Comparison of DCMP vs BH-AC.DMP in the treatment of acute promyelocytic leukemia (APL) was made among 21 patients who had been diagnosed in our hospital and Aichi-ken Shokuin Hospital between January 1974 and December 1982. Age ranged from 18 to 65 years. Thirteen patients in 1974 to 1978 were treated with DCMP (daunomycin (DM) 25 mg/m²/day day 1 to 3, cytosine arabinoside 80 mg/m²/day, 6 MP 70 mg/m²/day and predonine 20 mg/m²/day day 1 to 10) whereas 8 patients in 1979 to 1982 were treated with BH-AC. DMP (DM 25∼40 mg/m²/day, BH-AC 170 mg/m²/day, 6 MP 70 mg/m²/day and predonine 20mg/m²/day day 1 to 7). The patients' characteristics of two groups were nearly identical. Complete remission rate was estimated 23.1% in DCMP and 75% in BH-AC. DMP, respectively. Overall, the median duration of these remissions was 18 mos. Failures were mainly due to hemorrhage as a result of disseminated intravascular coagulation. The patients who had less than 1×10⁴/cmm of leukocyte counts at diagnosis attained CR at a rate of 2/7 (28.5%) in DCMP and 5/6 (83.3%) in BH-AC. DMP.
With respect to the total dose of DM administered while remission induction, the dose of more than 360 mg closely correlated with high CR rate; 100% CR was achieved in BH-AC. DMP group. Early death due to hemorrhage was greatly prevented in the patients of BH-AC. DMP group who received preventive or therapeutic massive platelet transfusion and heparin therapy.
Thus, the combination of high dose DM, massive platelet transfusion and heparin is a main strategy for the treatment of APL.

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The serum lactate dehydrogenase (LDH) levels and isozyme patterns in 88 adult patients suffering from acute leukemia were measured prior to the initial treatment and subsequently in connection with prognosis. When analyzed with respect to subtypes in the FAB classification, the M 3 cases (acute promyelocytic leukemia, n=14) showed significantly (p=0.01) lower serum LDH levels than those with other subtypes. Correlation between the initial LDH levels and the number of cell counts (NCC) in the bone marrow was also studied: generally no significant relationship was found, but a linear correlation after logarithmic conversion was found between LDH and NCC for M 1, M 2 and M 3 cases. The dominant LDH isozyme in the patient's sera was usually types II or III, but it was frequently type IV in M 3 cases.
The initial LDH levels were not associated with the complete remission (CR) rate. Patients with normal or only slightly elevated LDH levels (LDH≤500 W.U), however, survived longer than those with markedly high initial levels (LDH>1,500 W.U). The differences became more apparent when the CR rate and 50% survival rate were compared in relation to LDH/NCC index; they were 76.3% and 15 mos., respectively, for the low index (index≤40) group and 55.3% and 8 mos., respectively, for the high index (index>40) group.

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Twelve adult patients with idiopathic thrombocytopenic purpura (ITP) were treated with vinblastine-loaded platelet (VLP) therapy at Jichi Medical School Hospital from December 1979 through April 1983. They were 3 males and 9 females, aged from 27 to 62 years old. Total of 25 courses of VLP therapy were administered to these patients. They consisted of 4 patients with refractory ITP, 7 patients who were unresponsive to glucocorticoids, and one patient who had not been treated with glucocorticoid because of gastric ulcer. Platelet counts were increased to 10×10⁴/cmm or above in 3 patients, to 5×10⁴/cmm or above in 3 patients, and to 2×10⁴/cmm or above in 4 patients with VLP therapy but 2 out of 12 patients showed no elevation of platelet count with this therapy. As for 4 patients with refractory ITP, 2 patients showed more than 10×10⁴/cmm of platelet count elevation. One out of 7 patients who were unresponsive to glucocorticoids showed platelet count elevation to 10×10⁴/cmm.
However, only one patient maintained the platelet levels of approximately 10×10⁴/cmm for a long time, whereas in the rest of the patients the platelet count elevation was transient although there was some clinical improvement of hemorrhagic diathesis. These results suggest that VLP therapy is beneficial in some patients with refractory ITP and might be worthy of trial just antecedent to splenectomy to avoid severe hemorrhages during the operation.

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Bone marrow examinations were performed by aspiration and Jamshidi needle biopsy in patients with malignant lymphoma. At the time of diagnosis, none of 13 patients with Hodgkin's disease had bone marrow lesion, while twenty (28%) of 71 patients with non-Hodgkin's lymphoma had bone marrow lesion. In non-Hodgkin's lymphoma, incidence of bone marrow involvement was variable according to histology, 42% in diffuse medium cell lymphoma in contrast to 13% in diffuse large cell lymphoma. Bone marrow was the most frequent site of extralymphatic organs affected by lymphoma at diagnosis. Of 31 non-Hodgkin's lymphoma patients in stage IV, 20 (61%) had bone marrow lesion. Clinical stage was converted to stage IV from stage I, II or III as a result of positive bone marrow examination in 10 patients; one (13%) of 8 in stage I, three (19%) of 16 in stage II and six (23%) of 26 in stage III. Biopsy seemed to be superior to aspiration as a technique for bone marrow examination.

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Chromosome analysis was performed on the cells from 31 patients of various lymphoid malignancies, including 26 non-Hodgkin's lymphomas, 3 Hodgkin's diseases and 2 immunoblastic lymphadenopathies, with special reference to prognosis. An abnormal karyotype was found in 30 of 31 patients. Structural abnormalities were particularly remarkable in the chromosomes of No. 14, 6, 3 and 19, and the most commonly involved chromosome was No. 14. As previously reported, it appears to be sure that a 14 q+ is limited to lymphoproliferative disorders and that a 14 q+ having a break point at 14 q1 (2-3) as well as 14 q 32 is significant as a clonal marker. In addition, present observations on the cases without 14 q translocation suggested that the structural abnormalities of No. 6 centromere, No. 18 centromere and No. 19 p or q should be also marked as a clonal marker. In our series, the abnormality of No. 6 was closely related to prognosis. Especially, the patients with a structural abnormality of No. 6 proximal region, namely from its centromere to q 15, had extremely poor prognosis. On the other hand, donor chromosomes of 14 q translocation was not significantly correlated to the prognosis.

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To investigate leukemogenesis in atomic-bomb survivors, cytogenetic studies on bone marrow cells were performed on 167 patients with radiation-related leukemias. The patients comprised 70 with acute non-lymphocytic leukemia (ANLL), 61 with chronic myelocytic leukemia (CML) and 36 with CML in blast crisis. The results were compared with those obtained from 301 with radiation unrelated leukemias. Thirteen cases with refractory anemia with excess of blasts (RAEB) were also examined. Statistical analysis of the data on the frequencies of chromosomal aberrations in survivors who were classified according to the estimated exposure doses of T 65 D, revealed that heavily exposed patients tended to have significantly higher aberration rates as compared to unexposed patients. Furthermore, chromosomal aberrations in survivors were observed to be of more complex nature. These observations therefore suggest that patients with a history of heavy exposure to atomic-bomb radiation exhibit complex chromosomal aberrations when they subsequently develop leukemia.
RAEB patients, both exposed and unexposed, were characterised cytogenetically by the presence of mosaic clones of normal and abnormal chromosomal pattern. In addition, a high prevalence of 5 q- was noted in the present series.
Based on the present data, a possible mechanism of leukemogenesis in atomic-bomb survivors has been suggested.

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Seventeen patients with advanced of non-Hodgkin's lymphoma (Intermediate grade of working formulation, 12 cases) and Hodgkin's disease (5 cases) receiving no prior chemotherapy were treated with CVP or C-MOPP at Saitama Cancer Center during December 1975 to June 1981. The overall complete response rate was 65% (11/17), with 7 of 12 patients with non-Hodgkin's lymphoma and 4 of 5 patients with Hodgkin's disease. The median survival for all patients was 41 months, and survival curve became flat at 52 months and was well sustained with an actuarial survival of 28%. Major side effects are myelosuppression and infections. In addition, kyphosis and compression fracture in vertebra possibly due to over-dose of prednisolone occurred in one female elder patient. In conclusion, CVP or C-MOPP combination chemotherapy was very effective for the remission induction and duration of median survival, while survival rate at 5 years was reduced.

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A case of cutaneous T-cell lymphoma with γ-chain in serum and urine is reported.
A 67-year-old woman, who had been suffuring from collagen disease for about 10 years, developed indurated plaques and skin tumors. Physical examination showed skin lesions such as the tumor stage of mycosis fungoides (M.F.) and generalized lymphadenopathy.
The skin tumor was histologically interpreted as cutaneous lymphoma classified as diffuse, medium-sized cell type, and the lymphnode as diffuse, small cell type of LSG classification.
The tumor cells had not nucleus with irregular convolutions such as M.F. cells. There were no Pautrier's microabscesses. Laboratory examination showed no leukemic change, but showed hyper γ-globulinemia and M-components in serum and urine.
These M-components were identified as γ-chain. Most of the neoplastic cells of the skin and lymphnode showed OKT 3+, OKT 6-, ERFC +, indicating that these cells had peripheral T cell phenotype. The subset of the tumor cells could not be identified.
VEPA chemotherapy was effective, but the patient died of sepsis and gastrointestinal bleeding 6 months after the diagnosis. An autopsy was performed.

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An 80-year-old man with IgD (λ) myeloma and acute renal failure was successfully treated by plasma exchange. After admission, he soon became uremic due to Bence Jones protein nephropathy and acute pyelonephritis, in spite of treatment including chemotherapy, diuretics and antibiotics. In his serum, a high level of monoclonal IgD (λ) and λ-type Bence Jones protein was observed on electrophoresis and high speed liquid chromatography. Plasma exchange was carried out by using an IBM 2997, and the patient serum was replaced with 4,000 ml of fresh frozen plasma. After plasma exchange, an approximately 73% of IgD and Bence Jones protein was removed from his serum, and diuresis increased. An excellent recovery from impaired renal function has been maintained for five months.

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A 33-year-old woman with scattered petechiae, gingiva bleeding and genital bleeding was admitted to the Keio University Hospital on March 30, 1981. Hyperthyroidism has been diagnosed for the past five years. On admission, platelets count was 4,000/μl, with increased megakaryocyte in bone marrow and antiplatelets antibody. Also her T₃-RIA was 530 ng/dl and T₄ was 30 μg/dl and TSH was 1 μg/ml and she had a diffuse, soft goiter. Then her illness was diagnosed thrombocytopenia associated with hyperthyroidism and treated with PSL and Mercazol but platelets count did not increase. Since admission, her behavior and speech was abnormal. On April 3, 1981, she complained with a little headache, so that we examined her with brain CT scan which revealed high density area at her right frontal lobe. On May 21, splenectomy was done, then platelets count increased at level of 20×10⁴/μl and thyroid function was within normal limits and her psychotic state and intracranial hemorrhage was improved.
It suggested that intracranial hemorrhage in ITP was unexpectedly higher incidence, especially in ITP associated with hyperthyroidism.

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A 50-year-old man was admitted to the hospital in July, 1981 because of general amlaise, lymphadenopathy, hepatosplenomegaly and generalized trichophytosis. His white blood cell count was 177,000/cmm and peripheral blood smear showed marked increase of abnormal lymphoid cells with convoluted nuclei, which were compatible with adult T-cell leukemia. His chest X-ray films revealed pulmonary infiltration in both lower lung fields. Abdminal computed tomography showed multiple low density areas in the liver, suggesting leukemic infiltration. He was treated with total body irradiation as a primary therapy. Daily doses of 10 rad were given 5 times a week by using Linac, Mitsubishi ML III. A total dose of 150 rad was administered over a period of three weeks. Abnormal lymphoid cells in the peripheral blood rapidly decreased although significant pancytopenia developed as well. About a month after the completion of total body irradiation, he entered the complete remission with normalization of peripheral and bone marrow pictures. His remission continued over sixteen months without any maintenance therapy.
Most of the ATL patients are lost for a short period of time following multi-agent chemotherapy and/or conventional irradiation therapy. The clinical course of this patient suggests that total body irradiation could be a primary treatment of choice for adult T-cell leukemia patients.

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A case of adult T-cell leukemia/lymphoma was reported in a child of korean born Japanese. A 34-year-old man, suffering from upper abdominal pain, general fatigue and fever for a week, admitted on July 10, 1982. At admission, he had generalized lymphadenopathies, and his peripheral leukocytes count was 84,200/mm³ with 46% leukemic cells containing convoluted nucleus. In the bone marrow, 25.2% of nucleated cells were leukemic cells. Anti-ATLA antibody was 10-times positive. A histology of biopsied lymph node was compatible with that of non-Hodgkin's lymphoma, pleomorphic type. Based on above-mentioned findings, this case was diagnosed as adult T-cell leukemia/lymphoma. The parents of this patient were born in south-east Korea, and later emigrated into Japan. The patient was born and brought up at Ikeda City, Osaka. To our knowledge, there have been no report describing ATL in Korean.

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A 43 Year old woman, was admitted to our hospital with the complaints of wet cough due to bronchiectasis and low grade fever. Physical examination revealed the moist rales in the both middle pulmonary areas. Intravenous antibiotics [Piperacillin (PI-PC): 4 g/day] was continued for 19 days, also 4 g/day of PI-PC administration for 12 days after an interval of 1 week. High fever with markedly leucopenia was visited. WBC count was rapidly recoverd by an interruption of PI-PC. We investigated the effect of PI-PC by means of CFU-C derived colony assay system in vitro. The 2×10⁵ peripheral blood mononuclear cells, 10% patient's serum, PI-PC, and an equal number of patient bone marrow nucleated cells were seeded into 1.0 ml of 0.3% agar gel containing McCoy's 5 A medium, 20% FCS, 10% human placental conditioned medium in the plastic petri dish (# 3001, Falcon). Seven days incubation was done at 37°C under an atmosphere of fully humidified 5% CO₂. A mass of more than 40 cells was counted as a colony under an inverted-microscopy. As a result, the coexsisting of PI-PC, patient's mononuclear cells, and serum in our culture system suppressed patient's CFU-C originated colony formation especially granulocytic series specifically.
This result suggests that an immunological mechanism may play in the pathogenesis of our case.

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A 30-year-old male long term survivor, 2 years and 7 months, after blast crisis in CML was reported.
On admission after chronic phase, 7 years and 9 months, the bone marrow was replaced almost completely by the blasts.
Morphologically the blasts consisted of monocytoid cells (NAE (+), NaF (-)), and lymphoid cells (NAE (-)). The TdT activity of the blasts was high and the TdT by immunoenzyme method was positive in these two different kinds of the blasts simultaneously. At a year and 4 months after the onset of the blast crisis, a part of myeloid or monocytoid cells were positive for Fcγ-R and C₃b-R. At the last stage lymphoid cells were positive for Ia and CALLA. Moreover a part of myeloid or monocytoid cells were positive for OKM-1.
The patient has responded to the VP therapy temporarily but not attained any remission. In spite of the COAP and AraC-VAMP therapy, he died of cerebral hemorrhage.

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A 49 year old Japanese housewife suffered from easy infectibility since her childhood, and had many dental caries in her twenties. At age of 33 years, she was diagnosed as having a psychomotor seizure and so diphenylhydantoin (200 mg/day) has continuously been given until her death. About 4 years before admission, she noticed dry mouth and left parotid gland swelling, and was diagnosed as Sjögren's syndrome. About the same time she noticed a waxing and waning systemic adenopathy. At age of 48 years, the lymph node biopsy revealed reactive lymphadenopathy with obliterated normal structures due to a proliferation of large lymphoid cells and plasmacytoid cells, some of which possessed monoclonal cytoplasmic IgM, κ. Systemic lymphadenopathy (neck, axilla, inguinal lesion, etc.) was waxing and waning again spontaneously. At age of 49 years, she was diagnosed as malignant lymphoma (diffuse, large cell type, immunoblastic of B cell) by left axillar lymph node biopsy. She died of GI tract and pulmonary bleeding. At autopsy advanced distribution of malignant lymphoma was confirmed. In this report the relation between Sjögren's syndrome and malignant lymphoma is discussed.

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A family with storage pool disease, which is one of the abnormalities of platelet release reaction, was presented. A 28 year-old-female had been suffered from epistaxis since childhood. She also experienced episodes of massive bleeding due to appendectomy in 17 years old, and to left mastoidectomy by breast cancer in 27 years old. She has the tendency of hypermenorrhea and petechiae. There was no abnormalities of peripheral blood nor bone marrow pictures. Bleeding time, PT, APTT and factor XIII were normal. Platelet clot retraction was also normal. Adhesion to glass beads was slightly decreased. The absence of collagen-induced platelet aggregation, or second wave of ADP and epinephrine-induced platelet aggregation were observed. The uptake of serotonin was reduced and MDA formation by exogenous arachidonate was normal. The other study showed the deficiency of the granules themselves, but there was no defect of the intracellular mechanism by which the secretory process is mediated. In her family studies, collagen-induced aggregation was absent in her mother, and one of the brothers and sisters. Electron miroscopy revealed an absence of dense granules. From these findings, this patient was suggested to be a case of δ-SPD with autosomal dominant inheritance.

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A 41-year-old male who had been suffering from Ph¹-positive chronic myelogenous leukemia for 5 year was admitted to the Keio University Hospital on 16 August 1982 because of occasional nasal bleeding and easy fatigability. A peripheral blood examination on admission showed marked leukocytosis with a blast content of 10 percent and thrombocytopenia. Chromosomal aberrations, in addition to the high blast content, indicated that the patient was in the blastic phase.
The patient responded well to treatment with vincristine and prednisolone, but suddenly developed marked tachycardia and cyanosis while in a hematologically well-cotrolled condition and expired within a few hours. An autopsy revealed an enlarged pericardial sac containing a straw-colored effusion and a diffuse infiltration of immature leukemic cells into the patient's pericardium. Acute cardiac tamponade due to leukemic cell infiltration was confirmed as the cause of death.

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A 54-year-old housewife with acute myeloblastic leukemia in relapse was admitted because of vomiting, abdominal pain, palpitation and dyspnea. The hemoglobin value was 5.9 g/dl, RBC 310×10⁴/μl, platelets 10⁴/μl, and WBC 50.7×10⁴/μl with 76% myeloblasts. Chromosome analysis revealed monosomy 7. Arterial blood pH was 7.127, PO₂ 18.0 mmHg, Pco₂ 46 mmHg, HCO^-₃ 13.1 mmol/l. Serum Na value was 135 meq/l, K 5.4 mEq/l, Cl 100 mEq/l, blood glucose 87 mg/dl and creatinine 1.2 mg/dl. Serum lactate level was 132.1 mg/dl, pyruvate 4.9 mg/dl. A diagnosis of acute myeloblastic leukemia with lactic acidosis was made. The patient died soon after admission. Marked leukemic infiltrates were found in the liver, spleen, bilateral lungs and bone marrow at postmortem examination, which might account for the tissue hypoxia. Specimens of the liver obtained at autopsy were examined for key enzymes of gluconeogenesis. Reductions in enzymatic activities of pyruvate carboxylase, phosphoenolpyruvate carboxykinase, fructose-1-6-diphosphatase and glucose-6-phosphatase were observed. It is suggested that the suppressed gluconeogenesis due to leukemic infiltrates in the liver may be one of the causes of severe lactic acidosis.

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74-year-old woman, who was a native of Saitama prefecture, was admitted to our hospital because of discomfort in epigastrium in May 1982. Physical examination on admission revealed no lymphadenopathy, hepatosplenomegaly and skin lesions. RBC was 385×10⁴ per cmm, Hb 11.9 g per dl and Ht 36.4%. WBC was 39,400 per cmm with 92.5% lymphoid cells. Platelet was 20.5×10⁴ per cmm. Bone marrow showed 70% lymphoid cells. Lymphoid cells had not convoluted nuclei typical in ATL and responded normally to PHA and Con A. Immunological examination showed 98% sheep ERFC, 99% OKT 3⁺, 97% OKT 4⁺, positive C3d receptor, negative TdT, negative anti-ATLA antibody and negative proviral DNA, indicating that these lymphoid cells had peripheral mature T cell phenotype. Lymphangiography showed no abnormal accumulation. The clinical diagnosis of T cell CLL was made.
In September 1982, she was noted splenomegaly without lymphadenopathy. WBC count increased remarkably and reached 420,000 per cmm with 98% lymphoid cells. Immunological natures of these lymphoid cells were similar to those of leukemic cells before crisis. Combined chemotherapy with vincristine, methotrexate, ACNU and prednisolone was ineffective and she died in November 1982.
At autopsy, the infiltration of lymphoid cells was observed in bone marrow, liver, spleen, kidney, thyroid glands and cerebrum, and no remarkable lymphadenopathy was seen.

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The differentiation induction of leukemic cells was attempted with drugs in three cases of acute myeloid leukemia. These cases were acute myeloblastic leukemia, acute myeloblastic leukemia with myelofibrosis and refractory anemia with excess of blasts (RAEB). Two patients were treated with prednisolone (30 mg per day orally) or methylprednisolone (24 mg per day orally) and another patient with small doses of ara-C (15 mg per day intravenously). After the administration of drugs, peripheral and marrow leukemic cells decreased without cytopenia in all patients. Simultaniously, mature granulocytes or monocytes increased in the peripheral blood and bone marrow.
Theses results might suggest that leukemic cells differentiated into mature cells by prednisolone or small doses of ara-C. In a case of acute myeloblastic leukemia with myelofibrosis, NAP activity decreased on admission and was still low for a period of remission after chemotherapy, indicating that peripheral mature granulocytes originated from leukemic myeloblasts.
The analysis of many similar cases and the detection of specific markers for granulocytes or monocytes derived from leukemic cells might be necessary to elucidate the differentiation of leukemic cells.

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A case of acute myelogenous leukemia (AML) associated with acute febrile neutrophilic dermatosis (Sweet's syndrome) is reported.
The patient was a 62-year-old female who had been diagnosed as AML and received several courses of combination chemotherapy with aclarubicin, behenoyl-ara-C, 6-mercaptopurine and steroid hormone, but she did not reach complete remission for 9 months when the patient developed fever, arthralgia and raised painful erythema and her face was studded with vesicles. Histologically the lesions showed dense infiltration of mature polymorphonuclear leukocytes, although, no leukemic cells were found. Bacterial culture of blood and vesicular fluid were negative. The vesicles were diminished in size with scar formation without specific treatment, and after one month slightly atrophic patches were left at the site of cutaneous involvement.
In 1964 Sweet described this cutaneous syndrome and termed it acute febrile neutrophilic dermatosis. A hypersensitivity reaction to streptococcus is strongly suspected as the etiology and pathogenesis of this syndrome. The same mechanism of pathogenesis is also suggested in our case, because skin reactions to streptococcus were positive although ASLO value was low. The possible mechanism of the frequent association of Sweet's syndrome with malignancies especially with leukemia is discussed.

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A 79-year-old man with chronic bronchitis was hospitalized because of anemia and leukopenia. Peripheral blood smears revealed elliptocytes in 80% of red blood cells. Chemotactic activity as measured by the modification of Boyden's method was completely deficient; Chemotactic activity was O (normal, 220∼578), while in vivo neutrophil migration detected by skin window method was normal. Random motility was slightly decreased to 34μ (normal, 38∼55μ). Phagocytosis and NBT test showed a mild decrease. Serum chemotactic factor level was normal. In addition, serum IgE was elevated to 1739 IU/L (normal, less than 400). The number of B lymphocytes detected as EAC-rosette forming lymphocytes and surface-Ig bearing lymphocytes were markedly decreased to 1.3% (normal, 8.7∼17.2) and 2.9% (normal, 13.1∼29.5), respectively.
This is a very rare case in terms of elliptocytosis associated with defective neutrophil chemotaxis occurring at old age and B lymphocytopenia. It remains to be studied whether or not common defect in blood cell membranes is responsible for the deformity of red blood cells (elliptocytosis), impairment of neutrophil function (defective chemotaxis), and loss of surface Ig of lymphocytes (B lymphocytopenia).

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A 53-year-old man was diagnosed as having chronic myelogenous leukemia (CML) on January 8, 1982. Hematological findings of the peripheral blood and bone marrow were compatible with those in chronic stage of CML. Karyotype of the peripheral blood was 46, XY. t (9q+; 22q-). However, a few enlarged lymph nodes in which myeloblasts markedly infiltrated were felt in the left axilla. Chromosome analysis of the lymph node cells showed 46, XY, t (9q+; 22q-)/48, XY, t (9q+; 22q-), +19, +ph¹. Despite treatment with busulfan, 6 MP, prednisolone and vincristine, generalized peripheral lymphadenopathy developed 3 months after admission.
Increase of myeloblasts in the peripheral blood and bone marrow in number occurred in December, 1982. Karyotype of these cells was 46, XY, t (9q+; 22q-)/46, XY, t (9q+; 22q-), 2 q+/46, XY, t (9q+; 22q-), -7, +mar/48, XY, t (9q+; 22q-), +19, +ph¹. The patient was treated with intensive combination chemotherapy, but died of gastrointestinal bleeding on April 14, 1983.
At autopsy, there was generalized lymph node enlargenent which showed myeloblastic infiltration. Marked infiltration of the same cells was also seen in the bone marrow and spleen. There was ulcerative terminal ileitis with massive bleeding and peritonitis.
The evolution of blastic transformation in tumor formation pattern of CML was discussed.

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A case of 55-year-old man with T cell lymphoma of the left nasal hole origin was reported. The nasal lesion was a localized tumor with some ulceration and scale, and histology of the biopsied specimen showed proliferation of medium sized lymphoid cells in the form of “compartmentalization” and epidermal infiltration by the lymphoid cells. The lymphoid cells showed focal acid phosphatase activity, E_n rosette formation (84.7%), and Leu 2a positivity (16.9%). The lesion was diagnosed as malignant T cell lymphoma with probable nature of suppressor/cytotoxic T cells. He was treated by local irradiation of ⁶⁰Co (4,200 rads) with complete remission. Although this case may belong to the “nasal T cell lymphoma” (Ishii), considerable differences in the clinical findings and histological features were observed comparing with the five cases reported so far. Differential diagnosis between lymphomatoid granulomatosis (midline malignant reticulosis), “nasal T cell lymphoma” and cutaneous T cell lymphoma was discussed.

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