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PubMed2026

Insights into glandular trichome biology from analysis of organ-specific gene expression programmes in cannabis, hop and tomato.

Glandular trichomes (GTs) are epidermal outgrowths in which diverse specialised (secondary) metabolites are synthesised and stored. Cannabis (Cannabis sativa L.) and its close relative hop (Humulus lupulus L.) have pharmaceutical and industrial significance due to the presence of these metabolites in their GTs. We examined the conservation or divergence of the specific transcriptional programmes underlying GT biology. To achieve this, we generated transcriptome atlases of trichomes, flower, leaf, stem and root for cannabis, hop and tomato. We found that 12.9, 10.1 and 16.8% of cannabis, hop and tomato genes, respectively, were expressed organ/tissue specifically across all organs/tissues. Transcription factors (TFs) on average accounted for 7.5% of the organ-specific transcriptome and likely regulate organ-specific functions. We also conducted weighted gene co-expression network analysis and gene regulatory network (GRN) analysis to identify key regulators of GT function across the species and validated our predictions by DNA affinity purification sequencing for a subset of the cannabis and tomato GT TFs. The GRNs specific to cannabis or hop GTs were enriched for TFs and target genes associated with specialised metabolism, reflecting their species-specific nature. Conversely, the shared GRN components (identified via orthology analysis) were involved in highly conserved processes, such as flavonoid biosynthesis, solute transport and metabolite storage. Together, these GRNs and the associated transcriptome atlases are valuable resources to improve our knowledge of GT function and organ-specific genome regulation.

Solanum lycopersicum↗
PubMed2001

Species and organ specificity of fumonisin-induced endothelial alterations: potential role in porcine pulmonary edema.

Fumonisins, mycotoxins that commonly contaminate corn, induce cardiovascular toxicity and pulmonary edema in pigs, leukoencephalomalacia in horses, and nephropathy in rats, rabbits, and lambs. The mechanisms of these species-specific target organ toxicoses are poorly understood. We have previously reported perinuclear accumulation of membranous material in pulmonary capillary endothelial cells of pigs fed fumonisin-containing culture material. We hypothesized that these endothelial accumulations may be important in the pathogenesis of fumonisin-induced pulmonary edema and target organ toxicity in other species. Both target and non-target tissues from fumonisin-exposed pigs, sheep, rabbits, and rats were examined ultrastructurally. Specifically, lung, liver, heart and kidney were examined. In agreement with our previous work (Gumprecht, L.A., Beasley, V.R., Weigel, R.M., Parker, H.M., Tumbleson, M.E., Bacon, C.W., Meredith, F.I., Haschek, W.M., 1998. Development of fumonisin-induced hepatotoxicity and pulmonary edema in orally dosed swine: morphological and biochemical parameters. Tox. Pathol. 26, 777-788), endothelial alterations were present in the pulmonary capillary endothelial cells of pigs fed fumonisin-containing culture material, but at doses that did not induce pulmonary edema, as well as in pigs injected intravenously with purified fumonisin B(1). These alterations were present only in the pulmonary capillary endothelium of pigs and not in other species. In addition, these endothelial alterations were not present in any other organ of pigs or other species examined. Thus, these endothelial alterations are induced by fumonisin B(1), but only in pulmonary capillary endothelium and only in pigs. Although evidence that these alterations play a role in fumonisin-induced pulmonary edema is limited, other endothelial functions may be affected by fumonisin treatment.

Animals↗
PubMed2005

New approach to immunotherapy against organ-specific autoimmune diseases with T cell receptor and chemokine receptor DNA vaccines.

Organ-specific autoimmune diseases are characterized by the presence of relapse and remittance of the clinical signs, and last for a long period of time in most cases without an appropriate treatment. Immunopathologically, T cells that respond to organ-specific autoantigens play an important role in the development of inflammatory lesions in the target organ. These pathogenic T cells that had been activated by various stimuli including preceding infection infiltrate the target organ in an antigen-specific manner and break the homeostasis of the organ. Furthermore, they secrete a large number of pro-inflammatory cytokines and chemokines, which recruit by-stander inflammatory cells in the lesion. Although general immunosuppressive drugs such as corticosteroid and cyclosporine are effective in suppressing clinical signs and inflammation, immunospecific therapy is essential for the establishment of long-lasting remission or complete cure. In order to achieve effective immunospecific therapy, several groups have focused on two key molecules that are deeply involved in pathogenesis of autoimmune diseases. One is the T cell receptor (TCR) expressed on pathogenic T cells and the other is the cytokine and chemokine receptor expressed in the target organ. Another important aspect of this issue is the reagent that is used for the suppression of the function of the key molecules. So far, monoclonal antibodies, peptide vaccines and DNA vaccines are the major reagents used for immunosuppressive therapies. In the present review, I introduce the results of immunotherapy obtained in my laboratory using TCR-based and chemokine receptor (chemoR)-based DNA in experimental autoimmune encephalomyelitis (EAE) and myocarditis (EAC) and discuss its effectiveness and pathomechanisms of immunosuppression. First, we administered DNA vaccines encoding pathogenic TCR Vbeta8.2, 10 (to Lewis rats) and 15 (to DA rats) and observed that these vaccinations protected animals from the development of EAE. Similar results were obtained in EAC. Second, DNAs encoding several chemoRs were prepared and administered after the challenge to neutralize the function of chemokines that are highly upregulated in the lesions. It was demonstrated that these chemoR DNAs suppress the relapse of chronic relapsing EAE and block the progression of EAC to dilated cardiomyopathy (manuscripts submitted for publication). These findings clearly indicate that DNA vaccination can be a powerful tool for treatment of organ-specific autoimmune diseases.

Animals↗
PubMed1986

Islet cell and other organ-specific autoantibodies in healthy first-degree relatives to insulin-dependent.

The presence of organ-specific autoantibodies including islet cell surface, cytoplasmic and cytotoxic as well as thyroid-gastric antibodies were determined in healthy, non-diabetic, first-degree relatives to 30 insulin-dependent diabetic (IDDM) children. Thirty healthy families without family-history of diabetes mellitus served as controls. The prevalence of organ-specific autoantibodies among the healthy members in the diabetic families was increased compared to the control families (p less than 0.005). Islet cell cytoplasmic antibodies were only detected in diabetes families, since 23% (7/30) of the probands and 7% (2/31) of the siblings were positive and all others negative. Organ-specific autoantibodies were associated with HLA DR3 only in the diabetes families (p less than 0.025) while autoantibody positive members in the control families were associated with HLA B7 (p less than 0.01). This study suggests that childhood IDDM occurs in families with an increased prevalence of organ-specific autoantibodies.

Adolescent↗
PubMed2005

Impact of highly active antiretroviral therapy on organ-specific manifestations of HIV-1 infection.

In the last 10 years, interesting results have been reported concerning the impact of highly active antiretroviral therapy (HAART) on the changing pattern of organ-specific manifestations of HIV-1 infection. There has been a clear step-wise reduction in the incidence of several opportunistic infections (OIs), particularly Pneumocystis carinii pneumonia, whereas a nonsignificant reduction in incidence has been observed for other organ-specific diseases, including invasive cervical cancer and Hodgkin disease. In addition, several organ-specific manifestations, including HIV-associated nephropathy, wasting syndrome and cardiomyopathy, are a direct consequence of damage by HIV-1, and so HAART may have a therapeutic effect in improving or preventing these manifestations. Finally, the introduction of HAART has seen the emergence of several complications, termed immune reconstitution inflammatory syndrome, which includes OIs such as cytomegalovirus vitritis, Mycobacterium avium complex lymphadenitis, paradoxical responses to treatment for tuberculosis, and exacerbation of cryptococcosis. Because not all HIV-1 organ-specific manifestations are decreasing in the HAART era, this review will analyse the influence of HAART on several organ-specific manifestations, and in particular OIs related to several organs, cerebral disorders and HIV-1-related neoplasia.

AIDS-Related Opportunistic Infections↗
PubMed1976

Non-organ specific autoantibodies in malignant diseases.

A significant increase in non-organ specific autoantibodies is demonstrated in13 per cent of the sera from 202 patients with histologically proven malignancies, as compared with only 4 per cent of sera from 214 age and sex matched control patients. It appears that the incidence of autoantibodies is related to the histological type of the tumour but not to the presence or absence of tumour dissenmination. While the control group shows the expected increase in both incidence and titre of autoantibodies with increasing age, the malignant patients show no such pattern i.e. in cancer patients autoantibodies occur with equal frequency and at similar titres regardless of age. The absence of an age related increase in incidence and titre of non organ specific autoantibodies does not appear to have been reported previously. Our findings lend support to the hypothesis that cancer is associated with a breakdown of immunological surveillance, not only in old but also in young cancer patients. Thus the findings of non organ specific autoantibodies, especially to smooth muscle antigen, in an apparently healthy adult could be considered evidence of such a breakdown, carrying with it an increased risk of neoplasia.

Adult↗
PubMed1993

Differential organ-specific expression of three poly(A)-binding-protein genes from Arabidopsis thaliana.

Poly(A)-binding protein (PABP) is considered an essential component of a eukaryotic cell; deletion of the PABP-coding gene in yeast leads to a lethal phenotype. PABP is implicated in numerous aspects of posttranscriptional regulation, including mRNA turnover and translational initiation. A nested set of degenerate PCR primers designed from regions conserved among yeast, Xenopus, and human PABP sequences was used to amplify genomic DNA fragments from Arabidopsis thaliana. Hybridization screening of genomic and cDNA libraries with a genomic PCR probe led to the isolation of three diverse Arabidopsis genes encoding PABPs, PAB1, PAB3, and PAB5. All three sequences contain the expected four RNA-recognition motifs. Sequence diversity between these genes equals or exceeds the diversity among animal and fungal sequences. One of the genes, PAB5, and its cDNA were completely sequenced. Its open reading frame encodes a 73.2-kDa protein containing a number of amino acid motifs characteristic of PABPs from different species. Moreover, in vitro synthesized PAB5 protein bound to poly(A)-Sepharose with high specificity. All three genes isolated showed organ-specific patterns of expression. PAB5 and PAB3 RNAs were detected only in floral organs, with the highest level of expression in immature flowers. PAB1 RNA was observed predominantly in roots, was less abundant in immature flowers, and was not detected in any other organ examined (stems, leaves, mature flowers, siliques). This suggests a potentially unique role for PABPs in organ-specific posttranscriptional regulation in plants.

Amino Acid Sequence↗
PubMed1998

Organ-specific autoimmunity and genetic predisposition in interferon-treated HCV-related chronic hepatitis patients.

AIMS: Interferon alpha has been reported to enhance autoantibody production and to increase the risk of autoimmunity particularly against thyroid tissue. We designed a study with the following aims: 1) to assess the incidence of organ- and non-organ-specific autoantibodies during Interferon treatment; 2) to evaluate whether these autoantibodies have any clinical relevance; 3) to establish whether the development of autoimmune disorders can be related to a genetic predisposition. METHODS: A panel of 5 non-organ-specific and 6 organ-specific autoantibodies was evaluated in serum samples collected before treatment and then at 3 and 12 months in 47 patients enrolled in a treatment protocol with a 2b-recombinant Interferon (3 MU, 3 times a week for 12 months). In the second part of the study we explored genetic predisposition for autoimmune disorders in 31 patients by DNA-HLA class II typing using Restriction Fragment Length Polymorphism (RFPL). RESULTS: Non-organ-specific autoantibodies were absent in all patients before and after Interferon. During follow-up 6 patients showed an increment in thyroid microsomal antibody titres; 3 of these also developed thyroglobulin autoantibodies; 3 of the 6 patients developed persistent hypothyroidism; a fourth had a transient subclinical hypothyroidism and a fifth had a transient subclinical hyperthyroidism. Two patients with initial positivity for ICA and PCA maintained their reactivity during treatment without impairment of the respective target organs. Eight out of 39 initially negative patients developed one or more organ-specific autoantibodies during follow-up. One of these developed a persistent hypothyroidism, and another developed insulin-dependent diabetes. HLA-typing did not reveal any particular allele frequency in patients with thyroid antibody positivity as compared with those without autoantibodies and controls. Moreover, four of the 6 patients positive for islet-cell antibodies were carrying the non-Asp 57 allele which is considered a marker of a genetic predisposition for insulin-dependent diabetes. CONCLUSIONS: These findings suggest that, besides the thyroid gland, pancreatic beta-cells could be a target of autoimmunity during Interferon-treatment for chronic HCV hepatitis. A genetic predisposition may be important, though insufficient alone, in the development of Interferon-induced autoimmune phenomena.

Adolescent↗
PubMed1994

The role of the spleen in the organ-specific metastasis of murine BW 5147 T lymphomas.

Organ-specific metastasis of tumour cells may result from selective invasion and growth or from selective host cell responses. The present study demonstrates how selective interactions with the host affect the metastatic pattern of two murine T cell hybridoma lines, derived from the BW 5147 thymoma. Upon intravenous inoculation into syngeneic mice BW-14 cells preferentially colonize the kidneys, whereas BW-19 cells metastasize mainly to the spleen and the liver. The organ-specific behaviour of the two cell lines appears to be determined by a differential interaction with the spleen microenvironment. Inoculation of BW-14 cells into splenectomized mice results in increased liver colonization, indicating a negative effect of the spleen on BW-14 tumour development in the liver. Macrophages are likely to be involved in this inhibition, since inoculation of BW-14 cells into macrophage-depleted mice also leads to increased liver and spleen metastasis. In contrast, inoculation of BW-19 cells into splenectomized mice results in decreased liver metastasis, which indicates that the spleen exerts a stimulating effect on BW-19 cells. Macrophages also appear to be involved in this stimulation, since macrophage depletion causes a similar decrease in liver and spleen colonization. Hence components of the splenic microenvironment, probably macrophages, exert inhibiting or stimulating activities on BW-14 or BW-19 cells respectively, thereby determining the subsequent liver or kidney colonization.

Animals↗
PubMed2004

[The correlation between the distant metastases and organ-specific symptoms in the patients with lung cancer].

In this study, the correlation between distant metastases and metastatic organ-specific abnormalities in patients with lung cancer was evaluated. There were 197 patients who have lung cancer with distant metastases in this study. 141 (71.5%) of them were nonsmall cell lung cancer and 56 (28.5%) of them were small cell lung cancer. While one site of liver, brain and bone metastases were detected in 128 (64.9%) patients, remainders (69 patients, 35.1%) had surrenal, renal, pancreatic, skin, lung, thyroid, abdominal lymph node metastases. Organ-specific symptoms, findings on physical examination and abnormalities in laboratory data were detected in 121 (56.5%), 45 (21%) and 52 (24.2 %) patients, respectively. Sensitivity of predilection of organ-specific symptoms for bone, liver and brain metastases were 67%, 43% and 74% and specificity were 86%, 90% and 76%, respectively. We concluded that organ-specific abnormalities were not so effective to predict metastases in lung cancer. We considered that this result could be due to retrospective analysis and not included enough patients.

Bone Neoplasms↗
PubMed1997

Organ-specific autoantibodies in coeliac disease: do they represent an epiphenomenon or the expression of associated autoimmune disorders?

BACKGROUND AND AIMS: The occurrence of autoimmune disorders and organ-specific autoantibodies has been reported in coeliac disease. We assessed the prevalence of organ-specific autoantibodies in coeliac patients and evaluated whether their finding is an expression of associated autoimmune diseases. METHODS: Sera from 70 coeliac disease patients were tested for thyroid microsomal, gastric parietal cell, adrenal cortex and pancreatic islet cell antibodies by indirect immunofluorescence on O blood group human tissues. RESULTS: Eighteen coeliacs (26%) were positive for at least one of the autoantibodies studied; thyroid microsomal antibodies showed a higher prevalence (21%) than parietal cell (11%), adrenal cortex (4%) and islet cell antibodies (3%). In 15 (21%) of the 70 coeliacs studied an association with autoimmune diseases was found, including insulin dependent diabetes mellitus (6 cases), autoimmune hepatitis (3 cases), hypothyroidism (4 cases), thyrotoxicosis (1 case) and dermatomyositis (1 case). One or more organ-specific autoantibodies were positive in 12 (80%) of the 15 coeliacs with autoimmune disorders in comparison with their positivity in 6 (11%) of the 55 coeliacs without autoimmune diseases (p < 0.0001). CONCLUSIONS: The finding of organ-specific autoantibodies in coeliac patients discloses the coexistence of a wide spectrum of immunological diseases.

Adolescent↗
PubMed2004

Organ-specific autoantibodies in children with Helicobacter pylori infection.

BACKGROUND: We compared the prevalence of organ-specific autoantibodies in a group of Helicobacter pylori infected children and a group of uninfected children and investigated the relationship between the presence of relevant autoantibodies and the status of the target organs. PATIENTS AND METHODS: One hundred and twenty-four children with dyspepsia (54 boys, 70 girls; mean age 10.5 years; range 4-19) underwent gastroscopy: 56 had H. pylori infection (31 girls, 25 boys), while 68 (37 girls and 31 boys), were H. pylori-negative. All sera were tested for the presence of: parietal cell autoantibodies (PCA), intrinsic factor autoantibodies (IFA), microsomial autoantibodies, thyroglobulin autoantibodies, islet cell autoantibodies, glutamic acid decarboxylase autoantibodies, adrenal cortex autoantibodies, steroid-producing cell autoantibodies; gastrin, pepsinogen A, pepsinogen C and anti-H. pylori antibodies. The histological features and the ureA and cagA genes were also considered. RESULTS: The frequency of organ-specific autoantibodies was higher in patients with H. pylori infection than in uninfected patients (chi2-test p < .0001). Specifically gastric autoantibodies were significantly higher: seven of the 56 H. pylori-positive children were PCA-positive and one was IFA-positive (chi2-test p = .0004). The presence of autoantibodies was not associated with any clinical or biohumoral signs of disease. CONCLUSIONS: Our study detected a relationship between H. pylori infection in childhood and the presence of organ-specific autoantibodies unassociated with any clinical or biohumoral signs of disease. Helicobacter pylori infection in childhood could trigger the onset of clinical autoimmune gastritis, and/or other clinical autoimmune diseases.

Adolescent↗
PubMed1987

Use of in vivo/in vitro unscheduled DNA synthesis for identification of organ-specific carcinogens.

There are still only a few in vivo short-term assay methods for predicting potential organ-specific carcinogens and mutagens in mammals, although such methods are required for evaluating the in vivo effects of in vitro mutagens. In the in vivo/in vitro UDS assay methods described here, chemicals are given to experimental animals and induction of UDS in target organs is determined by in vitro organ culture or primary cell culture in the presence of [3H]dThd. Incorporation of [3H]dThd into DNA is measured with a liquid scintillation counter or by autoradiography. These methods have now been applied to the glandular stomach, forestomach, colon, liver, kidney, pancreas, tracheal epithelium, nasal epithelium, and spermatocytes. With minor modifications, they may also be applied to other organs. The present review shows that induction of UDS in various organs correlated well with the induction of cancer in these organs. The present authors have used the present methods to identify some potential organ-specific mutagens and carcinogens in mammals. The present authors found that three dicarbonyl compounds, glyoxal, methylglyoxal, and diacetyl, induced apparent UDS and TDS in the glandular stomach, and other groups found that 2-NT, MA6BT, and CNEt6BT induced UDS in the liver. These in vivo/in vitro UDS assays are better than in vitro UDS assay for identification of potential organ-specific mutagens and carcinogens in mammals and are especially useful for identifying potential mutagens and carcinogens that are specific for certain organs, such as the stomach, liver, and kidney. They are also useful for examining the potential mutagenicities and carcinogenicities of carcinogen analogs. However, these methods are not suitable for general in vivo screening because they are not yet available for all organs. A further advantage of the methods is that they can be used to examine larger numbers of animals at one time than other methods for detecting DNA damage, such as alkaline elution or alkaline sucrose density gradient centrifugation. Glyoxal enhanced cancer induction in the glandular stomach by the administration of a limited amount of MNNG and then glyoxal afterward in the two-stage stomach carcinogenesis.

Animals↗
PubMed2003

Histochemical analysis reveals organ-specific quantitative trait loci for enzyme activities in Arabidopsis.

To identify genetic loci involved in the regulation of organ-specific enzyme activities, a specific histochemical staining protocol was used in combination with quantitative trait locus (QTL) analysis. Using phosphoglucomutase (PGM) as an example, it is shown that enzyme activity can specifically, and with high resolution, be visualized in non-sectioned seedlings of Arabidopsis. The intensities of staining were converted to quantitative data and used as trait for QTL analysis using Landsberg erecta x Cape Verde Islands recombinant inbred lines. Independently, PGM activities were quantified in whole-seedling extracts, and these data were also used for QTL analysis. On the basis of extract data, six significant (P < 0.05) loci affecting PGM activity were found. From the histochemical data, one or more specific QTLs were found for each organ analyzed (cotyledons, shoot apex, hypocotyl, root, root neck, root tip, and root hairs). Loci detected for PGM activity in extracts colocated with loci for histochemical staining. QTLs were found coinciding with positions of (putative) PGM genes but also at other positions, the latter ones supposedly pointing toward regulatory genes. Some of this type of loci were also organ specific. It is concluded that QTL analysis based on histochemical data is feasible and may reveal organ-specific loci involved in the regulation of metabolic pathways.

Alleles↗
PubMed1982

Predisposition to organ-specific autoimmunity in Obese strain (OS) chickens: reactivity to thyroid, gastric, adrenal and pancreatic cytoplasmic antigens.

In addition to thyroglobulin autoantibodies, some Obese strain (OS) chickens gave organ-specific reactions with the cytoplasm of thyroid acinar cells when the sera were tested by immunofluorescence. The staining pattern was similar to that seen with human antibodies to thyroid microsomes. A proportion stained the proventricular glands of the chicken stomach in a manner indistinguishable from that of pernicious anaemia sera containing parietal cell antibodies. Isolated examples of organ-specific reactions with adrenal and exocrine pancreas were also recorded. These findings strengthen the notion that the OS chicken represents an authentic model for human organ-specific autoimmune disease. The high incidence of non-organ specific reactions complicates but does not necessarily invalidate this view since normal chickens show a propensity to develop such antibodies. However the OS chicken appears to differ from the human in being hyper-responsive to antigens in general.

Adrenal Glands↗
PubMed1991

Developmental and organ-specific changes in promoter DNA-protein interactions in the tomato rbcS gene family.

The five genes encoding ribulose-1,5-bisphosphate carboxylase (rbcS) from tomato are differentially expressed. Transcription of the genes is organ specific and developmentally regulated in fruit and light regulated in cotyledons and leaves. DNase I footprinting assays were used to map multiple sites of DNA-protein interaction in the promoter regions of all five genes and to determine whether the differential transcriptional activity of each gene correlated with developmental or organ-specific changes in DNA-protein interactions. We show organ-specific differences in DNase I protection patterns, suggesting that differential transcription of rbcS genes is controlled at least in part at the level of DNA-protein interactions. In contrast, no changes were detected in the DNase I footprint pattern generated with nuclear extracts from dark-grown cotyledons versus cotyledons exposed to light, implying that light-dependent regulation of rbcS transcription is controlled by protein-protein interactions or modification of DNA binding proteins. During development of tomato fruit, most DNA-protein interactions in the rbcS promoter regions disappear, coincident with the transcriptional inactivation of the rbcS genes. In nuclear extracts from nonphotosynthetic roots and red fruit, the only detectable DNase I protection corresponds to a G-box binding activity. Detection of other DNA binding proteins in extracts from these organs and expression of nonphotosynthetic genes exclude the possibility that roots and red fruit are transcriptionally inactive. The absence of complex promoter protection patterns in these organs suggests either that cooperative interactions between different DNA binding proteins are necessary to form functional transcription complexes or that there is developmental and organ-specific regulation of several rbcS-specific transcription factors in these organs. The DNase I-protected DNA sequences defined in this study are discussed in the context of conserved DNA sequence motifs and previously characterized binding sites.

Base Sequence↗
PubMed1989

Generation of a monoclonal antibody (G9) reactive with an organ-specific, tumor-associated epitope of human colon carcinoma.

A monoclonal antibody (G9), having an organ-specific and tumor-associated reactivity with colon carcinoma, has been generated. Monoclonal antibody G9 is an IgG1 immunoglobulin produced by immunization of mice with mucin which had been purified from a liver metastasis of a moderately differentiated human colon carcinoma. Examination of normal adult tissues, by enzyme immunoassay and immunohistochemical procedures, showed the G9-reactive epitope to be restricted to the gastrointestinal tract. Within the gastrointestinal tract the colon produced the highest amount of the epitope. A sharp, decreasing gradient of reactivity was observed, ending in the small intestine. Although the normal colonic epithelium did produce the G9-reactive determinant, there was a significant quantitative increase of the epitope in neoplastic colonic tissue; mucins derived from normal colon contained less than 10% of the specific epitope as compared with mucins derived from colon cancer tissues (P less than 0.01). In addition, a tumor xenograft contained 100 times the amount of epitope as did normal colonic tissue. By immunohistochemical procedures 70% of all colon carcinomas were positive. A relationship with differentiation was noted, with 80% of well differentiated and 83% of moderately differentiated tumors being positive, whereas only 1 of 6 poorly differentiated tumors were stained. The organ specificity was noted in neoplastic as well as normal tissues. Monoclonal antibody G9 was nonreactive with breast, lung, and ovarian tumors. The data suggest that at the level of sensitivity obtained by the immunoassays used, and within the range of tissues examined, monoclonal antibody G9 is organ specific and highly tumor associated in its reactivity.

Animals↗