS255 locus, which displays different methylation patterns according to the activation status of the corresponding X homolog. Five out of seven FA cases analysed for clonality displayed monoclonal hematopoiesis, including one case at the aplastic anemia stage, three cases with MDS and one with AML. Mutations of the N-ras and p53 genes were studied by a combination of single strand conformation polymorphism (SSCP) analysis and direct sequencing of the PCR product in the bone marrow and/or peripheral blood of 18 FA patients (seven with aplastic anemia, seven with MDS, four with AML). Only normal N-ras and p53 sequences were detected in all cases analyzed. These results suggest that monoclonal hematopoiesis is a frequent finding in the course of FA and may precede the onset of neoplasia in some cases. The genetic mechanisms underlying FA-associated leukemogenesis appear to be independent of N-ras and p53 mutations, which are relatively frequent events in myeloid tumors associated with other hematologic disorders.

Base Sequence↗
PubMed2004

[Clonality detection of cervical cancer and cervical intraepithelial neoplasia by human androgen receptor gene analysis].

OBJECTIVE: To assess the clonality of cervical cancer and cervical intraepithelial neoplasia (CIN) by the study of X-chromosome inactivation pattern with human androgen receptor gene (HUMARA) analysis. METHODS: Tissue DNA from samples of 26 invasive cervical cancers (9 in stage I, 10 in stage II and 7 in stage III), 31 CINs (12 CINI, 10 CIN II and 9 CIN III) and 33 normal cervixes was extracted, and then digested with methylation sensitive restriction endonuclease Hha I. HUMARA fragment was amplified with PCR method and PCR product was electrophoresed. Clonality was assessed by observing the electrophoresis bands. RESULTS: Heterozygotic rate of HUMARA was 89%. Monoclonal rates of cervical cancer, CIN, and normal cervix were 92%, 38% and 10%, respectively. Differences between cervical cancer and CIN and between cervical cancer and normal cervix were both extremely statistically significant (P < 0.001). Difference between CIN and normal cervix was also statistically significant (P = 0.012). Monoclonal rate of cervical cancer in stage I, II, III was 6/7, 90% and 7/7 respectively, without significant difference between them (P > 0.05). Monoclonal rate of CINI, II, III was 20%, 38% and 63% respectively, showing increasing tendency with grade, but without significant difference between them (P > 0.05). CONCLUSIONS: Invasive cervical cancer is a result of clonal proliferation of cancer cells. Active intervention or close follow up should be given to CIN with monoclonality.

Adult↗