dc.description.abstract | Burkitt’s tumour exemplifies the popular belief that lympho-reticular tumours are relatively more common in African than elsewhere. At the time the present studies were contemplated, its exact histogenesis was controversial, its aetiology and pathogenesis were unknown. It was however clear as a result of the pioneer work of Dr. Denis Burkitt, that the tumour is predominantly a childhood cancer with remarkable predilection for the jaws, and preponderate in the wet tropical Africa.
Morphological studies were therefore undertaken using histological and phase contrast criteria, to characterize the tumour and classify it within the framework of modern nomenclature for lymphoreticular and childhood tumours seen at U.C.H Ibadan.
From a histological review of biopsies of lymphoreticular tumours seen in the Department of Pathology, U.C.H. Ibadan, it became evident that a histological diagnosis of Burkitt’s tumour was possible in most, but the characteristic “starry-sky” pattern is not by itself unique to the tumour. A “starry-sky” appearance produced by closely packed, hyperchromatic, monomorphic blast cells, interspersed by large, pale, well-differentiated histiocytosis considered pathognomonic; the appearance is shared only by hyperblastic lymphoid germinal centre.
The blast cells of Burkitt’s tumour were characterized as lymphoblasts and distinguished from the cells of other round cell sarcomas of childhood by phase contract cytology. The close similarity of the cells to phytohaemagglutinin transferred lymphocytes already observed by Pulvertaft (1964) and Wright (1966a) was confirmed. It was however, also noted that there is close resemblance between the cells and certain blast cells seen in preparations from reactive lymph nodes, and pressured to be blast cells from hyperplastic lymphoid germinal centres.
It is submitted that the lymphoblasts of Burkitt’s tumour can be distinguished by phase contrast cytology from those of conventional childhood lymphosarcoma. This finding establishes the occurrence of both types of solid lymphoblastic neoplasms of childhood in Nigeria, and is in support of the contention of Burkitt and Wright (Burkitt and Wright 1966, Wright 1966b) that the two are distinct entities. The titles “Burkitt’s lymphoma” is in consequence adopted, to emphasis the lymphomatous origin of the tumour and to distinguish it from conventional childhood lymphosarcoma.
Eight lymphoblast cell lines (OB1, OB2, OB3, OB4, OB5, OB6, OB7, OB8) Established from Burkitt’s Lymphoma provided readily available tumour material for use in experimental studies of the immunopathology of the tumour.
Immunofluorescence and in vitro cytotoxic tests as well as growth inhibition of Burkitt’s lymphoma cells were the parameters used to provide evidence for the conclusion that Burkitt’s lymphoma patients (untreated and in remission), as well as individuals with no history of the disease, do possess antibodies to antigens in Burkitt’s lymphoma. Significant differences in the incidence of positive individuals in the various groups tested led to the conclusion that the antibody was against a ubiquitous infective antigen to which Nigerians (and presumably individuals in other areas where the tumour is “endemic”) are readily exposed, more so than Americans.
The conclusions support the virus-induced hypothesis of Davies, (1962), Burkitt (1962b) and Stanley (1966) for Burkitt’s lymphoma. Speculative submissions are made on the pathogenesis of Burkitt’s lymphosa. Finally, capacity of Burkitt’s lymphosa cells for immunoglobin synthesis and secretion, demonstrated in preliminary experiments in collaboration with the Burkitt’s lymphoma study Group at U.C.H. Ibadan, confirms the suspicion of existence of host-defence mechanisms, raises hope of immunotherapy, and encourages future search for specific infective antigens related to the aetiology of the tumour. | en_US |