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Biomedical subjects

C M Haskell

Publications and source records attributed to C M Haskell.

At least 37 records · Page 2Linked to original sources
PubMed1981

L-Asparaginase: human toxicology and single agent activity in nonleukemic neoplasms.

The early hope that L-asparaginase would be a breakthrough in medical treatment, with selective toxic effects based on the qualitative presence or absence of a specific enzyme (asparagine synthetase), has not been realized. Despite its failure to live up to early hopes, L-asparaginase is now commercially available because of its usefulness in treating selected forms of acute leukemia and T-cell lymphoid neoplasms. By and large, hints of useful activity in other tumors have not been confirmed, and L-asparaginase remains experimental for all other indications. It is variably toxic in man, and severe toxic effects are not unusual. Toxic reactions are generally hypersensitivity reactions or depression of protein synthesis.

Adult↗
PubMed1981

Increased inactive creatine kinase B protein in the plasma of patients with malignancy.

Using a specific radioimmunoassay for enzymically inactive creatine kinase (EC 2.7.3.2) B protein (CK-Bi), we studied 139 patients with various malignancies. We found it to be increased in certain adenocarcinomas, including colorectal, lung, and prostate, as has also been reported for enzymically active CK-BB. Of 15 patients with leukemia or lymphomas with active disease, 12 also had increased values for CK-Bi in plasma. In these patients, concentrations of CK-Bi in plasma tended to correlate with disease activity, increasing with aggressive malignancy and decreasing on successful treatment. Thus, measurement of CK-Bi may constitute a sensitive means for detecting malignancy and, in certain subsets of patients, for monitoring therapeutic response.

Adenocarcinoma↗
PubMed1978

Chemo-immunotherapy for unresectable bronchogenic carcinoma.

Seventy-nine patients with metastatic or unresectable bronchogenic carcinoma were treated with a regimen of combination chemotherapy which included methotrexate, Oncovin (vincristine), cyclophosphamide, and adriamycin (MOCA), and were randomized to receive no additional therapy, immunotherapy with bacillus Calmette-Guérin, or immunotherapy with Corynebacterium parvum (C. parvum). The response rate and estimated median survival time were 68% and 42 weeks in small cell carcinoma and 18% and 29 weeks in other histologic types. Improved survival correlated with high performance status and response to therapy. Immunotherapy did not improve response, time to progression, or hematopoietic tolerance of chemotherapy. C. parvum was associated with significant morbidity and was poorly tolerated. MOCA appears to be of modest value in the treatment of bronchogenic carcinoma, particularly of the small cell type. A role for immunotherapy remains unproven.

BCG Vaccine↗
PubMed1977

Systemic therapy for metastatic breast cancer.

The data reviewed in this conference suggest that initial therapeutic decisions for patients with metastic breast cancer be based on the presence or absence of an estrogen receptor in the tumor. Patients with estrogen receptor in their original primary breast cancer or in a subsequent metastitic lesion are candidates for hormonal manipulation, whereas patients lacking estrogen receptor in their tumor are treated for their metastic disease with nonhormonal chemotherapy. Nonhormonal therapy usually consists of a combination of cytotoxic drugs including cyclophosphamide, methotrexate, and 5-fluorouracil (CMF). Other programs of combination chemotherapy are under active study, especially programs that include nonspecific immune stimulation with Corynebacterium parvum or bacillus Calmette-Guérin (BCG). Inasmuch as patients with Stage II primary breast cancer frequently have "micrometastatic" disease, combination chemotherapy is also under study as an adjuvant to surgery. Preliminary results strongly support the use of such therapy.

BCG Vaccine↗
PubMed1975

Metastatic carcinoid presenting as a spinal tumor.

A case of carcinoid tumor metastatic to the thoracic spine with associated myelopathy is described. Multiple posterior explorations were singularly unsuccessful in locating and indentifying the metastasis, but an anterior transthoracic exposure allowed identification of the tumor, removal of the osteoblastic epidural mass, and fusion of the spine with a rib graft. The patient's myelopathy improved steadily following surgery without evidence of tumor recurrence or regression of neurologic status. The reasons for the relative absence of central nervous system carcinoid metastases are not known.

Carcinoid Tumor↗