Showing papers on "Cancer published in 1983"

Hypomethylation distinguishes genes of some human cancers from their normal counterparts.

Abstract: It has been suggested that cancer represents an alteration in DNA, heritable by progeny cells, that leads to abnormally regulated expression of normal cellular genes; DNA alterations such as mutations, rearrangements and changes in methylation have been proposed to have such a role. Because of increasing evidence that DNA methylation is important in gene expression (for review see refs 7, 9-11), several investigators have studied DNA methylation in animal tumours, transformed cells and leukaemia cells in culture. The results of these studies have varied; depending on the techniques and systems used, an increase, decrease, or no change in the degree of methylation has been reported. To our knowledge, however, primary human tumour tissues have not been used in such studies. We have now examined DNA methylation in human cancer with three considerations in mind: (1) the methylation pattern of specific genes, rather than total levels of methylation, was determined; (2) human cancers and adjacent analogous normal tissues, unconditioned by culture media, were analysed; and (3) the cancers were taken from patients who had received neither radiation nor chemotherapy. In four of five patients studied, representing two histological types of cancer, substantial hypomethylation was found in genes of cancer cells compared with their normal counterparts. This hypomethylation was progressive in a metastasis from one of the patients.

A Detergent-trypsin method for the preparation of nuclei for flow cytometric DNA analysis†

Abstract: A new modification of our detergent technique for the preparation of nuclei for flow cytometric DNA analysis is described. The attainment of low coefficients of variation of the peaks and of quantitative staining of nuclei from different tissues was a problem with the original method. This was solved in the new modification by trypsinization of the unfixed nuclei. The nuclei were stabilized by spermine. A simple procedure for long-term storage of samples at —80°C was integrated into the method. The fluorescence of the nuclei was stable for at least 3 hours after staining. Light exposure protection of the samples was essential. No cell loss was caused by storage or staining. The method was successfully applied on samples including: (a) Normal tissues— human lymphocytes, granulocytes and spleen. Mouse lymphocytes, bone marrow, spleen, liver, kidney and thymus. (b) Human neoplasms— lung cancer, breast cancer, lymphoma, leukemia, bladder cancer and cancer of the oral cavity. (c) Human tumors in nude mice— breast cancer, lung cancer, melanoma and colon cancer. (d) Mouse ascites tumors— JB-1, L 1210, Ehrlich and P 383. It therefore seems well suited as a routine clinical procedure.

Cancer: Principles and Practice of Oncology

Abstract: Anyone who cares for or aspires to care for cancer patients should buy and read this book It will become the standard reference for what now is popularized as "multimodal" cancer therapy (chemotherapy, radiotherapy, and surgery) The arguments for reading this huge tome are straightforward: (1) cancer continues to be an overwhelming health problem; (2) more kinds of cancers are curable now than when most clinicians were trained; and (3) effective cancer therapy is becoming more complicated For those who have difficulty justifying the considerable purchase price, remember that the cost per pound for Cancer is less than that for veal (pointed out first to me by one of the editors!) DeVita, Hellman, and Rosenberg have organized their exposition superbly Initial summary chapters outline the magnitude of the clinical cancer problem, recent changes in the incidence of particular kinds of cancer, and the principles that underlie each of the three

The 5-methylcytosine content of DNA from human tumors

Abstract: The over-all 5-methylcytosine (m5C) content of DNA from normal tissues varies considerably in a tissue-specific manner. By high-performance liquid chromatography, we have examined the m5C contents of enzymatic digests of DNA from 103 human tumors including benign, primary malignant and secondary malignant neoplasms. The diversity and large number of these tumor samples allowed us to compare the range of DNA methylation levels from neoplastic tissues to that of normal tissues from humans. Most of the metastatic neoplasms had significantly lower genomic m5C contents than did most of the benign neoplasms or normal tissues. The percentage of primary malignancies with hypomethylated DNA was intermediate between those of metastases and benign neoplasms. These findings might reflect an involvement of extensive demethylation of DNA in tumor progression. Such demethylation could be a source of the continually generated cellular diversity associated with cancer.

Role of retinoids in differentiation and carcinogenesis.

Abstract: It has been known for more than 50 years that retinoids, the family of molecules comprising both the natural and synthetic analogues of retinol, are potent agents for control of both cellular differentiation and cellular proliferation (70). In their original clas sic paper describing the cellular effects of vitamin A deficiency in the rat, Wolbach and Howe clearly noted that there were distinct effects on both differentiation and proliferation of epithelial cells. During vitamin A deficiency, it was found that proper differentia tion of stem cells into mature epithelial cells failed to occur and that abnormal cellular differentiation, characterized in particular by excessive accumulation of keratin, was a frequent event. Furthermore, it was noted that there was excessive cellular proliferation in many of the deficient epithelia. Although the conclusion that an adequate level of retinoid was necessary for control of normal cellular differentiation and proliferation was clearly stated in the original paper by Wolbach and Howe, a satisfactory explanation of the molecular mechanisms underlying these effects on both differentiation and proliferation still eludes us more than 50 years later. It was inevitable that the basic role of retinoids in control of cell differentiation and proliferation would eventually find practical application in the cancer field, and there have been great ad vances in this area, particularly for prevention of cancer. Many studies have shown that retinoids can suppress the process of carcinogenesis in vivo in experimental animals (for reviews, see Refs. 7, 33, 51, 54, 56, and 57), and these results are now the basis of current attempts to use retinoids for cancer prevention in humans. Furthermore, there is now an extensive literature on the ability of retinoids to suppress the development of the malignant phenotype in vitro (for reviews, see Refs. 6, 8, 30, and 31 ), and these studies corroborate the use of retinoids for cancer prevention. Finally, most recently, it has been shown that reti noids can exert effects on certain fully transformed, invasive, neoplastic cells, leading in certain instances to a suppression of proliferation (30) and in other instances to terminal differentiation of these cells, resulting in a more benign, nonneoplastic pheno type (10,11,60,62). Even though there are many types of tumor cells for which this is not the case (33, 52) (indeed, at present there are only a limited number of instances in which such profound effects of retinoids on differentiation and proliferation of invasive tumor cells have been shown), this finding neverthe less has highly significant implications for the problem of cancer treatment. It emphasizes that in many respects cancer is fun damentally a disease of abnormal cell differentiation (36,44), and it raises the possibility that even invasive disease may eventually be controlled by agents which control cell differentiation rather than kill cells. Since carcinogenesis is essentially a disorder of cell differentiation, the overall scientific problem of the role of retinoids in either differentiation or carcinogenesis is essentially

Flow Cytometry in Clinical Cancer Research

Abstract: The prognosis of patients with cancer is largely determined by the specific histological diagnosis, tumor mass stage, and host performance status. The management of neoplastic disease with the currently available treatment armamentarium may be further advanced if individual patients' risk factors could be better defined. Some of the determinants of tumor response seem to be expressed at the cellular level in terms of degree of tumor cell differentiation, growth kinetics, and hormone receptor expression, which are not readily appreciated by descriptive morphology. Quantitative cytology in the form of flow cytometry has greatly advanced the objective elucidation of tumor cell heterogeneity by using probes that discriminate tumor and normal cells and assess differentiative as well as proliferative tumor cell properties. Abnormal nuclear DNA content is a conclusive marker of malignancy and is found with increasing frequency in leukemia (23% among 793 patients), in lymphoma (53% among 360 patients), and in myeloma (76% among 177 patients), as well as in solid tumors (75% among 3611 patients), for an overall incidence of 67% in 4941 patients. The degree of DNA content abnormality varies according to disease type, with a predominant excess of 10 to 20% in the hematological cancers, whereas ploidy levels in solid-tissue neoplasms span the entire range from almost haploid to hyperoctaploid abnormalities, with near-triploid mean and median DNA content values. The proportion of cells in the S phase of the cell cycle increases with increasing DNA excess in a number of different solid tumors and in acute leukemia. This cytokinetic parameter permits discrimination of low- and high-grade malignant lymphomas. Several reports demonstrate increasing morphological immaturity to be associated with increasing DNA content abnormality and increasing S percentage, all of which adversely affect prognosis. Among phenotypic tumor cell markers, surface membrane antigens have been extensively studied in lymphoid and myeloid neoplasms by the use of hybridoma-generated monoclonal antibodies, which have recently also found in vitro and in vivo therapeutic application. Cellular RNA content is useful for the objective discrimination of acute leukemias and of multiple myeloma. Newer applications of flow cytometry concern studies in the areas of cytoenzymology and cellular pharmacology. Current research is dedicated to the identification of neoplastic marker probes for DNA-diploid disease ( e.g. , nucleolar antigen) and additional phenotypic ( e.g. , hormone receptors) and cytokinetic ( e.g. , cycle traverse rate, growth fraction) parameters. From a patient management perspective, a role for flow cytometry is emerging as a tool for diagnosis of cancer (abnormal DNA content), specific histopathological diagnosis (RNA for hematological cancers; surface markers for lymphoid and myeloid neoplasms), prognosis (adverse impact of aneuploidy and high S percentage), and treatment (cytokinetically oriented, monoclonal antibodies, drug pharmacology). The pace of past progress justifies the hope that cytometry may soon provide “fingerprinttype” information of an individual patient's tumor which, if proven prognostically relevant, may provide the basis for treatment selection in the future.

‘Hormonal’ risk factors, ‘breast tissue age’ and the age-incidence of breast cancer

Abstract: For most cancer sites there is a linear log-log relationship between incidence and age. This relationship does not hold for breast cancer, and certain 'key' breast cancer risk factors suggest that breast tissue does not 'age' in step with calendar time. A quantitative description of 'breast tissue age' is suggested which brings the age-incidence curve of breast cancer into line with the common log-log cancers and explains quantitatively the known key risk factors. The model also explains the 'anomalous' finding that although early first birth is protective, late first birth carries a higher risk than nulliparity. US breast cancer rates are some four to six times the rates in Japan--the model suggests that the key risk factors, when considered jointly with weight, can explain about 85% of the difference.

Pathology of hepatocellular carcinoma in Japan. 232 Consecutive cases autopsied in ten years.

Abstract: The pathologic findings of 232 consecutive cases of hepatocellular carcinoma (HCC) autopsied during the past ten years at Kurume, Japan, were analyzed from the point of view of global epidemiology, in relation to clinical feature, and in regard to incidence, age, sex, etiologic factors, size of liver, changes in noncancer parenchyma, gross type of tumor, extrahepatic metastases, intravascular and intraductal growths, cancer cell histology, hepatitis B surface antigen (HBsAg) in hepatocytes and cancer cells, liver cell dysplasia, and frequency and clinicopathologic characteristics of minute HCC. Furthermore, postmortem hepatic arteriography and portography were done in 152 livers for comparison with gross anatomy and celiac angiograms. It was found that: (1) epidemiologically, HCC in Japan is distinct from that in the West that it is frequently encapsulated, livers are generally small because of frequent and advanced cirrhosis and small cancer, minute HCC, is not uncommon at autopsy, cirrhosis most commonly associated is the one with thin stroma and medium size nodules, and micronodular cirrhosis is very rare despite frequent alcohol abuse; (2) HCC is increasing in incidence; (3) HBsAg is frequently found in parenchyma; (4) liver cell dysplasia is indirectly related to HBsAg with no evidence for premalignancy; (5) the lung is the most frequent site of metastasis but peritoneal dissemination is unusual; (6) intraportal tumor growth is very common and the hepatic vein is less frequently affected; (7) growth in the major bile duct is frequently associated with intraportal growth and clinically presents as obstructive jaundice; and (8) tumor is supplied solely by arteries and celiac arteriograms are closely correlated with gross pathologic findings.

Tumor heterogeneity: biological implications and therapeutic consequences

Abstract: It is now appreciated that cancers can be composed of multiple clonal subpopulations of cancer cells which differ among themselves in many properties, including karyotype, growth rate, ability to metastasize, immunological characteristics, production and expression of markers, and sensitivity to therapeutic modalities. Such tumor heterogeneity has been demonstrated in a wide variety of animal tumors of differing etiology, tissue and cellular origin, and species. It has been shown in autochthonous, as well as transplanted, tumors. Similar results have been reported for human cancers, although much of the evidence that heterogeneity of human cancers, also reflects, at least in part, the existence of clonal subpopulations, is still indirect. Heterogeneity is not a unique property of malignancy. Preneoplastic tumors, as well as normal tissues, are also composed of cellular subpopulations. Proposed mechanisms for the origin of tumor heterogeneity include coalescence of multiple foci of cancer clones and the generation of diverse subpopulations from a single clone. This latter process could be due to genetic errors arising from classical genetic mechanisms or to the production of cellular variants as in normal tissue differentiation. Indeed, certain tumor subpopulations have been shown to produce variants at high frequency. In some cases this frequency can be modified by environmental circumstances. Nontumor cells may also contribute to production of cancer cell variants, perhaps, in the case of infiltrating phagocytic cells, by producing mutagens or by somatic hybridization with cancer cells. Production of tumor cell variants is a dynamic process which can occur at any time. Although tumors are mixed populations of cells, knowledge of the characteristics of individual components is not sufficient to predict the behavior of the whole. Individual cancer subpopulations can interact to affect each other's growth, immunogenicity, ability to metastasize, sensitivity to drugs, and clonal stability. The existence of multiple, interactive subpopulations provides a basis for the well-known phenomenon of ‘tumor progression’ in which tumors undergo qualitative changes in characteristics over the course of time. Selection of subpopulations better able to survive changing environmental circumstances allows for such changes as autonomy in regard to endogenous growth regulation, more ‘malignant’ behavior, and loss of response to therapy. Tumor subpopulation interactions may play a regulatory role in this process. Tumor heterogeneity has obvious consequences to the design of effective therapy. It provides one rationale for combination therapies and suggests that initial treatment should be early and comprehensive. The continuing emergence of new clones suggests that treatment which is unsuccessful at one point might be effective later. Assays to predict effective therapy for individual patients need to address the multiplicity of tumor subpopulations and the ability of these subpopulations to influence each other. Subpopulation interactions may also be useful in therapy design, as may be efforts to control the extent of tumor heterogeneity by agents which effect cellular differentiation. Thus, tumor heterogeneity presents both problems and, perhaps, new solutions for control of cancer.

Tumor recurrence in the abdominal wall scar tissue after large-bowel cancer surgery.

Abstract: In the Melbourne (Monash) series reviewed here the development of apparently isolated incisional scar tissue recurrences after curative excisions for large-bowel cancer proved unusual. Eleven patients with such a recurrence all died of disseminated disease within four years, and most within 12 months, of its development. This suggests that an incisional recurrence is a manifestation of disseminated cancer rather than isolated implantation.

Tumor localization in patients by radiolabeled monoclonal antibodies against colon carcinoma.

Abstract: A radiolabeled monoclonal antibody (MAb) that has been shown to react specifically in vitro and ex vivo to human colorectal carcinoma and to inhibit growth of human carcinomas grafted in nude mice was administered to 52 colorectal carcinoma patients and 15 patients with other types of cancer. Of 63 colorectal carcinoma tumor sites studied, 34 showed significant accumulation of antibody by external photoscanning and tomoscintigraphy, whereas none of the 20 sites of other cancer types gave positive results. One-third of the patients received F(ab')2 fragments of the MAb, which gave a slightly higher percentage (61%) of positive results than did intact MAbs (51%). A few patients scheduled for tumor resection were given injections simultaneously of 131I-labeled MAb and 125I-labeled normal immunoglobulin G. Antibody concentration in resected tumors was 3.6 to 6.3 times higher than the average antibody concentration in adjacent normal tissues (1.5, 3.4, and 9.4 as compared with normal mucosa, serosa, and fat, respectively), and the specificity indices, calculated by differential radioactivity analysis, ranged from 2.1 to 5.1. The results show the potential value and limitations of this particular MAb for tumor detection by immunoscintigraphy.

New approach in the treatment of prostate cancer: Complete instead of partial withdrawal of androgens

Abstract: To completely eliminate androgens of both testicular and adrenal origin, 37 previously untreated patients with advanced (stages C or D) prostatic cancer received the combination therapy using an LHRH agonist (HOE-766) and a pure antiandrogen (RU-23908). The response criteria developed by the National Prostatic Cancer Project were used. A positive response (assessed by bone scan and/or serum prostatic acid phosphatase measured by radioimunoassay was observed in 29 of the 30 cases who could be evaluated by these objective criteria (97%). The objective response was parallel to a rapid and marked improvement of the clinical signs and symptoms related to prostate cancer (prostatism, bone pain, and general well being). In marked contrast, the same combination therapy applied to patients previously treated with high doses of diethylstilbestrol (13 patients) showed a positive objective response in only 55% of cases. In 23 previously castrated patients showing relapse, an objective response was seen in only 25% of cases after neutralization of adrenal androgens by the antiandrogen. Previous treatment with chlorotrianisene (TACE) had no detectable effect on prostatic cancer and patients having previously received such treatment had a rate of positive response similar to previously untreated patients (five of five). In the previously untreated patients receiving the combination therapy, a 60% fall in serum prostatic acid phosphatase was observed as early as five days after starting treatment, at a time when the serum androgen concentration was 100% to 200% above control. Combined treatment with the pure antiandrogen completely prevents flare-up of the disease, a complication previously found in a significant proportion of patients treated with an LHRH agonist alone. The present data show that complete withdrawal of androgens by combined hormonal therapy with the LHRH agonist (or castration) and a pure antiandrogen leads to a positive objective response in more than 95% of cases as opposed to 60%-70% as reported by many groups using the previous partial hormonal therapy (castration or high doses of estrogens). Adrenal androgens are most likely responsible for this difference. The present study also shows that the proportion of androgen-sensitive cells decreases from more than 95% in untreated patients to 25% to 55% after previous partial hormonal therapy. Such data clearly indicate that the previous partial hormonal therapy exclusively aimed at neutralizing testicular androgens left 25% to 55% of cancer cells having a relatively low sensitivity to adrogens in a hormonal milieu compatible with their continuous growth. No clinical or biochemical side effect could be detected except those related to reduced serum androgen levels. Due to the ease of its application and the lack of secondary effects other than those related to hypoandrogenicity, the present data clearly suggest that complete (instead of partial) androgen withdrawal should be performed as early as possible after diagnosis, at least in advanced prostatic cancer, to reduce the development of androgen-insensitive cell clones and to facilitate the adjuvant treatment with chemotherapeutic agents and/or radiotherapy of androgen-insensitive tumors in the appropriate cases.

Inhibition of Human Cancer Cell Growth by 1,25-Dihydroxyvitamin D3 Metabolites

Abstract: Specific high-affinity 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] receptors, which can undergo hormone-dependent activation and nuclear localization, have been demonstrated in a wide variety of established human cancer cell lines and surgically obtained human cancer tissues. 1,25-(OH)2D3 has been reported by some workers to stimulate cancer cell replication at low "physiological" concentrations and by ourselves and others to inhibit at higher concentrations. We report here that 1,25-(OH)2D3 had a biphasic effect on the replication of two distinct human cancer cell lines, i.e., the breast cancer T-47D and the malignant melanoma MM96, an effect analogous to that of estrogens on the breast cancer cell line MCF-7. These inhibitory effects were accompanied by marked morphological changes. Furthermore, two known metabolites of 1,25-(OH)2D3, i.e., 1,24,25-trihydroxyvitamin D3 and 1,25,26-trihydroxyvitamin D3, which compete for binding to the 1,25-(OH)2D3 receptor, did not stimulate but were almost equipotent with 1,25-(OH)2D3 in inhibiting the replication of both cell lines. The stimulatory but not the inhibitory effect of 1,25-(OH)2D3 was abolished by cortisone. These 1,25-dihydroxyvitamin D3 metabolites show promise for the inhibition of cancer growth, analogous to the effect of estrogens and antiestrogens in breast cancer but with potential application in a much wider range of human cancers.

Cancer and pregnancy.

Abstract: I: Clinical Aspects: Diagnosis and Management.- 1 The Epidemiology of Cancer in Pregnancy.- 2 Placental and Fetal Cancers.- 3 Breast Cancer and Pregnancy.- 4 Gynaecologic Malignancies in Pregnancy.- 5 Hematologic Malignancies in Pregnancy.- 6 Melanoma in Pregnancy.- 7 Rare Tumours in Pregnancy.- 8 Colorectal Cancer in Pregnancy.- 9 Radiologic Diagnosis of Cancer in Pregnancy.- 10 Pregnancy Derived Tumor Marker.- 11 Chemo and Radiation Therapy During Pregnancy.- 12 Management of Cancer in Pregnancy (Case Reports).- 13 Transplacental Carcinogenesis: Role of Chemicals, Radiation and Viruses.- II Comparative Aspects of Pregnancy Development and Tumour Biology.- 14 Metabolism of Chemotherapeutic Drugs by Maternal and Conceptus Tissues.- 15 Adverse Reproductive Outcome Potential of Cancer Therapies During Pregnancy.- 16 Immunomodulatory Analogies Between Trophoblastic and Cancer Cells and Their Hosts.- 17 Protective Role of Human Chorionic Gonadotrophin and Luteinizing Hormone Against Breast Cancer.- 18 Proliferation, Differentiation and Apoptosis in Pregnancy and Cancer.- 19 Controlled vs Uncontrolled Angiogenesis: Color Doppler Studies.- 20 Angiogenesis and Vasculogenesis in Pregnancy and in Tumor Development.- 21 Trophoblast Implantation Versus Tumor Invasion.- 22 Pregnancy Derived Compounds that Control Proliferation.- 23 Cancer and Pregnancy: Bioethical and Legal Dilemmas.- Epilogue Cancer and Pregnancy: a Reason for Hope.

Estrogen Exposure During Gestation and Risk of Testicular Cancer

Abstract: In this case--control study of 108 cases of testicular cancer in men under 30 years of age, cryptorchidism was a major risk factor [relative risk (RR) = 9.0]. Low birth weight was also associated with increased risk (RR = 3.2). Having severe acne at puberty was protective (RR = 0.37). Interviews with mothers of cases revealed that exposure of the mother to exogenous estrogen during pregnancy created a significant risk in the son (RR = 8.0). In first pregnancies, excessive nausea indicated an increased risk of testicular cancer (RR = 4.2). Increased body weight in the mother also increased the risk. The relation between these factors and testicular hypoplasia is discussed. Severe perimenopausal menorrhagia was a factor in the mother associated with reduced risk of testicular cancer in the son (RR = 0.10). A modified hormonal milieu in the mother appears to be important in the later development of testicular cancer in her sons.

Chemotherapy in head and neck cancer.

Abstract: SQUAMOUS-CELL carcinoma of the head and neck accounts for five per cent of the cases of cancer in the United States. Only one third of patients with this neoplasm present with localized disease easily curable by surgery and radiation. These treatment methods, however, have not provided adequate tumor control in the majority of patients who present with advanced local and regional disease. Local recurrences occur in up to 60 per cent of these patients, and distant metastases develop in 20 to 30 per cent; survival remains poor (0 to 40 per cent).1 , 2 Until recently, chemotherapy has been reserved only for . . .

Diet in the Epidemiology of Carcinoma of the Prostate Gland

Abstract: In vivo, in vitro, prospective, and retrospective epidemiologic inquiries have suggested that retinoids inhibit cancer, and fats have been hypothesized to enhance and ascorbic acid to reduce cancer risk. Comparison of 260 patients from Buffalo with cancer of the prostate gland was made with two different control series of similar size and age distribution. Regardless of the control group, risk of prostate cancer gained with increases in ingestion of retinoids, animal fats, and vitamin C. These anomalous findings may be due to peculiarities in methodology. From the possible specificity of effect of the nutrients studied, as shown in experimental animals and in vitro, a hypothesis could be made that a substance like vitamin A or C, which may inhibit certain cancers, also may enhance risk of other cancer types or have neither effect.

Copper and Zinc levels in normal and malignant tissues

Abstract: The copper and zinc levels in 53 malignant and 47 normal human tissue samples were measured. In the malignant tissues, the mean copper concentration was 46% higher (P less than 0.001) than in the normal ones. Analysis of the individual organs showed this increment to be statistically significant in malignancies of the large bowel, stomach, urinary bladder and female reproductive organs, while in cancer of the breast, kidney and testis, the increase in copper level was not significant. The mean zinc concentration in the malignant tissues was not significantly different from that in the corresponding normal tissue specimens (-11%; P less than 0.2). In breast cancer, however, tissue zinc levels were increased by 72% (P less than 0.01), and decreased markedly in carcinoma of the kidney (-73%). A hypothesis for the possible mechanism involving elevated tissue copper levels in biological damage (previously caused by free radicals) which may be responsible for the malignant process, is presented and discussed.

Familial Pancreatic Cancer

Abstract: Excerpt To the editor: I write to add to the report of Dat and Sontag (1) with a brief description of another family with pancreatic carcinoma. I treated an 80-year-old white man who presented with...

Patterns of care outcome studies. Results of the national practice in cancer of the cervix.

Abstract: This report summarizes the national data collected by the Patterns of Care Study in the process and outcome of care in the treatment of carcinoma of the cervix. Substantial variation was found from a consensus of best current management, although training facilities tended to score higher than non-training on a compliance measure. Four year national averages for control of cervical cancer are: Stage I, 87%, Stage II, 66%, Stage III, 28%. Factors relating to recurrences include failure to use intracavitary irradiation, the type of equipment, the central dose, and Karnofsky Score. The presence of complications is associated with daily dose, lateral dose and central dose, among other factors, and was shown to be unacceptably high in Stage I.

Gallstone Size and the Risk of Gallbladder Cancer

Abstract: Gallstones are a major risk factor for gallbladder cancer, but few persons with stones experience development of tumors. To examine this relationship, a case-control study was performed. Each of 81 cancer cases was matched for age, sex, hospital, and admission date with two controls, one with benign gallbladder disease and one with a nongallbladder diagnosis. Persons with large gallstones were found to be at increased risk for cancer. For those with stone diameters of 2.0 to 2.9 cm, the odds ratio ( v stone size ( JAMA 1983;250:2323-2326)

Multimodal treatment of locoregionally advanced breast cancer.

Abstract: Fifty-two patients with locally advanced primary breast cancer (T3, T4/N2, N3) without distant metastases were treated with three cycles of combination chemotherapy consisting of 5-FU, Adriamycin and cyclophosphamide (FAC) and immunotherapy with Bacillus Calmette-Guerin (BCG) followed by local therapy (simple mastectomy and/or radiotherapy to breast/chest wall and regional lymphatics) and adjuvant chemotherapy to complete two years of treatment. Forty-nine of 52 (94%) patients were rendered free of clinically detectable disease. The median disease-free interval was 24 months. At a median follow-up time of 60 months, 40% of patients remained free of disease, off all therapy. Those patients who completed two years of therapy and started adjuvant chemotherapy promptly after local treatment had a 48% disease-free survival at five years. Local recurrences were observed in 21% of patients. Distant metastases developed in 40% of patients. Despite good tolerance, treatment compliance was poor. The complete remission rate with this multimodal approach is high and long-term disease-free survival is achieved in a considerable number of patients.