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D M Thomson

Publications and source records attributed to D M Thomson.

At least 19 recordsLinked to original sources
PubMed1992

Routine use of hair root or buccal swab specimens for PCR analysis: advantages over using blood.

We report the use of hair roots and buccal cells as specimens of choice for DNA analysis of genetic diseases in a service laboratory. Our protocols using these specimen types show superiority to those using blood specimens in the areas of collection, transport, storage and overall cost. Our experience using these specimen types for 319 cystic fibrosis delta F508 mutation tests and 62 Leber's hereditary optic neuroretinopathy mutation tests leads us to recommend that hair roots and buccal cells should be evaluated as specimens of first choice when developing PCR DNA analysis.

Base Sequence↗
PubMed1979

Tube leukocyte adherence inhibition (LAI) assay in gastrointestinal (GIT) cancer.

Tumor-specific immunity to carcinoma of the colon, pancreas and stomach was assayed by tube LAI. Cancers of the colon, pancreas and stomach, were shown to possess organ-type specific neoantigens. In 115 patients with colon cancer, 100%, 75%, 61% with Dukes' A, B and C cancer were LAI positive, respectively. Even a microfocus of in situ cancer in a colon adenoma was sufficient to stimulate measurable tumor-specific immunity in the host. In Dukes' D cancer, 25% of patients with widespread metastasis were positive, whereas 100% with solitary lesions were positive. Reactive leukocytes from patients with colon cancer did not react to extracts of normal bowel mucosa or villous adenoma from LAI-negative patients. Leukocytes from 19% (3 of 16) of patients with colon adenomas reacted to the extract of colon cancer but not normal colon mucosa. Moreover, the LAI-positive response of the patients with colon adenomas or colon cancer is directed to a colon cancer TSA which is linked to beta2-microglobulin. These studies suggest that some colon adenomas express TSA before morphological evidence of cancer. It is not known if the acquisition of a cell surface TSA is an irreversible step toward unrestrained growth and metastasis. In pancreatic cancer, 100% of patients with cancers less than 5 cm and without metastasis were LAI positive, whereas 29% were positive when the cancer was greater than 5 cm or had metastasized. In Patients with stomach cancer, 100% with Stage II and 46% with Stage III and IV cancer were LAI-positive. Leukocytes from patients with other GIT cancers and from patients with inflammatory bowel disease or pancreatitis did not react with extracts of colon, stomach or pancreatic cancer. Leukocytes from patients with metastatic cancer, usually did not react in the tube LAI assay because their surfaces were coated in vivo with TSA. LAI reactivity was present when CEA was not detectable and when CEA levels were elevated LAI activity was often absent. The present study suggests that the automated tube LAI shows sufficient promise to warrant studies to determine its efficacy for the diagnosis of GIT cancers.

Adenoma↗
PubMed1979

Moiré topography.

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Interferometry↗
PubMed1979

Demonstration of tube leukocyte adherence inhibition assay with coded samples of blood.

Heparinized samples of blood from three different patients were coded by impartial observers. The buffy coat leukocytes from the coded samples of blood were isolated and incubated separately with extracts of colon and pancreatic cancer in the tube leukocyte adherence inhibition assay. At the completion of the assay, the leukocytes from Patient 1 were equally nonadherent to both cancer extracts with a nonadherence index value of 8. By contrast, leukocytes from Patient 2 exhibited increased nonadherence to the extract of colon cancer (p = 0.02) with a nonadherence index value to colon cancer antigen of 89. Leukocytes from Patient 3 displayed increased nonadherence to the extract of pancreatic cancer (p less than 0.05) with a nonadherence index value to pancreatic cancer antigen of 39. When the code was broken, patients 1, 2, and 3 had diagnoses of malignant melanoma, colon cancer, and pancreatic cancer, respectively. Hence, this was a classical criss-cross experiment; the patient with malignant melanoma reacted to neither of the antigens, whereas the patients with colon and pancreatic cancer reacted to the sensitizing cancers which had unique organ-type specific neoantigens.

Antigens, Neoplasm↗
PubMed1978

Leucocyte adherence inhibition for detecting specific tumour immunity in early pancreatic cancer.

Tumour-specific immunity to pancreatic tumour antigens, assayed by an automated tube leucocyte-adherence inhibition assay (L.A.I.), was detected in 3 of 3 patients with localised pancreatic cancer and 3 of 8 patients with more extensive pancreatic cancer. Leucocytes from pancreatic cancer patients with L.A.I. reactivity did not react to antigens of stomach, colon, or lung tumours; leucocytes from patients with stomach, colon, or lung cancer of inflammatory disease of the pancreas and bowel did not show L.A.I. reactivity to pancreatic tumour antigens.

Adenoma, Islet Cell↗
PubMed1978

Isolation of HLA and tumor antigens by means of affinity chromatography employing anti-beta2-microglobulin (beta2m) antiserum.

A method for the isolation of HLA antigen molecules from normal and cancerous solid human tissue is described. The method employs anti-beta2-microglobulin (beta2m) antiserum coupled to Sepharose beads as an immunosorbent affinity medium. The anti-beta2m affinity chromatography procedure greatly purifies and selectively enriches HLA and any material that copurifies by affinity, with beta2m and/or HLA molecules. The HLA isolated by this purification procedure was used to immunize rabbits. The antisera obtained were absorbed on beta2m to remove all anti-beta2m antibody activity. The use of such anti-HLA antisera in radioimmunoassays, immunoprecipitation studies, and F(ab')2 blocking experiments demonstrated that these antisera are directed against a common HLA determinant present on the heavy (alloantigen-bearing) chain of all HLA molecules. The use of an identical procedure employing human tumor tissues has resulted in the isolation of HLA-like or HLA-associated tumor-specific antigens as demonstrated by the leukocyte adherence inhibition (LAI) assay.

Antigens, Neoplasm↗
PubMed1978

Isolation of human tumour-specific antigens associated with beta2 microglobulin.

In the present study the tube LAI assay was used to monitor the isolation of the TSA of 4 different types of human cancers. Each tumour antigen was found to be specific for tumours arising in the organ from which the TSA was initially derived and which were histopathologically similar. Immunochemical studies revealed that these molecules co-isolate with normal human HLA antigens and are associated with beta2m. On Sephadex G-150, the majority of the papain-solubilized tumour antigen eluted in the mol. wt range 70,000-150,000. Analysis of this material by SDS-PAGE and 6M guanidine-HC1 column chromatography indicated that the material is composed of smaller subunits with prominent peaks at approximately 40,000, 25,000 and 12,000 mol. wt. Immunoadsorbent affinity chromatography of the solubilized tumour-membrane constituents on AH-Sepharose-linked horse anti-human-beta2m indicated that the tumour antigens, like HLA molecules, contain a beta2m subunit. The specificity of binding of TSA to the immunoadsorbent columns and the immunologically specific abrogation of LAI reactivity were clearly shown. The present study, therefore, indicates that by the isolation of beta2m, human tumour antigens can also be isolated, since human tumour antigens are associated with beta2m. Whether human TSAs may perhaps be modified histocompatibility antigens remains to be answered. Although the change upon malignant transformation in the pattern of the cell-surface proteins expressing the TSA determinant remains obscure, it would appear that for tumours arising within a given organ, a consistent alteration of cell-surface proteins occurs.

Antigens, Neoplasm↗
PubMed1978

The natural history of antitumour immunity in human breast cancer assayed by tube leucocyte adherence inhibition.

The specificity of the tube LAI in breast cancer was examined in a study with coded samples of PBL. In addition, 64 patients with breast cancer had their LAI reactivity monitored and correlated with their clinical status for up to 3 years after mastectomy. When patients were assayed by tube LAI, 83, 72, and 29% with Stage I, and II and III breast cancer respectively were positive. In Stage IV brest cancer, 88% of those with local recurrence and 15% of those with disseminated cancer were positive. By contrast, 3% of control subjects were LAI+. A select group of patients admitted to hospital with suspicious breast lumps that histopathologically proved to be benign breast disease (BBD) had a higher incidence of LAI+ (12%), whereas of outpatients with BBD only 2% were LAI+. Most breast cancer patients LAI reactivity became negative 2--4 months after mastectomy, even when some harboured micrometastases. LAI reactivity remained absent in those patients who remained clinically "cancer-free". In the follow-up patients, LAI activity returned about 4 months before local recurrence. LAI reactivity was observed in 7/8 patients in the coded study and 14/15 patients in the follow-up study preceding and/or at the time of local recurrence. A few patients (15%) progressed to widespread cancer without preceding positive LAI activity. The results suggest that tumour-specific immunity rapidly fades after surgery and may play no role in the rejection of micrometastases by 6 months after surgery. In addition, the present study has shown that the human hose manifests tumour-specific immunity when the cancer is small, and suggests that the early detection of human cancer would depend upon reliable methods to measure the tumour-specific immune response.

Breast Neoplasms↗
PubMed1978

A study of false positive and negative responses in the tube leucocyte adherence inhibition (tube LAI) assay.

A panel of 5 different breast-cancer and 2 other cancer extracts was used to clarify the false-negative responses in patients with Stage I and II breast cancer and the false-positive responses in control subjects. Most patients with Stage I and II breast cancer who had an initially negative LAI response were positive when tested against the panel. The false negatives occurred because of (1) the experimental errors of the assay; (2) changes in the antigenic strength of the extracts; (3) antigenic heterogeneity of a few tumours and (4) lack of tumour-specific reactivity of the host. 3% of control subjects had a false-positive LAI response. The leucocytes from most of these positive patients did not react to the panel of antigens, and hence the false positives appeared to result from experimental error. In-hospital patients with benign breast disease had a 12% positivity rate when initially assayed, and 63% of these patients reacted to the panel of breast-cancer antigens. Those patients with benign breast disease who reacted to the panel of breast-cancer antigens had cytophilic anti-breast-cancer antibody in their serum; their leucocyte LAI reactivity was blocked in an immunologically specific manner by serum from advanced Stage IV breast-cancer patients; their leucocytes reacted to extracts of breast cancer and not fibrocystic breast tissue; their leucocyte reactivity was blocked by isolated breast-cancer TSA that was linked to beta 2 microglobulin, but not by normal breast-tissue proteins; and the kinetics of the LAI response after excision of the breast mass was identical to that observed with breast-cancer patients after mastectomy. In these patients, the breast tissue within the breast lump expressed breast TSA similar to unequivocal breast cancer.

Antigens, Neoplasm↗