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PubMed2001

Circadian rhythms of basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), insulin-like growth factor-1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3), cortisol, and melatonin in women with breast cancer.

BACKGROUND: Circadian rhythms in plasma concentrations of many hormones and cytokines determine their effects on target cells. METHODS: Circadian variations were studied in cortisol, melatonin, cytokines (basic fibroblast growth factor IbFGF], EGF, insulin-like growth factor-1 [IGF-1]), and a cytokine receptor (insulin-like growth factor binding protein-3 [IGFBP-3]) in the plasma of 28 patients with metastatic breast cancer. All patients followed a diurnal activity pattern. Blood was drawn at 3h intervals during waking hours and once during the night, at 03:00. The plasma levels obtained by enzyme-linked immunoassay (ELISA) or radioimmunoassay (RIA) were evaluated by population mean cosinor (using local midnight as the phase reference) and by one-way analysis of variance (ANOVA). RESULTS: Cortisol and melatonin showed a high-amplitude circadian rhythm and a superimposed 12h frequency. bFGF showed a circadian rhythm with an acrophase around 13:00 with a peak-to-trough interval (double amplitude) of 18.2% and a superimposed 12h frequency. EGF showed a circadian rhythm with an acrophase around 14:20, a peak-to-trough interval of 25.8%, and a superimposed 12h frequency. IGF-1 showed a high value in the morning, which is statistically different (t test) from the low value at 10:00, but a regular circadian or ultradian rhythm was not recognizable as a group phenomenon. IGFBP-3 showed a low-amplitude (peak-to-trough difference 8.4%) circadian rhythm with the acrophase around 11:00 and low values during the night. CONCLUSIONS: (1) Circadian periodicity is maintained in hospitalized patients with metastatic breast cancer. (2) Ultradian (12h) variations were superimposed on the circadian rhythms of the hormones and several of the cytokines measured. (3) Studies of hormones and cytokines in cancer patients have to take their biologic rhythms into consideration. (4) The circadian periodicity of tumor growth stimulating or restraining factors raises questions about circadian and/or ultradian variations in the pathophysiology of breast cancer.

Analysis of Variance↗

PubMed2006

Integrative molecular concept modeling of prostate cancer progression.

Despite efforts to profile prostate cancer, the genetic alterations and biological processes that correlate with the observed histological progression are unclear. Using laser-capture microdissection to isolate 101 cell populations, we have profiled prostate cancer progression from benign epithelium to metastatic disease. By analyzing expression signatures in the context of over 14,000 'molecular concepts', or sets of biologically connected genes, we generated an integrative model of progression. Molecular concepts that demarcate critical transitions in progression include protein biosynthesis, E26 transformation-specific (ETS) family transcriptional targets, androgen signaling and cell proliferation. Of note, relative to low-grade prostate cancer (Gleason pattern 3), high-grade cancer (Gleason pattern 4) shows an attenuated androgen signaling signature, similar to metastatic prostate cancer, which may reflect dedifferentiation and explain the clinical association of grade with prognosis. Taken together, these data show that analyzing gene expression signatures in the context of a compendium of molecular concepts is useful in understanding cancer biology.

Androgens↗

PubMed1995

Lack of concordant p53 mutations in some paired primary and metastatic mouse squamous cell carcinomas induced by chemical carcinogenesis.

We studied the frequency and pattern of p53 mutations in 16 mouse skin primary squamous carcinomas induced by chemical carcinogens and their 19 matched metastases. The molecular changes were analyzed by polymerase chain reaction-single-strand conformation polymorphism and subsequent direct sequencing analysis. Eleven mutations of the p53 gene were detected in a total of eight primary tumors, and 10 mutations were detected in nine metastases. Only four pairs had identical mutations in primary and paired metastatic tumors. Eight mutations in six pairs were detected in primary tumors but not in their metastases, and four mutations from three matched pairs were detected in metastases but not in primary tumors. The four pairs that contained the same mutations in both the primary and secondary tumors had lymph-node metastases, and all mutations occurred in exon 8. Conversely, five of six pairs with p53 mutations only in primary tumors had lung metastases, and only one of the mutations occurred in exon 8. None of the mutations found only in metastases were located in exon 8. These data indicate that p53 mutations are prevalent in lymph-node metastases and infrequent in lung metastases of mouse skin tumors and that primary tumors with exon 8 mutations may be more likely to metastasize to the lymph nodes.

Animals↗

PubMed1987

Colon carcinoma metastatic to the thigh--an unusual site of metastasis. Report of a case.

Metastasis from colorectal carcinoma occurs by either lymphatic or hematogenous spread. The pattern of metastasis in patients with colorectal malignancy has been characterized by numerous clinical, surgical, and autopsy studies. The most common sites of colorectal metastasis are the liver and lung. Only two previous instances of colorectal carcinoma metastatic to skeletal muscle have been reported. The present report documents the third case of colorectal cancer metastatic to skeletal muscle and reviews the typical pattern of distant metastasis from colorectal carcinoma.

Adenocarcinoma, Mucinous↗

PubMed2001

EMA: a differentiation antigen related to node metastatic capacity of breast carcinomas.

Epithelial membrane antigen (EMA), also known as MUC1, is a mucinous glycoprotein fixed to the luminal domain of the epithelial cell membrane of normal breast ducts. However, in breast cancer cells, it is usually dispersed in the cytoplasm. EMA staining patterns of 330 breast carcinomas were examined, and three groups formed: lineal (16%), cytoplasmic (75%), and negative (9%). Although these patterns were somewhat related to histological cancer types, this was not statistically significant. However, EMA showed statistically significant univariate relationships to tumor grade, tumor size, estrogen and progesterone receptors, and nodal stage. Logistic regression analysis showed that among these variables, all of which were univariately related to node metastasis, only tumor size and EMA were independent nodal stage predictors. A combined analysis of these two factors revealed that the statistical probability of a tumor metastasizing to four or more nodes increased in each tumor size group from 0.9% to 12% for pT1, from 2% to 29% for pT2 and from 10% to 63% for pT3, depending on the EMA staining. The tumors showing a lineal pattern were the least metastasizing, while the EMA-negative tumors were the most. After recognizing these relationships between EMA staining patterns and other well-known differentiation markers and the lymph node metastatic capacity of carcinomas, and considering the results obtained by others on survival, one might conclude that EMA is both a differentiation marker and a histological prognostic factor.

Axilla↗

PubMed1985

Pathologic analysis of primary brain tumors.

Diffuse astrocytomas of the cerebrum, cerebellum, brain stem, and spinal cord are classified into three groups according to the degree of tumor anaplasia. These groups are the astrocytoma, anaplastic astrocytoma, and glioblastoma multiforme. Juvenile pilocytic astrocytomas have a better prognosis and are clinically and biologically distinct from the diffuse, fibrillary astrocytomas. The prognosis of astrocytomas depends not only on histologic characteristics, but also age of the patient, location of the tumor, and extent of surgical resection. The pattern of invasion into surrounding brain distinguishes gliomas from metastatic carcinomas and sarcomas. Topographic correlations have shown that malignant gliomas may invade the brain for distances of up to several centimeters from the enhancing rim seen on CT scan. However, the junction between glioblastoma and adjacent brain may also be fairly abrupt, with a peripheral margin of less than 1 mm. Recurrent glioblastomas are more widely invasive and often extend into areas that appear normal on CT scan. The optimal site for tumor biopsy corresponds to areas of contrast enhancement. Primitive neuroepithelial tumors are malignant neoplasms with a poor prognosis. They tend to recur locally and metastasize throughout the neuraxis via the CSF. It remains controversial whether these tumors should be classified as a single entity with the potential for differentiation along different cell lines, or whether the categories of neuroblastoma, spongioblastoma, ependymoblastoma, pineoblastoma, and medulloblastoma should be retained as specific entities. The medulloblastoma is the most common of these neoplasms, its clinicopathologic features are well characterized, and the current 5-year survivals of 50 to 60 per cent are better than for other "primitive" neoplasms. Glial fibrillary acidic protein is a specific marker for immature, reactive, and neoplastic astrocytes and ependymal cells. Although the absence of GFAP in a neoplasm does not exclude an astrocytic origin, the presence of GFAP indicates astrocytic or ependymal differentiation. This has important diagnostic applications. The expression of GFAP is used to distinguish astrocytic neoplasms from epithelial or mesenchymal tumors that may on occasion mimic a glioma. The detection of GFAP is also useful in the investigation of tumor histogenesis and differentiation both in vivo and in vitro. Although meningiomas exhibit a wide variety of histologic patterns, most tumors exhibit similar biologic and clinical behavior regardless of the histologic subtype.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed2006

[Vasculogenic mimicry--potential target for tumor therapy].

In 1999, Maniotis described a novel process by which tumors develop a highly patterned microcirculation that was independent of angiogenesis: in aggressive primary and metastatic melanomas, tumor cells generate non-endothelial cell-lined microcirculatory channels composed of extracellular matrix and lined externally by tumor cells. They named the process "vasculogenic mimicry" (VM). Folberg used PAS staining to show VM network, and identified 7 morphologic patterns of PAS-positive channels uveal melanomas which were confirmed as tubular type and patterned matrix type. Maniotis suggested PAS-positive patterns of VM in uveal melanoma are indeed a form of tumor microcirculation which is different from angiogenesis, and it is not a stromal host response at the interface between the tumor and the surrounding host stroma. VM has also been observed in carcinomas of the breast, prostate, ovary and lung, glioblastoma, synoviosarcoma, rhabdomyosarcoma, and phaeochromocytoma, and in the process of placenta formation from cytotrophoblasts. The molecular "signature" of aggressive melanoma cells is illustrative of an undifferentiated cell with a gene expression profile that is similar to that of embryonic-like cells. VE-cadherin, EphA2, laminin5 gamma2, matrix metalloproteinases (MMPs), vascular endothelial growth factor-C (VEGF-C), LYVE1, TF and NOTCH are important components of molecular switch of vasculogenic mimicry. The heterogeneity of tumor vasculature and the molecular regulation mechanisms present an opportunity for tumor therapy.

Animals↗

PubMed1999

Cutaneous lymphatic drainage in patients with grossly involved nodal basins.

BACKGROUND: The development of lymphatic mapping techniques has facilitated the identification of the sentinel lymph node (SLN), the first node in the regional basin into which cutaneous lymphatics flow from a particular skin area. Previous studies have shown that SLN histology reflects the histology of the entire basin, because melanoma metastases progress in an orderly fashion, involving the SLN before higher nodes in the basin become involved with metastatic disease. It is uncertain whether these orderly cutaneous lymphatic flow patterns are maintained in grossly involved basins. Lymphatic mapping was performed in a population of melanoma patients with clinically palpable lymphadenopathy to address this question. We aimed to determine whether the presence of gross nodal disease in the basin alters lymphatic flow into that basin so that lymphatic mapping techniques are not applicable, and, in patients referred with a grossly involved basin, whether preoperative lymphoscintigraphy should be performed to identify other regional basins at risk for metastases. METHODS: Eight patients presented with grossly palpable disease in the regional basin and underwent preoperative lymphoscintigraphy. All patients with palpable disease and all basins indicated by lymphoscintigraphy to be at risk were dissected. Three patients presented with clinically palpable nodes at the time of diagnosis, and five developed nodal disease on clinical follow-up after undergoing initial wide local excision only. A total of 10 basins in the eight patients were dissected. Of these, eight of the basins had grossly palpable regional nodal disease, and the other two basins were identified by preoperative lymphoscintigraphy as being at risk for metastases. The SLN was identified with intraoperative mapping, harvested, and submitted to pathology. Complete therapeutic lymph node dissections were performed following the SLN harvest in the basins with grossly palpable disease. SLN biopsy alone was performed in the two basins that did not have clinically palpable adenopathy but showed cutaneous lymphatic flow from the scintigram. RESULTS: Sixteen SLNs were harvested from these eight basins with grossly palpable disease, and 14 (87.5%) contained tumor. In each case, one of the SLNs was the grossly palpable node, and in six of the basins (75%) it was the only site of melanoma metastases. An additional 190 higher level, non-SLNs were removed, 32 (16.8%) of which contained microscopic foci of metastatic melanoma (P = .015). The null hypothesis that melanoma nodal metastasis is a random event is rejected. Two patients with trunk melanoma primary sites were identified to have other basins at risk for metastatic disease on lymphoscintigraphy. SLN biopsies were performed in these two patients, and one had microscopic nodal disease in the SLN. CONCLUSIONS: These data support the fact that cutaneous lymphatic drainage patterns are maintained in patients with grossly involved basins, thus buttressing the idea that the SLN is the node most likely to develop metastatic disease. Gross disease in the basin does not significantly alter cutaneous lymphatic flow into the regional basin, as the sentinel lymph node identified under these circumstances is the same as with the grossly involved node. Preoperative lymphoscintigraphy in patients who present with grossly involved nodes in one basin may identify other regional basins with micrometastatic disease and deserves further study in this setting.

Adult↗

PubMed1980

Metastasis-enhancing effect of heparin and its relationship to a lipoprotein factor.

The effect of low-dose heparin on spontaneous metastasis formation was studied with the PA-III rat prostate adenocarcinoma cell line model system. In LW rats given heparin iv at a dose of 1,000 U/kg body weight (three times/wk), the metastatic spread of implanted PA-III cells from the footpad through ipsilateral lymphatics to the lungs was enhanced. The weights of the draining lymph nodes (popliteal, inguinal, and axillary) and the number of lung tumor colonies were significantly increased compared with those in the saline-treated control tumor-bearing rats. The growth of the primary tumor was also enhanced. Heparin alone did not induce enlarged lymph nodes in rats nor did it change the growth pattern of PA-III cells in vitro. The accelerated metastatic spread of the PA-III cells was possibly related to the destruction of the oncolytic activity of the very low-density lipoprotein by the lipoprotein lipases induced by the iv administration of heparin. However, the possibility that other mechanisms could be operative in this phenomenon has not been ruled out.

Adenocarcinoma↗

PubMed2001

Monitoring metastatic behavior of human tumor cells in mice with species-specific polymerase chain reaction: elevated expression of angiogenesis and bone resorption stimulators by breast cancer in bone metastases.

Tumor-stroma interactions are of primary importance in determining the pathogenesis of metastasis. Here, we describe the application of sensitive competitive polymerase chain reaction (PCR) techniques for detection and quantitation of human breast cancer cells (MDA-MB-231) in an in vivo mouse model of experimental metastasis. Human-specific oligonucleotide primers in competitive PCR reactions were used to quantify the amount of MDA-MB-231 cells per tissue per organ. Using this species-specific (semi)quantitative PCR approach, gene expression patterns of (human) tumor cells or (mouse) stromal cells in metastatic lesions in the skeleton or soft tissues were investigated and compared. In all metastatic lesions, MDA-MB-231 cells express angiogenic factors (vascular endothelial growth factors [VEGFs]; VEGF-A, -B, and -C) and bone-acting cytokines (parathyroid hormone-related protein [PTHrP] and macrophage colony-stimulating factor [M-CSF]). In these metastases, PECAM-1-positive blood vessels and stromal cells of mouse origin are detected. The latter express angiogenic factors and markers of sprouting vessels (VEGF receptors flt-1/flk - 1/flk-4 and CD31/PECAM-1). Strikingly, steady-state messenger RNA (mRNA) levels of VEGF-A and -B and the major bone resorption stimulators PTHrP and M-CSF by tumor cells were elevated significantly in bone versus soft tissues (p < or = 0.05, p < or = 0.0001, p < or = 0.001, and p < or = 0.05, respectively), indicating tissue-specific expression of these tumor progression factors. In conclusion, MDA-MB-231 breast cancer cells express a variety of factors in vivo that have been implicated in metastatic bone disease and that correlate with poor survival of patients with breast cancer. We hypothesize that the observed up-regulated expression of angiogenic and bone-resorbing factors by the breast cancer cells in the skeleton underlie the clinically observed osteotropism of breast cancer cells and pathogenesis of osteolytic bone metastases. The application of the species-specific competitive PCR-based assay in vivo can provide new information concerning the involvement of gene families in tumor progression and metastatic disease and greatly facilitates the study of tumor-stroma interactions in cancer invasion and metastasis.

Animals↗

PubMed1995

Immunolocalization of interleukin-6 in salivary gland tumors.

Interleukin-6 (IL-6) is a multifunctional cytokine that regulates immune responses and acute phase reactions. It has demonstrated a growth factor function in several tumors, including those of salivary, plasma cell, and renal origin. We performed immunohistochemical staining for IL-6 localization on 57 salivary tumors. Reactivity was scored by intensity (0 to 4+) and percentage of cells staining, and the tumors were classified into three groups representing low (0 to 1+, 0% to 30%), moderate (2 to 3+, 31% to 75%), or high (> 3 to 4+, 76% to 100%) reactors. High reactivity was found in all primary pleomorphic adenomas (N = 10), five of eight recurrent pleomorphic adenomas, and all polymorphous low grade adenocarcinomas (N = 4). Moderate reactivity was observed in four of seven basal cell adenomas and three of five myoepitheliomas. Low reactivity characterized all acinic cell carcinomas (N = 3) and mucoepidermoid carcinomas (N = 3) as well as six of nine primary adenoid cystic carcinomas and all metastatic adenoid cystic carcinomas (N = 3). Carcinoma ex pleomorphic adenoma (N = 5) had three low and two moderate reactors. A pattern emerged in which the benign and low grade malignant tumors showed stronger reactivity than the metastatic or high grade malignant tumors. This suggests an inverse relationship between the presence of IL-6 and the biological aggressiveness of salivary gland tumors. The function of IL-6 in salivary gland neoplasia awaits further study and elucidation.

Humans↗

PubMed1998

Do HPA and PHA-L have the same binding pattern in metastasizing human breast and colon cancers?

Glycoconjugates on the tumour cell surface are functionally important for the interaction of the tumour cell with its environment. Several studies have demonstrated that particular carbohydrate residues on primary cancers are associated with metastasis. Identification of such residues is possible using lectins, including Helix pomatia agglutinin (HPA) which has a nominal monosaccharide specificity for N-acetyl galactosamine (GalNAc) and Phaseolus vulgaris leucoagglutinin (PHA-L) which recognizes beta1-6 branched oligosaccharides. Both lectins have been reported to be valuable prognostic markers in breast and colon cancers. In the present study, the binding patterns of both lectins were investigated on serial sections of human breast cancers and on metastatic and non-metastatic human breast and colon cancer cell lines grown in severe combined immunodeficient (SCID) mice. The two lectins gave very different staining patterns and HPA was more often associated with metastases than PHA-L. Our results indicate that both lectins are not simply recognizing different oligosaccharides associated with the same common metastasis-related glycoconjugate.

Animals↗

PubMed1994

Hormone-regulated genes (pS2, PIP, FAS) in breast cancer and nontumoral mammary tissue.

Expression of the hormone-regulated genes, pS2, prolactin-inducible protein (PIP) and fatty acid synthetase (FAS), was investigated by Northern blotting in primary breast carcinoma, metastatic breast cancer in axillary lymph nodes, in uninvolved breast tissue from mastectomies and in normal lymph nodes. There were considerable differences in expression of the genes between the tissues. The proportion of tissues containing PIP-mRNA decreased from uninvolved breast tissue to primary breast carcinoma to metastatic carcinoma. The reverse applied to FAS-mRNA which was found more often in metastatic cancer than in primary cancer, and least frequently in uninvolved breast tissue. Yet another pattern was observed for pS2 expression. The highest proportion of tissues demonstrating gene expression was found in primary breast cancer with both metastatic tumor and uninvolved breast tissue expressing the gene less frequently. pS2-mRNA and PIP-mRNA could only rarely be detected in trace amounts in normal lymph nodes. In contrast, FAS-mRNA was present in about one third of normal lymph nodes. Only pS2-mRNA showed an association with estrogen and progesterone receptor status.

Blotting, Northern↗

PubMed2005

Lymphangitic spread of breast carcinoma: scintigraphic pattern with chest x-ray and computed tomography correlation.

Lymphangitic spread of metastases has distinct patterns on pulmonary scintigraphy and radiographic imaging. A 43-year-old woman with metastatic breast cancer presented with shortness of breath. Symptomatology was studied with ventilation and perfusion (V/Q) scintigraphy, chest radiograph, and computed tomography (CT). The scintigraphic pattern is consistent with prior descriptions of lymphangitic spread of tumor. The chest x-ray and CT were both performed within the prior 2 months and were confirmatory.

Adult↗

PubMed2004

Mammaglobin and CRxA-01 in pleural effusion cytology: potential utility of distinguishing metastatic breast carcinomas from other cytokeratin 7-positive/cytokeratin 20-negative carcinomas.

BACKGROUND: The most common causes of malignant pleural effusions in women are metastatic lung carcinomas and breast carcinomas. It is often very difficult to distinguish between breast carcinomas and other metastatic carcinomas when they share a similar morphology and a similar cytokeratin profile (CK7-positive/CK20-negative [CK7+/CK20-]). To better differentiate between metastatic mammary carcinomas and other metastatic carcinomas in pleural effusion cytology, the authors studied the potential use of a novel antibody, CRxA-01, which was identified by a cDNA subtraction library, together with a well characterized antibody against mammaglobin. METHODS: A computer search for patients with malignant pleural effusion specimens between January 1992 and November 2002 generated 228 patients, 71 of whom had cell block material and a known clinical history. Primary malignancies among these patients included 20 breast carcinomas, 32 lung carcinomas, 4 endometrial carcinomas, 9 ovarian carcinomas, 4 gastrointestinal carcinomas, and 2 genitourinary carcinomas. All specimens were immunostained with anti-CK7, CK20, CRxA-01, and mammaglobin antibodies. Only CK7-positive/CK20-negative (CK7+/CK20-) specimens were included in the current study, and only definitive membranous staining for CRxA-01 and cytoplasmic staining for mammaglobin were considered to be positive. RESULTS: For patients with metastatic breast carcinomas, mammaglobin was positive in 11 of 20 (55%) tissue specimens and CRxA-01 was positive in 12 of 20 (60%) tissue specimens. When CRxA-01 and mammaglobin were used together, 16 of 20 (80%) tissue specimens were positive for mammaglobin or/and CRxA-01 antibodies. This staining pattern was not seen for tissue specimens from patients with other metastatic carcinomas. Two of 4 (50%) uterine carcinoma specimens and 6 of 9 (67%) ovarian carcinoma specimens were positive for CRxA-01 only. CONCLUSIONS: CRxA-01 and mammaglobin were expressed in most metastatic breast carcinoma specimens. Other CK7+/CK20- carcinoma specimens did not express mammaglobin and showed weak or negative staining for CRxA-01. When used together, CRxA-01 and mammaglobin greatly improved the sensitivity and specificity for the detection of metastatic breast carcinoma in pleural effusion specimens.

Antibodies, Neoplasm↗

PubMed2002

Identification of HLA-A3-restricted CD8+ T cell epitopes derived from mammaglobin-A, a tumor-associated antigen of human breast cancer.

Mammaglobin-A is highly overexpressed in breast cancer cell lines and primary breast tumors. This pattern of expression is restricted to mammary epithelium and metastatic breast tumors. Thus, mammaglobin-A-specific T cell immune responses may provide an important approach for the design of breast cancer-specific immunotherapy. The purpose of our study was to define the T cell-mediated immune response to mammaglobin-A. We determined that the frequency of mammaglobin-A-reactive CD8+ and CD4+ T cells in breast cancer patients is significantly higher than that observed in healthy female controls using limiting dilution analyses (p = 0.026 and p = 0.02, respectively). We identified 8 mammaglobin-A-derived 9-mer peptides with the highest binding affinity for the HLA-A3 molecule (Mam-A3.1-8) using a computer-assisted analysis of the mammaglobin-A protein sequence. Subsequently, we determined that CD8+ T cells from breast cancer patients reacted to peptides Mam-A3.1 (23-31, PLLENVISK), Mam-A3.3 (2-10, KLLMVLMLA), Mam-A3.4 (55-63, TTNAIDELK) and Mam-A3.8 (58-66, AIDELKECF) using an IFN-gamma enzyme-linked immunospot assay. A CD8+ T cell line generated in vitro against HLA-A*0301-transfected TAP-deficient T2 cells loaded with these peptides showed significant cytotoxic activity against the Mam-A3.1 peptide. This CD8+ T cell line showed a significant HLA-A3-restricted cytotoxic activity against mammaglobin-A-positive but not mammaglobin-A-negative breast cancer cells. In summary, our study identified four HLA-A3-restricted mammaglobin-A-derived epitopes naturally expressed by breast cancer cells, indicating the immunotherapeutic potential of this novel antigen for the treatment and prevention of breast cancer.

Breast Neoplasms↗

PubMed1982

A monoclonal antibody (B72.3) defines patterns of distribution of a novel tumor-associated antigen in human mammary carcinoma cell populations.

We report here both the range and patterns of reactivity of an IgG1 monoclonal antibody, B72.3, prepared against human, metastatic mammary carcinoma cells. When the avidin-biotin complex (ABC) immunoperoxidase technique was used on tissue sections, monoclonal B72.3 reacted with 19 of 41 (46%) primary mammary carcinomas and 13 of 21 (62%) metastatic lesions, either in axillary lymph nodes or at distal sites. Variable concentrations of antigen, recognized by B72.3, were observed among mammary tumors, as well as among different cell populations of a given tumor mass. Several patterns of antigen distribution were observed: membrane, diffuse cytoplasmic, focal and marginal. No reactivity was observed to normal mammary epithelium, stroma, or lymphocytes of the breast, nor to any cell types in a variety of other normal human tissues, melanomas, and sarcomas. Reactivity with all of four colon carcinomas was also observed. Assay of serial sections of mammary carcinomas with B72.3 and a monoclonal antibody directed against carcinoembryonic antigen demonstrated that these antigens were both distinct and non-coordinately expressed.

Antibodies, Monoclonal↗

PubMed1983

Characterization of the pharmacokinetics of bisantrene (NSC-337766).

The pharmacokinetics of bisantrene, 9,10-anthracenedicarboxaldehyde bis [4,5-dihydro-1 H-imidazol-2-yl) hydrazone) dihydrochloride were evaluated during a Phase I clinical investigation. Bisantrene at doses of 20 to 280 mg/m2 was administered by variable infusion rates to nine patients with advanced metastatic cancer. Bisantrene's plasma clearance followed a triexponential pattern with a harmonic mean terminal half-life (t1/2 gamma) of 26 h. The steady state volume of distribution (Vdss) was large, averaging 627 l/m2. Plasma clearance averaged 42.6 +/- 6.7 l/h/m2. The cumulative urinary excretion of bisantrene was 3.6 +/- 1.6% at 48 h.

Aged↗