[High-dose cytarabine treatment: a promising therapy modality in acute resistant myeloid leukemias in recurrence]. / Hochdosierte Cytarabin-Behandlung: Erfolgversprechende Therapie-modalität bei resistenten akuten myeloischen Leukämien im Rezidiv.

High dose Cytarabin in relapsed and refractory acute leukaemia. High dose cytarabin can be very effective for the treatment of acute leukaemia resistent to conventional cytarabin doses. Therefore 10 patients (6 males, 4 females) with ages ranging from 18 to 58 years (median: 34 years) refractory to conventional induction therapy were treated with 1 hour infusions of high dose cytarabin (3 g/m2 q 12 h for 6 days) 2 patients got additional 20 mg/m2 doxorubicin on days 7 to 9. According to this treatment, in 5 of the 10 patients complete remissions could be achieved. Without further treatment 3 patients relapsed after 4, 7 and 15 months leading to death in 2 or 3 months. 19 months after treatment 1 patient is in complete remission, though demonstrating meningosis leukaemica 5 months after high dose cytarabin. Another patient relapsed 14 months after high dose cytarabin, reaching another complete remission after treatment according to a ALL/AUL protocol [7]. 2 patients died in bone marrow aplasia and 2 patients did not show any response, dying 11 months after high dose cytarabin application. All patients demonstrated vomiting, nausea, diarrhea and allopecia. Bone marrow was profoundly depressed in all patients with severe granulocytopenia and thrombocytopenia for periods from 7 to 34 days. 3 to 5 days after the end of high dose cytarabin therapy 3 patients developed acute ceratitis and 2 patients conjunctivitis. 3 patients showed erythrodermia of their skin with epidermolysis in 2 of these patients.

[Angioimmunoblastic lymphadenopathy. Evolution into malignant lymphoma (author's transl)]. / Angioimmunoblastische Lymphadenopathie mit Entwicklung eines malignen Lymphoms.

In the last years angioimmunoblastic lymphadenopathy (AIL) was interpreted mainly as a benign reactive lymphnode disease. Recently, the reports about a progression into malignant lymphomas have become more numerous. We present a case of a 74-years-old woman which was diagnosed as lymphogranulomatosis X at first. Four weeks later criteria of malignancy were evident. 7 months after beginning of the disease the patient died. Histological, cytochemical, cytophotometrical, electron microscopical and immunological findings are reported. With regard to the diagnosis AIL it must be kept in mind that an evolution into malignant lymphoma is not infrequent. Hereby obviously a variable differentiation can be expected.

Penetration of an ascitic reticulum cell sarcoma of the golden hampster into the body wall and through the diaphragm. A scanning electron microscopic (SEM) study.

SEM studies on infiltration of the ascitic form of the hamster reticulum cell sarcoma HaTu 25 into the ventral body wall and through the diaphragm were performed during 6 consecutive days after intraperitoneal transplantation. The findings allow an interpretation of the course of events based on 3 main stages: 1) Contraction of mesothelial cells with partial exposure of the submesothelial stratum. 2) Preferential attachment of tumor cells to these denuded areas. 3) Advance of tumor cells within defects gradually extening from the submesothelial stratum of the musculature. These stages were more pronounced and took a more rapid course at the peritoneal side of the diaphragm than at the body wall. At the pleural side of the diaphragm the appearance of single tumor cells within widened intercellular spaces of the mesothelium was recorded prior to the onset of penetration at the peritoneal surface. The rapid migration of tumor cells through the diaphragm as well as the particularly intensive tumor infiltration into this organ is thought to be connected with the mechanism of intravasation of tumor cells into the lymphatic plexus of the diaphragm. During the whole sequence of events, HaTu 25 cells were found to have maintained their spherical configuration and characteristic surface architecture. Apparently, growth pressure is of minor or no importance in this spacial mode of tumor penetration, rather the action of proteolytic enzymes elaborated by the tumor cells has to be taken into consideration.