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Biomedical subjects

A Lipton

Publications and source records attributed to A Lipton.

206 records · Page 12Linked to original sources
PubMed1966

Intracellular forms of lambda deoxyribonucleic acid in Escherichia coli infected with clear or virulent mutants of bacteriophage lambda.

Weissbach, Arthur (National Institutes of Health, Bethesda, Md.), Allan Lipton, and Arnold Lisio. Intracellular forms of lambda deoxyribonucleic acid in Escherichia coli infected with clear or virulent mutants of bacteriophage lambda. J. Bacteriol. 91:1489-1493. 1966.-Infection of either the sensitive or lysogenic strain of Escherichia coli K-112S by lambda(+) leads to the formation of a new phage deoxyribonucleic acid (DNA) species having the properties of a twisted circular DNA duplex. This new phage DNA species is also seen in cells infected with clear or virulent mutants of lambda which cannot lysogenize, or do so at a low frequency. The sedimentation rate of circular lambda DNA duplex at various pH values and its lability were examined.

Carbon Isotopes↗
PubMedDate not supplied

The impact of 2D versus 3D quantitation of tumor bulk determination on current methods of assessing response to treatment.

PURPOSE: Measurements from sequential axial "2D" data in cancer patients are commonly used to assess treatment response or disease progression. This study compares the volume of tumor bulk calculated with 3D reconstructions with that calculated by conventional methods to determine if it might change patient classification. METHOD: All medical, gynecologic, and pediatric oncology patients under treatment who were evaluated with serial CT scans between January 1, 1992, and July 31, 1994, for whom the digital data were available were included in this study. For each tumor site, the maximum diameter and its perpendicular were measured and multiplied together to yield an area. The sum of areas of the measured lesions was used as an approximation of overall 2D tumor volume. In addition, the 2D area of each site was multiplied by its height, yielding a 2D volume. Last, the digital data were loaded into a 3D computer system and total 3D tumor volumes determined. All medical and gynecologic oncology patients were treated based upon the 2D area of tumor. The pediatric oncology patients were treated based upon the 2D volume of tumor measured as per standard practice. The members of each treating oncologic service assessed their patients as to how the other two methods would have changed their classification of the patients' response category. RESULTS: Four hundred thirty-three CT scans were performed in 139 patients, which included 204 baseline and 294 follow-up CT examinations. Seventy patients had new tumor foci and would have been classified as failure by all three methods of tumor bulk measurement. The 3D volume versus the 2D area method of tumor bulk assessment would have changed response categories in 52 of the 294 follow-up CT examinations (p < 0.0001). Thirty-five patients were recategorized from either "no response" to "failure" (21 patients) or "no response" to "response" (14 patients) categories. If only those follow-up studies without new metastatic foci are considered, the 3D volume versus the 2D area methods of tumor assessment would have changed the treatment response category in 23.2%. The use of the 2D volume method of calculating tumor volume of bulk tended to overestimate the overall tumor size by an average of 244 cm3 (p = 0.001). CONCLUSION: The 3D method of tumor volume measurement differs significantly from conventional 2D methods of tumor volume determination. Large prospective studies analyzing the usefulness of 3D tumor volume measurements and assessing possible changes in patient response categories would be required for full utilization of this more accurate method of following disease bulk.

Adolescent↗
PubMedDate not supplied

Hormone stimulation and chemotherapy in advanced prostate cancer: interim analysis of an ongoing randomized trial.

We report here in the interim analysis of an ongoing randomized clinical trial designed to test whether androgen priming enhances tumor chemosensitivity in men with stage D prostate cancer refractory to orchiectomy. All patients are continuously treated with aminoglutethimide and hydrocortisone, to lower adrenal androgen secretion, and are given cyclic chemotherapy. Patients in the stimulation arm receive also the synthetic androgen, fluoxymesterone, for 3 days before and on the day of chemotherapy. Of 57 patients entered to date, 41 have received adequate treatment to be evaluable. Response to therapy (objective remissions + stabilizations of disease) occurred in 17 of 18 evaluable patients (94%) randomized to the stimulation arm, and in 16 of 23 evaluable patients (70%) in the control group (p less than 0.025). Duration of response was not significantly different in the two groups (median: 9 months in the stimulation and 12 months in the control arm). With 30% of the total of 57 patients still alive, survival is not significantly different in the stimulation (median: 13 months) and control arm (median: 16 months). As expected, patients who responded to treatment lived significantly longer than those who failed to benefit. Two episodes of reversible spinal cord compression occurred during androgen administration. (The risk of this serious side effect may be reduced by performing a screening myelogram to rule out subclinical spinal metastasis). Our preliminary data suggest that androgen priming may enhance the tumoricidal effect of cytotoxic drugs in advanced prostate cancer. The lack of improvement in duration of response and survival may be explained by the large fraction of hormone-independent cells probably present in patients with tumors refractory to orchiectomy.

Aged↗
PubMedDate not supplied

Hormone stimulation and chemotherapy in advanced prostate cancer: preliminary results of a prospective controlled clinical trial.

Preliminary evidence suggests that the sensitivity of endocrine-dependent neoplasms to chemotherapy may be enhanced by transient hormonal stimulation of tumor growth. To test this concept, we are conducting a prospective controlled trial in men with stage D2 prostate cancer who have relapsed following orchiectomy. All patients are continuously treated with aminoglutethimide and hydrocortisone to lower adrenal androgen secretion plus cyclic chemotherapy. Patients in the stimulation arm receive, in addition, the synthetic androgen fluoxymesterone for 3 days before and on the day of chemotherapy. Of 41 patients entered to date, 26 are evaluable. Twenty-one (81%) obtained either an objective remission or stabilization of disease with a mean duration of 9+ months and 10 patients still responding. Thus far, the response rate is similar in the control and stimulation groups. Androgen administration was associated with a rise in acid phosphatase and usually a modest flare of symptoms except for 2 patients who developed spinal cord compression. These preliminary data indicate that the combination of aminoglutethimide and chemotherapy has a potent antitumor effect on advanced prostate cancer refractory to orchiectomy. A large number of patients and a longer follow up are needed to assess whether transient androgen administration potentiates the effect of chemotherapy.

Acid Phosphatase↗
PubMedDate not supplied

Evaluation of CEA and GCDFP-15 plasma level during hormonally induced cancer stimulation.

Preliminary clinical trials indicate that transient stimulation of breast and prostate cancer growth by hormonal means may enhance tumor sensitivity to chemotherapy. In none of these studies, however, has an attempt been made to measure parameters that might reflect perturbations in cell kinetics induced by the treatment schedules. While conducting two, controlled, randomized clinical trials in advanced breast cancer and prostate cancer using a similar approach, we have measured plasma levels of two tumor markers, carcinoembryonic antigen (CEA) and breast gross cystic disease fluid protein (GCDFP-15). These served as a possible means of monitoring hormonal stimulation of tumor growth. Both markers failed to increase following administration of estrogens to patients with breast cancer and of androgens to men with prostatic carcinoma. In contrast, transient stimulation of tumor growth probably occurred as shown by exacerbation of symptoms and, in patients with prostate cancer, rise in acid phosphatase. We conclude that CEA and GCDFP-15 are not useful for monitoring pertubations in tumor cell kinetics induced by hormone stimulative protocols.

Antineoplastic Combined Chemotherapy Protocols↗
PubMedDate not supplied

Growth inhibition of breast cancer cell lines by combinations of anti-P185HER2 monoclonal antibody and cytokines.

The p185HER2 oncogene is associated with poor prognosis in patients with breast cancer. Both anti-p185HER2 MAb and cytokines have been shown to downregulate p185HER2 expression. We investigated the effect of combinations of humanized 4D5, and anti-p185HER2 MAB, and the cytokines IFN-alpha, IFN-gamma or TNF-alpha on the growth of three p185HER2 positive human abreast carcinoma cell lines, SK-BR-3, BT-474, and MDA-MB-453. All three cell lines were treated with IFN-alpha (1000 U/ml) or IFN-gamma (1000 U/ml) or TNF-alpha (100 U/ml) with or without huMAb 4D5 (100 microM), and cell growth was determined on days 3-7. While IFN-alpha, IFN-gamma, TNF-alpha, and huMAb 4D5 all inhibited growth, an apparently additive inhibitory effect occurred using combinations of huMAb 4D5 plus cytokine, with huMAb 4D5 plus TNF-alpha causing the greatest growth inhibition. These results demonstrate the potentiation of growth inhibition of breast cancer cell lines by the combination of anti p185HER2 MAb and cytokines, and suggest that combinations of anti-growth factor receptor MAb and cytokines may be useful in the treatment of breast cancer.

Antibodies, Monoclonal↗
PubMedDate not supplied

Protein tyrosine kinase activity in breast cancer and its relation to prognostic indicators.

Tyrosine kinase dependent oncogenes and growth factor receptors are of prognostic importance in breast cancer, but the relation of cytosolic protein tyrosine kinase (PTK) activity to traditional prognostic indicators is poorly defined. We determined cytosolic PTK activity in tumor extracts of 61 women with invasive breast cancer, including 51 primary specimens and 12 nodal or metastatic specimens, 7 women with in situ breast cancer, and 8 control breast specimens. PTK activity (pmol/min/mg) was measured in a dot blot assay using phosphotyrosine antibodies to detect phosphorylated tyrosyl residues in the tissue extracts. Compared with control specimens (mean PTK = 20.5), tyrosine kinase activity was significantly greater in invasive primary cancers (mean PTK = 298.1; p = 0.0008), and nodal/metastatic specimens (mean PTK = 491.5; p = 0.0009). PTK levels of invasive cancers did not correlate with age (p = 0.36), tumor size (p = 0.83), nodal status (p = 0.37), estrogen receptor status (p = 0.66), or progesterone receptor status (p = 0.09). Thus, while tyrosine kinase activity is increased in breast cancer, correlations with traditional prognostic indicators were not found.

Breast↗