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PubMed2003

Expression of a novel immunoglobulin gene SNC73 in human cancer and non-cancerous tissues.

AIM: To investigate the expression of immunoglobulin gene SNC73 in malignant tumors and non-cancerous normal tissues. METHODS: Expression level of SNC73 in tumors and non-cancerous tissues from the same patient was determined by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay (RT-PCR-ELISA) in 90 cases of malignant tumors, including colorectal cancer, gastric cancer, breast cancer, lung cancer and liver cancer. Analysis on the correlation of SNC73 expression with sex, age, site, grade of differentiation, depth of invasion, and metastases in colorectal cancer patients was made. RESULTS: Expression level of SNC73 in non-cancerous colorectal mucosa and colorectal cancerous tissues was 1.234+/-0.842 and 0.737+/-0.731, respectively (P<0.01), with the mean ratio of 7.134+/-14.092 (range, 0.36-59.54). Expression of SNC73 showed no significant difference among gastric cancer, breast cancer, lung cancer and liver cancer when compared with non-cancerous tissues (P>0.05). No correlation was found between SNC73 expression level and various clinicopathological factors, including sex, age, site, grade of differentiation, depth of invasion and metastases of CRC patients. CONCLUSION: Down-regulation of SNC73 expression may be a relatively specific phenomenon in colorectal cancer. SNC73 is a potential genetic marker for the carcinongenesis of colorectal cancer. The relationship of SNC73 expression and carcinogenesis of colorectal cancer merits further study.

Base Sequence↗

PubMed1993

[Multiple primary cancers in patients with head and neck cancer and history of tobacco smoking and drinking].

In a total of 2083 cases of hollow organ cancer of the head and neck region treated in our institute in the past 20 years, the relative risk of second primary cancers was statistically studied by the person-year approach. The organ association in multiple primary cancers and the relationship between tobacco and alcohol consumption and the development of second primary cancers were also reviewed. The incidence of second primary cancers was significantly (p < 0.05) higher in patients having a lesion at the tongue (n = 502), mesopharynx (n = 188), hypopharynx (n = 224) and larynx (n = 621) and in the oral cavity (n = 203) than in the general population. With regard to organ association in multiple primary cancers, cancers in the oral cavity, esophagus and at the pharynx were found to occur as second primary cancers of the tongue, oral cavity, meso-hypopharynx and larynx at significantly high rates in males. Male laryngeal cancer was related to the lung. No relation of female lingual cancer to the esophagus was noted. The incidence of second primary cancer was very high in persons who had been heavy smokers and/or heavy drinkers before the occurrence of their primary cancer in the head and neck region. In these people, second primary cancers were found to occur at high rates as cancers related to tobacco smoking and drinking. Otherwise, in cases with head and neck cancers less related to tobacco smoking and drinking, the incidence of second primary cancers was low. From the above results, tobacco smoking and drinking may be closely related to a high incidence of second primary cancer following the first primary cancer in the head and neck region.

Aged↗

PubMed1993

Smoking cessation after successful treatment of small-cell lung cancer is associated with fewer smoking-related second primary cancers.

OBJECTIVE: To determine the incidence of second primary cancers developing in patients surviving free of cancer for 2 or more years after treatment for small-cell lung cancer and to assess the potential effect of smoking cessation. DESIGN: Retrospective review of 540 patients from a single institution with a median follow-up of 6.1 years. SETTING: A single government institution (the National Cancer Institute). PATIENTS: Consecutive sample of 540 patients with histologically confirmed small-cell lung cancer treated from 1973 through 1989 on therapeutic clinical trials. MEASUREMENTS: The relative risk for second primary cancers and death were calculated in patients who remained free of cancer for 2 years after initiation of therapy. The relation of these end points to smoking history was also determined. RESULTS: Fifty-five patients (10%) were free of cancer 2 years after initiation of therapy. Eighteen of these patients developed one or more second primary cancers, including 13 who developed second primary non-small-cell lung cancer. The risk for any second primary cancer compared with that in the general population was increased four times (relative risk, 4.4; 95% CI, 2.5-7.2), with a relative risk of a second primary non-small-cell lung cancer of 16 (CI, 8.4-27). Forty-three patients discontinued smoking within 6 months of starting treatment for small-cell lung cancer, and 12 continued to smoke. In those who stopped smoking at time of diagnosis, the relative risk of a second lung cancer was 11 (CI, 4.4 to 23), whereas, in those who continued to smoke, it was 32 (CI, 12 to 69). CONCLUSIONS: Patients with small-cell lung cancer who survive cancer-free for more than 2 years have a significantly increased risk for development of a second primary smoking-related cancer. Cigarette smoking cessation after successful therapy is associated with a decrease in risk for a second smoking-related primary cancer.

Aged↗

PubMed2002

[Cancer in siblings of children with cancer].

INTRODUCTION: In some rare inherited disorders, such as Li-Fraumeni syndrome, relatives of children with cancer are at increased risk of cancer. We aimed to assess relations between childhood cancer and sibling risk, and evaluate the influence of recessive conditions in cancer causation. MATERIAL AND METHODS: We did a population-based cohort study in the Nordic countries of 42,277 siblings of 25,605 children with cancer. Children with cancer were identified from records in the five Nordic cancer registries, and their siblings from nationwide population registries. Cancers in siblings were documented through record linkage with cancer registries and compared with national incidence rates. We also assessed cancer incidence in parents to identify familial cancer syndromes. RESULTS: 284.2 cancers were expected in siblings, whereas 353 were diagnosed (standardised incidence ratio 1.24 95% CI, 1.12-1.38). Risk ratios for siblings were highest in the first decade of life (2.59; 1.89-3.46). We excluded 56 families with genetic syndromes linked to cancer, which reduced this ratio from 1.7 to 1.0 (0.7-1.3) for siblings younger than 20 years and from 1.3 to 1.0 (0.8-1.3) for those aged 20-29 years. We found no new patterns of familial cancer that indicated inherited susceptibility, or evidence that recessive conditions might contribute to cancers not explained by syndromes. 40% of cancers in siblings that occurred before age 20 years could be attributed to known genetic factors, whereas 60% remained unexplained. DISCUSSION: Apart from rare cancer syndromes, paediatric cancer is not an indicator of increased risk in siblings.

Adolescent↗

PubMed2001

Why Did Cancer Deaths Increase in Japan after the Introduction of the Tenth Version of the International Classification of Disease? : Assessment Based on a Population-Based Cancer Registry.

Considerable increase in cancer deaths has been observed since 1995, after when the tenth version of the international classification of disease (ICD) was introduced in Japan according with the revision of a death certificate form at the same time. We assessed the contributing factors for this unnatural fluctuation, using a population-based cancer registry data as a model. All deaths of the prefectural residents are collated with the cancer registry database in the registration process. For all Japanese deaths of Aichi Prefecture in 1994 (n=41,111) and in 1995 (n=42,944), the description of the death certificates were compared with the ICD classified as the cause of death. It was ascertained that 97-99% of cancer and 97-98% of non-cancer deaths classified by ICD were proper. Among those classified as cancer as the cause of death and stated as other than the direct cause of death (n=92 in 1994, n=428 in 1995), only 22% (1994) and 8% (1995) were considered to be classifiable to both cancer and non-cancer as the cause of death. Among those who were classified as non-cancer as the cause of death in spite of including cancer in the original statement (n=770 in 1994, n=638 in 1995), 24% (1994) 10% (1995) were considered to be non-cancer as the cause of death, and the rest were considered classifiable into both cancer and non-cancer. Even if all cancer deaths classifiable to non-cancer were classified as non-cancer deaths, change in the number of cancer deaths was inconsiderable in both years. Therefore, it is suggested that the increase of cancer deaths after introduction of the new ICD was caused not by the artifact such as change in selection rule of disease when classify the cause of death, but by the improvement of the description of death certificate by physicians as a result of revision of death certificate form.

Journal Article↗

PubMed1986

Risk factors of multiple primary cancers in breast cancer patients.

To clarify risk factors of multiple primary cancers in breast cancer patients, a case-control analysis based on data from medical records was conducted at the Aichi Cancer Center Hospital. For each of a total of 115 multiple primary cancer patients affected by one or two other primary cancers after or concurrently with breast cancer, two patients with unilateral breast cancer were selected as controls by matching age, time of the operation for breast cancer, and survival period. Multiple primary cancer patients were then divided into two groups, 61 cases of bilateral breast cancer and 56 cases of other multiple primary cancers. Conditional multiple logistic regression analysis indicated that relatively heavy smoking (more than 10 cigarettes per day) decreased the risk of multiple primary cancers taken overall (relative risk (RR) = 0.23); overweight status elevated the risk of bilateral breast cancer (RR = 3.01); and greater than average height (RR = 2.20), history of gallstone or cholecystitis (RR = 6.29), and late first birth or nulliparous status (RR = 6.85) elevated the risk of other multiple primary cancers. The effects of weight and height were predominant in the postmenopausal women. As to family history, we could not obtain clear results, though history of cancer among siblings tended to increase the risk of multiple primary cancers (P less than 0.10) and family history of breast cancer was more frequent in patients with bilateral breast cancer (not significant).

Alcohol Drinking↗

PubMed1985

Second cancer following lymphatic and hematopoietic cancers in Connecticut, 1935-82.

The risk of developing a second primary cancer was evaluated in approximately 19,000 persons with initial cancers of the lymphatic and hematopoietic system in Connecticut between 1935 and 1982. Significant excesses for all second cancers were observed among patients with leukemia (34%), Hodgkin's disease (70%), non-Hodgkin's lymphoma (25%), and multiple myeloma (24%). In general, the risk of second cancers was greater in males than in females, even for cohorts not showing an excess of surveillance-related prostate cancer. Among patients with leukemia, significant excesses of cancers of the lung, kidney/ureter, and prostate were noted; cutaneous melanoma was elevated only in males. These excesses did not persist in the small number of long-term survivors. Possible etiologic factors included tobacco smoking for lung and kidney cancers, medical surveillance artifact for prostate cancer, and immunosuppression for malignant melanoma and lung cancer. The large number and good prognoses of patients with chronic lymphocytic leukemia strongly influenced the pattern of second cancers when all leukemias were analyzed together; no evidence was found for an increased risk of second cancer in patients with acute lymphocytic leukemia. A disproportionate number of subsequent cancers, particularly those of the kidney and ureter, were diagnosed incidentally at autopsy. Patients with Hodgkin's disease displayed significant excesses of cancers of the buccal cavity and pharynx, lung, female breast, and thyroid. The latter 3 sites remained significantly elevated in long-term survivors (10 yr or more postdiagnosis), so that radiation therapy may have contributed to their development. Among persons with non-Hodgkin's lymphoma, cancers of the stomach, lung, brain, and connective tissue occurred excessively. The first 3 sites, plus cancers of the urinary bladder, remained elevated among long-term survivors. The brain cancer excess, not previously reported, may represent misclassification of central nervous system lymphoma. The risk of gastric cancer is reminiscent of similar findings in patients with both acquired and genetically determined immunodeficiency disorders. The alkylating agent, cyclophosphamide, used extensively in the treatment of non-Hodgkin's lymphoma, is known to cause bladder cancer in man.(ABSTRACT TRUNCATED AT 400 WORDS)

Connecticut↗

PubMed1985

Second cancer following cancer of the female genital system in Denmark, 1943-80.

Between 1943 and 1980, approximately 53,000 women in Denmark survived 2 or more months after initial diagnosis of cancers of the cervix uteri, corpus uteri, ovaries, fallopian tubes, and ligaments. No significant excess of new cancers was observed following cancers of the cervix and corpus uteri. However, after second cancers of both the cervix and corpus uteri were eliminated from the analysis (because it was likely they were surgically removed or not recorded due to conservative coding practices), 6 and 4% excess risks of borderline significance were found among women with cancer of the cervix and uterus, respectively. A significant 25% excess of all second primary cancers was observed following cancer of the ovary (relative risk = 1.25; 95% CI = 1.14-1.37). Significant excesses of colon and breast cancers followed cancers of the ovary and corpus uteri. Subsequent to cervical cancer, the risk of cancers of the lung, esophagus, bladder, and kidney occurred significantly above expectation. These associations may be explained by common risk factors related to reproduction and possibly diet for cancers of the breast, colon, ovary, and corpus uteri; and to cigarette smoking for cancers of the lung, esophagus, bladder, and cervix uteri. The significant deficit of breast cancer after cervical cancer could be due to different patterns of risk factor (i.e., reproductive and socioeconomic variables) and loss of functioning ovaries as a part of the treatment for cervical cancer. Each of the female genital sites showed significant excesses of second bladder cancers, and the risk increased significantly with time, which indicate a relation to radiotherapy. The pattern of risk of leukemia observed following cancer of the ovary was also compatible with effects of treatment, especially chemotherapy.

Denmark↗

PubMed1985

Second cancer following cancer of the urinary system in Denmark, 1943-80.

The risk of second primary cancer was evaluated in 29,128 patients who developed tumors of the urinary tract, including benign and malignant tumors of the renal pelvis and ureter and bladder papillomas in Denmark between 1943 and 1980. Among 9,162 persons with kidney cancer, 416 developed a second primary tumor [relative risk (RR) = 1.4]. Among 19,966 persons with bladder cancer, 1,423 developed a second primary tumor against 1,239 expected (RR = 1.1). The risk of bladder cancer was increased following kidney cancer in both men (RR = 6.3) and women (RR = 10.1), and kidney cancer was increased in both men (RR = 2.9) and women (RR = 4.5) following bladder cancer. These risks were particularly pronounced for cancers occurring in the ureter and renal pelvis. Etiologic similarities are likely explanations for these observations, which also emphasize the role of host factors and the multifocal nature of urothelial tumors. A decrease in relative risks since diagnosis of the first primary cancer was seen that may partly be attributed to a lessening of the intensity of medical surveillance with time. Among long-term survivors with kidney cancer, increased risks were observed for colon and pancreatic cancers, which may be related to treatment; approximately 25% received radiotherapy. Among bladder cancer patients, increased risks of cancers of the lung and larynx occurred, probably due to tobacco smoking. A slight elevation of prostate cancer (RR = 1.3) may be attributable to medical surveillance. Unexpected findings were the significant deficits of cancers of the stomach and rectum among patients with bladder cancer and stomach cancer among those with kidney cancer.

Denmark↗

PubMedDate not supplied

Recurrent pattern of digestive tract carcinoma in the Japanese: comparison of gastric cancer to colon cancer.

Six hundred and two consecutive cases of gastric cancer and 204 of colorectal cancer in recent decades were investigated for recurrence. Recurrence occurred in 103 cases of gastric cancer and 31 cases of colorectal cancer. We classified three categories of recurrent patterns; A: local, B: peritoneal dissemination, and C: distant metastasis. In gastric cancer, 11 cases (11%) were grouped A, 50 (48%) were B, and 42 (41%) were C. Similarly, 12 (39%) were grouped A, 5 (16%) were B, and 14 (45%) were C in colorectal cancer. The incidence of local recurrence was more increased in colorectal cancer than in gastric cancer (p < 0.01). On the contrary, that of peritoneal dissemination was more increased in gastric cancer than in colorectal cancer (p < 0.01). In gastric cancer, 8 cases of 103 survived more than 5 years after operation, furthermore 7 cases obtained more than 5 years of tumor-free interval. At the time of diagnosis of recurrence, data of serum CEA was available in 77 for gastric cancer and 29 for colon cancer. CEA positive cases were revealed 32 (42%) for gastric cancer and 24 (83%) for colorectal cancer (p < 0.01). Our data clarified the different recurrence patterns between gastric cancer and colorectal cancer. And suggest that more than 5 years follow-up should be needed in patients with gastric cancer.

Adult↗

PubMed1996

Characteristics of familial ovarian cancer: a report of the first 1,000 families in the Gilda Radner Familial Ovarian Cancer Registry.

BACKGROUND: To determine the demographics of the first 1,000 families in the Gilda Radner Familial Ovarian Cancer Registry. METHODS: Any woman with a family history of two or more first or second degree relatives with ovarian cancer who was referred to the Registry was entered into a database. The demographics of the Registry population were analyzed, including total number of ovarian cancer cases, cases per family, age at diagnosis, prevalence of other malignancies, and histology. Comparisons were made to expected norms in the general population using the most recent surveillance, Epidemiology, and End Results data from the National Cancer Institute. RESULTS: There were 2,425 reported cases of ovarian cancer among the 1,000 registered families. The number of cases per family ranged from 2-10 with 72.4% of the families having two cases of ovarian cancer and 27.6% with three or more cases of ovarian cancer. The mean age at diagnosis was 53.5 years, significantly younger than the 60.8 years reported in the general population (p < 0.1). The mean age at diagnosis was even younger, 52.1 years, in the subset of patients with a family history of three or more cases of ovarian cancer. Moreover, in the mother/daughter pairs of ovarian cancer where age of onset of ovarian cancer was known, the mean age of the mothers was 58.8 compared to a mean age of 50.2 among the daughters (p < 0.01). There was a significantly larger proportion of serous adenocarcinoma (40%) and a significantly smaller proportion of mucinous adenocarcinoma (3%) and stromal cell tumor (0%) when compared to the general population (p < 0.01). Breast and colon cancer were the two most common other cancers reported. CONCLUSIONS: given the limits of the study due to the voluntary nature of the Registry, the data suggests that familial ovarian cancer occurs at a younger age than the general population, daughters of mothers with ovarian cancers develop ovarian cancer at an age significantly younger than their mothers, mucinous and stromal tumors occurred significantly less often than in the general population, and the most common associated other cancers are female breast cancer and female and male colon cancer.

Adolescent↗

PubMed1996

A population-based study of endometrial cancer and familial risk in younger women. Cancer and Steroid Hormone Study Group.

Endometrial cancer remains an important cause of morbidity and mortality in the United States, and recent genetic evidence supports the hypothesis that hormonal dysregulation is not the only important risk factor for this tumor. This multicenter, population-based case-control study investigated familial aggregation of endometrial cancer and other cancers. Cases were 455 women 20-54 years of age diagnosed with histologically confirmed primary epithelial carcinoma of the endometrium. Controls consisted of 3216 women 20-54 years of age identified by random-digit dialing. Family histories of cancer in female relatives were obtained by interview of cases and controls. Endometrial cancer in a first-degree female relative increased the risk of endometrial cancer by nearly 3-fold [odds ratio (OR), 2.8; 95% confidence interval (CI), 1.9-4.2]. Cases also reported significantly more colorectal cancer in family members than did controls (OR, 1.9; 95% CI, 1.1-3.3). Family history of cancer of the cervix, lung, ovary, and thyroid was not significantly associated with endometrial cancer, and breast cancer was not related unless more than one relative was affected. Family history of endometrial cancer is an independent risk factor for cancer of the endometrium. In addition, the observed association with a family history of colorectal cancer suggests that genes important in familial colorectal cancer may have substantial implications for endometrial cancer. Nearly 5% of incident endometrial cancer among women between the ages of 20 and 54 may be attributable to a family history of endometrial cancer, and 2% may be related to colorectal cancer.

Adult↗

PubMedDate not supplied

Tissue expression of neu differentiation factor/heregulin and its receptor complex in prostate cancer and its biologic effects on prostate cancer cells in vitro.

BACKGROUND: Prostate cancer is the most common cancer in American men and the second leading cause of cancer death. All clinical observations correlate poorly differentiated high-grade prostate cancer with disease-specific mortality. The HER2 cell membrane tyrosine kinase, a member of the epidermal growth factor receptor family that is the transcription product of the erbB2neu oncogene, and HER3, a receptor protein of the same family, are overexpressed in prostate cancer and prostatic intraepithelial neoplasia. The ligand for these receptors and another related family member, HER4, has recently been identified by independent investigator groups and called neu differentiation factor (NDF) or heregulin. In vitro treatment of HER2- and HER3- or HER2- and HER4-expressing breast cancer cells stimulates tyrosine phosphorylation of HER2 and produces changes in the rate of proliferation, degree of cellular differentiation, and synthesis of physiologic secretion products. There are no published reports on the expression of NDF and HER4 in prostate cancer or the in vitro effects of NDF in prostate cancer cells. METHODS: Expression of NDF, HER2, HER3, and HER4 was studied in 24 frozen prostatectomy specimens by immunohistochemistry. The biologic effect of human recombinant NDF was studied in vitro, using the LNCaP, PC3, and DU145 human prostate cancer cell lines. HER and NDF protein expression was studied by immunohistochemistry. NDF mRNA was analyzed using reverse transcriptase polymerase chain reaction from whole RNA. The biologic effects of NDF on prostate cancer cells in vitro included cell proliferation, thymidine synthesis, induction of prostate-specific antigen mRNA, anchorage-dependent and anchorage-independent cell growth, and ploidy analysis. Data analysis was performed using Student's t test. RESULTS: Observations in clinical prostatectomy specimens: Immunohistochemistry studies in clinical prostatectomy specimens demonstrate absence of significant NDF expression in prostate cancer, whereas it is expressed in 100% of the stroma, 100% of basal epithelial cells, and 58% of luminal cells in normal and benign hyperplastic prostatic tissue. The HER4 receptor protein is strongly expressed by normal prostate luminal cells, but not prostate cancer. Benign prostate tissue exhibits strong expression of HER2, HER3, and HER4 by basal cells, but only luminal cells significantly express HER4. Only 23% of prostate cancer specimens express HER4, while 95% express HER3 and 82% HER2. Prostatic intraepithelial neoplasia stained similarly to cancer for all proteins studied. Observations in prostate cancer cell lines: In vitro treatment with NDF significantly reduces aneuploidy and proliferation and growth of androgen-sensitive prostate cancer cells. Incubation with NDF also induces prostate-specific antigen mRNA in prostate cancer cells. In spite of displaying NDF mRNA, prostate cancer cells do not produce detectable NDF protein, but express HER2 and HER3 proteins. DISCUSSION: These data suggest that NDF may be a paracrine differentiation factor involved in normal adult prostate physiology and that functional loss of the NDF/HER ligand/ receptor loop may be an early event associated with prostate tumorigenesis.

Antineoplastic Agents↗

PubMed1996

Cancer mortality in relatives of women with ovarian cancer: the OPCS Study. Office of Population Censuses and Surveys.

Mortality from cancer and other causes in first-degree relatives of women with ovarian cancer diagnosed before age 60 has been examined in a large population-based cohort study in England and Wales. Relatives of 1,188 ovarian-cancer cases diagnosed between 1954 and 1981 were identified through a register of households established in 1939. Some 4,111 first-degree relatives living in the same household and having the same surname as the index case were followed up through national records until the end of 1992. Over this period, 1,950 deaths (including 574 cancer deaths) occurred in the relatives. Mortality rates within the cohort were compared with age-, sex- and period-adjusted mortality rates for England and Wales. Mortality from ovarian cancer in first-degree relatives was significantly raised (SMR 223, 95% CI 155-310) although the excess was smaller than that found in case-control studies. The SMR increased with decreasing age of the relative, though not with decreasing age of the index case. After allowing for age, sisters of cases had higher ovarian-cancer mortality than mothers (sister:mother SMR ratio 1.89, p = 0.06). The SMR was greater in individuals having 2 first-degree relatives with ovarian cancer (4 deaths versus 0.17 expected, SMR 242). Relatives of ovarian cancer cases also had significantly increased mortality from cancers of the stomach (SMR 146, 69 deaths) and rectum (SMR 150, 33 deaths), and increased mortality from colon cancer, breast cancer and pancreatic cancer which failed to reach statistical significance. Individuals having a relative with colorectal cancer and a relative with ovarian cancer showed a high mortality from both cancers (11 colorectal-cancer deaths versus 1.23 expected, 4 ovarian-cancer deaths versus 0.66 expected.

Adult↗

PubMed1996

Oestrogen-related cancer risk in mothers of testicular-cancer patients.

The belief that oestrogens are involved in the pathogenesis both of testicular cancer in young men and of cancers of the endometrium and female breast has become widespread. In a search for possible hormonal links between these cancers, we investigated the cancer pattern in a cohort of women who had given birth to sons who developed testicular cancer. Particular focus, was given to oestrogen-related cancers. The present retrospective population-based cohort study is based on data from the Danish Cancer Registry. Mothers of 2,204 testicular-cancer patients were followed for the occurrence of cancer over a total of 70,063 person years. The ratio of observed cancers in the cohort over the expected numbers based on cancer incidence in the underlying female population served as measure of the relative risk (RR). The RR of developing breast cancer among mothers of testicular-cancer patients was 0.8 (95% confidence interval 0.6-1.1), the relative risk of endometrial cancer 0.6 (0.3-1.0) and of ovarian cancer 1.0 (0.6-1.6). Mothers of testicular-cancer patients are not at increased risk of developing oestrogen-related cancers.

Adult↗

PubMed1991

Prostate cancer: transrectal ultrasound and pathology comparison. A preliminary study of outer gland (peripheral and central zones) and inner gland (transition zone) cancer.

A study was conducted to compare results of transrectal ultrasound with pathologic findings on 116 patients who underwent radical prostatectomy for treatment of prostate cancer. In 96% (111 of 116), transrectal ultrasound guided biopsies of a hypoechoic lesion proved cancer; seven patients had known Stage A cancer; one patient had cancer detected by palpation and not detected by ultrasound. Cancers in the outer gland (peripheral and central zones) were compared with cancers in the inner gland (transition zone) by both ultrasound and pathology. Forty-eight percent (52 of 108) of cancers originating in the outer gland showed extraprostatic extension (Stage C disease). The primary sites of tumor escape from the outer gland were the prostatic capsule (38%), anterior fibromuscular stroma (5%), seminal vesicle (18%), the base of the gland at the neurovascular bundle (21%), and the apex (31%). Twenty-two percent (17 of 54) of cancers originating in the inner gland (transition zone) showed extraprostatic extension (Stage C disease). The primary sites of tumor escape from the inner gland were the anterior fibromuscular stroma (6%) and apex (11%). Both histologic and biologic differences between outer and inner gland cancers were found when tumor size was controlled. Gleason scores were significantly different for inner and outer gland cancers, with mean scores of 6.2 +/- 1.6 and 7.4 +/- 0.9, respectively. An odds ratio of 8.6 confirmed the increased risk of extraprostatic extension for outer gland cancer. Outer gland cancers showed increased aggressive behavior of both histologic and biologic nature. The difference in biologic aggressiveness of outer and inner gland cancers has definite implications for treatment options. Use of other diagnostic parameters, such as DNA ploidy, may help to determine which cancers to treat and when to treat them; this may have more relevance for cancers originating in the inner gland. Strategic transrectal ultrasound guided biopsy affords accurate tumor mapping and staging when modes of internal spread and escape of cancer from both outer and inner gland are known. Thus, transrectal ultrasound may be our "window of observation" through which additional research may explain the histologic and biologic discrepancies between outer and inner gland cancers.

Adenocarcinoma↗

PubMed1995

Risks of cancer among members of families in the Gilda Radner Familial Ovarian Cancer Registry.

BACKGROUND: Increasing scientific and public interest in hereditary cancer syndromes has created a need for estimates of lifetime cancer risks among members of families with such syndromes. METHODS: Data from the Gilda Radner Familial Ovarian Cancer Registry were used to evaluate risk for cancers of the breast, cervix, uterus, colorectum, and prostate in members of 143 families containing three or more reported cases of ovarian cancer among first- or second-degree relatives. These risks were compared with those that were expected based on general population rates obtained from the Connecticut Tumor Registry. RESULTS: Overall, family members' risk of cancer at any nonovarian site was 1.5 times that of the general population (P < 0.001). Among female members, risk for cancer of the breast was 2.5 times that of the general population. Risk for cancer of the uterus was 5 times that of the general population and increased with increasing number of first-degree relatives with ovarian cancer. Among male family members having three or more first-degree relatives with ovarian cancer, prostate cancer risk was 4.5 times that of the general population. No excess risks were observed for cancer of the colorectum. CONCLUSIONS: These data support previous reports of coaggregation of cancer of the breast, uterus and ovary, and suggest coaggregation between cancer of the ovary and prostate. Differences in cancer risk profiles observed in these families with multiple ovarian cancer and in carriers of the gene BRCA1 suggest that hereditary ovarian cancer is genetically heterogeneous.

Female↗

PubMed2002

Completeness and accuracy of registration of ovarian cancer in the cancer registry of Norway.

Completeness of reporting and accuracy of the diagnosis of ovarian cancer from one health region in Norway to the Cancer Registry were examined. Data kept by the Cancer Registry were evaluated against discharge diagnosis data from all 8 hospitals in the health region during the period of 1987-1996. The assessment of the accuracy of the diagnosis recorded in the Cancer Registry was based on review of all medical records in the hospital setting and on slide review of all histologic diagnoses. The overall completeness of reporting ovarian cancer to the Cancer Registry was 99.6%. The organ specific completeness of registration of histologic verified ovarian cancer within the Cancer Registry was 95.3%; 0.9% was erroneously coded and 3.5% had their diagnosis changed to ovarian cancer at re-evaluation. Of all ovarian cancer cases registered at the Cancer Registry, 91% had a primary histologic diagnosis. Among 591 cases identified with a histologic diagnosis in the Cancer Registry, the accuracy of the diagnosis was estimated at 92%. Coding errors were found in 2% of these cases, while in 6% of the cases it was not possible to reproduce the original diagnosis of ovarian cancer at re-evaluation. In order to provide data of high quality for cancer surveillance a cancer registry needs several data providers, such as histopathologic laboratory reports and clinical reports. In addition, assessment of reported data through stringent quality assurance procedures within the registry are necessary for reaching a nearly 100% completeness of registration as found for ovarian cancer in the Cancer Registry of Norway.

Female↗