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Biomedical subjects

B Acker

Publications and source records attributed to B Acker.

6 recordsLinked to original sources
PubMed1995

Small cell carcinoma of the cervix treated with concurrent radiotherapy, cisplatin, and etoposide.

A multimodality regimen of four cycles of cisplatin and etoposide with concurrent locoregional radiotherapy (XRT) has been, since May 1988, the standard therapy for women with small cell carcinoma of the cervix (SCCC). Prophylactic cranial irradiation was to be used in all but primary progressors. All 11 patients (median age 47; 4 with pure SCCC and 7 with mixed histology) seen by us were treated with this regimen. Only 1 patient progressed while on treatment. The 3-year overall and failure-free survivals were 28%. Four patients remain alive in first remission; the remaining 7 died (2 from toxicity, 5 from cancer). Although not statistically significant due to the small numbers, it appeared that the chance of long-term survival depended both on the amount of the cancer as indicated by the FIGO stage and size of the primary and also the performance status. The toxicity was significant with 70% experiencing severe neutropenia and 40% being admitted for control of emesis. This regimen is only appropriate for those women in whom all of the apparent tumor can be encompassed within a radiation field and who, in addition, have a performance status of 0 or 1. For the remainder it does not offer any chance of long-term survival and its toxicity renders it antipalliative.

Adult↗
PubMed1989

Potentiation of the tumor cytotoxicity of melphalan by vasodilating drugs.

Previous studies have shown that several vasoactive drugs can selectively reduce blood flow and increase hypoxia in experimental tumor systems. Our studies with one such agent, the vasodilator hydralazine, have clearly demonstrated that it can increase the tumor cytotoxicity of drugs which are known to be more toxic under hypoxic conditions. We have now extended our investigations to determine whether such selective reductions in tumor blood flow induced by hydralazine can increase the tumor cytotoxicity of other classes of cancer chemotherapeutic drugs. Our initial studies have involved the alkylating agent melphalan. Administration of hydralazine (5 mg/kg IP) at various times before or after melphalan results in increased tumor cytotoxicity in the Lewis lung carcinoma. An enhancement factor of between 2 and 3 was obtained in this tumor system. Similar results are observed if the vasodilator cadralazine is used. In contrast to the enhancement of the tumor cytotoxicity of melphalan by hydralazine, systemic toxicity is only increased by a factor of 1.2. Therefore, therapeutic gain may accrue from the use of vasodilating agents in combination with melphalan. Studies using spheroids to establish the mechanism responsible for the enhanced tumor cytotoxicity indicate that both hypoxia and pH can influence melphalan toxicity.

Animals↗
PubMed1987

The effect of hydralazine on the tumor cytotoxicity of the hypoxic cell cytotoxin RSU-1069: evidence for therapeutic gain.

The effect of the vasodilator hydralazine on both the tumor and systemic toxicity of RSU-1069 has been evaluated in C57B1 mice bearing Lewis lung tumors. The results obtained indicate that both hydralazine and RSU-1069 are cytotoxic to the Lewis lung tumor on their own. However, administration of hydralazine (5 mg/kg PO) at times up to either 3 hr before or 3 hr after RSU-1069 (0.1 mg/g IP) results in a level of cell killing greater than expected from additive effects. This potentiation by hydralazine was observed with doses of RSU-1069 from 0.01 to 0.1 mg/g. The results obtained using excision assays were confirmed using in situ growth delay as the endpoint. Growth delay (+/- s.e.m.) values for tumors to double in volume of 1.5 (+/- 1.2), 2.0 (+/- 1.3) and 6.0 (+/- 0.9) were obtained for hydralazine (5 mg/kg PO) alone, RSU-1069 (0.1 mg/g IP) alone and for hydralazine administered at the same time as RSU-1069 respectively. In contrast to the potentiating effect of hydralazine on the tumor cytotoxicity of RSU-1069, it had no significant effect on the systemic toxicity of RSU-1069 as measured by LD50/30d. No detailed studies to examine the mechanism responsible for the potentiation of tumor cytotoxicity have been performed in the present study. However, the results obtained would be consistent with previous reports that vasodilators such as hydralazine can selectively reduce tumor blood flow and thus oxygenation. Such reduced tumor oxygenation would increase the cytotoxic effects of RSU-1069 which is known to be more toxic to cells at reduced oxygen levels.

Animals↗
PubMed1983

Histologic conversion in the non-Hodgkin's lymphomas.

Between July 1, 1971 and December 31, 1978, 150 patients with favorable subtypes of non-Hodgkin's lymphoma [nodular poorly differentiated lymphocytic (NLPD), nodular mixed, or diffuse well differentiated lymphocytic] were entered into prospective randomized clinical trials at Stanford University. Treatments included involved field, total lymphoid, or whole body irradiation, single alkylating agent chemotherapy, combination chemotherapy with cyclophosphamide, vincristine and prednisone (CVP) or with cyclophosphamide, vincristine, procarbazine, and prednisone (C-MOPP), or various combinations of chemotherapy and irradiation. The initial complete response rate (CR) was 79%. Among patients who achieved a CR, 31% later relapsed. There were 78 patients who either failed to achieve a CR or achieved a CR and later relapsed. Histologic conversion (change from initially favorable to an unfavorable subtype of non-Hodgkin's lymphoma) was documented in 22/78 patients (28%). However, the actuarial risk for conversion was actually much greater (60% at 8 yr). The median time to documentation of conversion was 51 mo. The most common type of histologic conversion was from NLPD to diffuse histiocytic lymphoma. Documented histologic conversion was often associated with a more aggressive clinical behavior of the lymphoma, and the median survival after conversion was less than 1 yr. However, those patients who achieved a CR after conversion had a more favorable outcome (actuarial survival 75% at 5 yr). No specific risk factors predictive of histologic conversion could be identified.

Actuarial Analysis↗
PubMed1981

Delayed cerebral embolization of a shotgun pellet with fatal consequences.

A case of shotgun pellet embolization to the middle cerebral artery is presented. Embolization occurred approximately 36 hours following successful resuscitation of blood pressure, respirations, and neurologic function in a 21-year-old man who had sustained a massive chest wound. The diagnosis of pellet embolization was made within 8 hours of the onset of neurologic deficits; however, fatal cerebral infarction had occurred before surgery could be undertaken. Seven similar cases are briefly reviewed and it is concluded that low velocity and low kinetic energy missiles are more likely to embolize, and that left lower extremity injuries are more frequently involved in embolization. In all cases of shotgun trauma to the chest cerebral embolization of pellets should be considered at any sign of neurologic change and skull films obtained. Surgical intervention is necessary before cerebral infarction.

Adult↗