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At least 19 recordsLinked to original sources
PubMed1996

Pattern of second primary neoplasms following breast cancer.

BACKGROUND: Second primary neoplasms (SPN) have been seen with diseases such as breast cancer and Hodgkin's disease. Therapeutic agents used for their treatment have been found responsible for the development of SPN in some cases. In addition, genetic factors are known to contribute to their development. METHODS: A retrospective study of 15 patients who had primary breast cancer and developed SPN concurrently or sequentially was conducted. RESULTS: Of 15 patients analysed in this study, five had haematological SPN, four had ovarian cancer, and six had different types of non-haematological SPN. Familial clustering was found in two patients. A peculiar abnormality of chromosome 5 and 7 was detected in one patient with haematological SPN, suggesting therapy-related leukaemia. CONCLUSIONS: It is postulated that alkylating agents with or without p53 gene inactivation may predispose to leukaemia, whereas ovarian tumors following breast cancer could be related to BRCA 1 gene inactivation.

Adult↗
PubMed2003

TP53, BRCA1, and BRCA2 tumor suppressor genes are not commonly mutated in survivors of Hodgkin's disease with second primary neoplasms.

PURPOSE: Despite recognition that second malignant neoplasms (SMNs) contribute significantly to mortality after the successful treatment of Hodgkin's disease (HD), little is known about the molecular events leading to secondary tumors. Factors contributing to second cancer risk include the carcinogenic effects of ionizing radiation and chemotherapy, in combination with possible host susceptibility. To clarify whether host genetic factors contribute to secondary tumorigenesis, we performed mutational analyses of the TP53, BRCA1, and BRCA2 tumor suppressor genes in a cohort of 44 HD patients developing one or more SMN. PATIENTS AND METHODS: Family cancer histories and constitutional DNA samples were obtained from 44 HD patients with SMNs identified. Using DNA-based sequencing, we evaluated the TP53 gene in all 44 patients. Nineteen female patients developing one or more secondary breast cancer were also analyzed for mutations in the BRCA1 and BRCA2 breast cancer-susceptibility genes. RESULTS: Nineteen patients (43%) had more than one SMN, and 12 patients (27%) had a positive family history of cancer. One of 44 patients tested for TP53 harbored a novel homozygous germline abnormality. One of 19 patients tested for BRCA2 carried a previously described heterozygous inactivating mutation. We identified no germline BRCA1 mutations. CONCLUSION: Despite features suggestive of genetic predisposition, the TP53, BRCA1, and BRCA2 genes were not frequently mutated in this cohort of HD patients developing SMNs. Larger studies of these genes or investigations of other genes involved in cellular DNA damage response pathways may identify host genetic factors that contribute to secondary tumorigenesis.

Adult↗
PubMed1996

Second primary neoplasms in thyroid cancer patients.

To determine risk patterns for second primary neoplasms after the occurrence of thyroid cancer, we conducted a retrospective cohort study of 3321 thyroid cancer patients who were operated and histologically confirmed at the Noguchi Thyroid Clinic and Hospital Foundation between 1946 and 1985. They were followed from the date of operation through the end of 1990 with an observation period from 45 to 5 years. The average observation period of the patients was 13.4 years and the follow-up rate reached 98%. The standardized mortality ratio (SMR) was computed to assess possible risk increase by cancer site. In this computation, the time period less than 5 years after operation was omitted to reduce the influence of deaths related to the original thyroid cancer. A total of 103 deaths from malignant neoplasms other than thyroid cancer were observed during this time period (SMR = 1.6, 95% confidence interval [CI] = 1.3-2.0). Analyses of site-specific cancer mortality revealed significantly elevated risks for the central nervous system (SMR = 16.1, CI = 5.2-37.6) and respiratory organs (SMR = 2.6, CI = 1.5-4.1). Based on a review of available medical records with histological findings, we concluded that the risk increases for these sites were most likely to be attributable to second primary neoplasms. Whether or not the patients had received radiotherapy was not significantly associated with elevated risk. Further investigations are needed to clarify the risk factors responsible for the above findings.

Adolescent↗
PubMed1989

Relationship between immunophenotype and the development of second primary neoplasms in patients with non-Hodgkin's lymphoma.

We reviewed the records of 107 patients with non-Hodgkin's lymphoma (NHL) to evaluate the relation between second primary neoplasms and the NHL immunophenotype. The incidence of second primary neoplasms was 3.7%. There were one case of hepatocellular carcinoma and 3 cases of gastric adenocarcinoma including one patient who had a history of metachronous malignant lymphomas. Three patients had B cell lymphoma with monoclonal IgM kappa phenotype, and one patient had follicular mixed cell type lymphoma with serum monoclonal IgM kappa. The dominant immunophenotype of B cell lymphomas in Japanese patients is IgM lambda. We believe that the association of the uncommon phenotype of IgM kappa with second primary neoplasms, especially gastric cancer, reflects an underlying genetic predisposition. NHL patients with IgM kappa phenotype should be evaluated carefully for second primary neoplasms.

Adenocarcinoma↗
PubMed2000

Second primary neoplasms in patients with laryngeal carcinoma.

OBJECTIVES: To better define the characteristics of second primary malignancies appearing in patients suffering from head and neck cancers, and more specifically laryngeal carcinoma, and to elicit those parameters that may be of assistance in better diagnosing, treating, and predicting outcome in such patients. STUDY DESIGN: Retrospective review of a group of 514 compliant subjects, examined and treated during an 8-year period until 1996. After initial diagnosis and subsequent treatment, rigorous follow-up ensured systematic screening of the subjects, who underwent standard examinations in outpatient clinics for periods of up to 56 months. RESULTS: Of 514 cases followed, presence of second primary neoplasms was established in 42 or 8.17%, 8 being synchronous and 34 metachronous of the original primary lesion. CONCLUSIONS: Respiratory and upper gastrointestinal localizations were primarily affected, incidence was highest in septuagenarians, and staging of the primary was found to be irrelevant to the incidence rates of second primaries. No statistical significance was attached to the fact that supraglottic primary tumors showed slightly higher second primary rates; the same applying for well-differentiated primary tumors compared with poorly differentiated ones. Modality of treatment surgery, and radiotherapy being the options in question-did not in the long run statistically influence incidence rates. Throughout, reference to current literature and this study's relevance in light of similar efforts were taken into account.

Adult↗
PubMedDate not supplied

The etiology of second primary neoplasms.

Neoplasms are derived from normal tissues of the body by cellular transformation. Tumors often represent a less differentiated or an undifferentiated version of the histology of the neoplasms original tissue. Primary tumor(s) may spread by direct extension or by metastasis. For the purpose of this review, second primary tumors will be defined to exclude metastatic lesions or recurrences from an original primary tumor. Second primary tumors arise in several different clinical situations that basically are the result of either inherited or acquired genetic mutations. Second primary tumors may develop soon or very late after treatment of the first primary tumor and may reflect an underlying genetic or immunologic defect in the patient, treatment related genetic damage, or environmental exposure to carcinogens. With the greater success of modern chemotherapy and radiotherapy in achieving long-term remissions in many patients, second primary tumors are a rapidly developing disease-category. This paper will review the clinical circumstances associated with a significantly higher incidence of second primary tumors in patients with an initial primary tumor.

Humans↗
PubMed1993

Second primary neoplasms following breast cancer in Saarland, Germany, 1968-1987.

A statewide cohort study on the occurrence of second primary neoplasms was conducted among 9678 women first diagnosed with breast cancer in Saarland, Germany between 1968 and 1987. A total number of 409 second primary neoplasms was observed compared to 328 cases that would have been expected based on the incidence rates of the general population (standardised incidence ratio, SIR = 1.25). This elevation in incidence of second neoplasms was primarily due to increased occurrence of cancer of the opposite breast (SIR = 2.48), which was most pronounced for patients below the age of 50 (SIR = 4.20) and within the first 5 years after diagnosis (SIR = 2.91). There was a moderate elevation in incidence of malignant tumours of the ovaries (SIR = 1.46), while the incidence of most other malignancies was lower than in the general population. Our results, which are in agreement with previous findings from Northern Europe, the U.S.A. and Japan provide valuable background information for aetiological research, as well as for surveillance of breast cancer patients.

Breast Neoplasms↗
PubMed2001

Second primary neoplasms after 19281 endocrine gland tumours: aetiological links?

The nationwide Swedish Family-Cancer Database of 9.6 million individuals was used to analyse the development of second neoplasia after 6909 thyroid and 12697 other endocrine tumours. Tumour cases were retrieved from the Swedish Cancer Registry from 1958 to 1996. The risk of a second endocrine tumour was markedly increased compared with first endocrine tumour; e.g. the standardised incidence ratios (SIRs) were well over 10 for adrenal tumours after thyroid cancer, and vice versa. Familial risks were higher for the development of second compared with first neoplasms, and the SIRs for men were usually higher than those for women. Many increases between different endocrine glands can probably be ascribed to known cancer syndromes. Even cancers at some other sites were increased after the development of primary endocrine tumours. Notably, small intestinal carcinoids were increased after thyroid and other endocrine tumours, and brain menigiomas were increased after parathyroid and pituitary adenomas. These novel associations suggest shared risk factors for these sites. However, many endocrine tumours are benign and the diagnosis of the first tumour may increase the likelihood of a second diagnosis.

Endocrine Gland Neoplasms↗
PubMed1986

Second primary neoplasms in patients with retinoblastoma.

In a series of 882 retinoblastoma patients, 384 known to have the genetic form of the disease and 498 others, 30 patients developed second primary neoplasms. The spectrum of these second neoplasms is discussed in relation to the forms of treatment used for the retinoblastoma. Cumulative incidence rates of second tumours in the whole series are 2.0% at 12 years after diagnosis and 4.2% after 18 years. For patients with the genetic form of retinoblastoma the cumulative incidence rate after 18 years is 8.4% for all second neoplasms and 6.0% for osteosarcomas alone. The inherent risk among survivors from genetic retinoblastoma of developing an osteosarcoma, excluding all possible effects of treatment, is estimated to be 2.2% after 18 years. Within the field of radiation treatment the cumulative incidence rate for all second neoplasms after 18 years is 6.6% and for osteosarcomas alone 3.7%. There is some evidence that patients with genetic retinoblastoma are particularly sensitive to the carcinogenic effects of radiation. The results also suggest that the use of cyclophosphamide may increase the risk of second primary neoplasms in patients with genetic retinoblastoma. The incidence rates of second primary neoplasms in retinoblastoma survivors reported here are lower than those quoted for previously published series. Evidence from this and other papers strongly suggests an association between retinoblastoma and malignant melanoma.

Child, Preschool↗
PubMed1994

Second primary neoplasms in a population-based series of patients diagnosed with renal tumours in childhood.

Eight second malignant tumours developed in a population-based series of 218 patients diagnosed with renal tumours in childhood: renal cell carcinoma of the contralateral kidney, hepatocellular carcinoma, Hodgkin's disease, and 4 basal cell and 1 squamous cell carcinomas of skin. Excess risk of developing a second malignancy (excluding skin carcinomas but including a registrable spinal neurofibroma) was 14.7 (95% CI 4.0-37.7, P = 0.0003) for Wilms' tumour patients. Cumulative incidence of second malignant neoplasms (excluding skin carcinoma) was zero at 10 years, 5.0% at 20 years, and 10.2% at 30 years. The most common second neoplasms seen were benign osseous/chondromatous tumours and 4 of the 7 Wilms' tumour patients with malignant tumours had previous or synchronous tumours of this kind. Development of bony exostoses may be a marker for those patients at particularly high risk of subsequent malignancy.

Adolescent↗
PubMed2005

DNA repair gene polymorphisms and risk of second primary neoplasms and mortality in oral cancer patients.

OBJECTIVES/HYPOTHESIS: We tested the hypothesis that polymorphisms in genes involved in DNA repair pathways are associated with the development of second primary neoplasms of the upper aerodigestive tract (UADT), as well as mortality, in patients previously diagnosed with oral squamous cell cancer (OSCC). METHODS: DNA specimens from 279 OSCC patients who had participated in two previous population-based case-control studies were assayed for the following polymorphisms: X-ray repair cross-complementing (XRCC) 1 Arg399Gln, XRCC3 Thr241Met, xeroderma pigmentosum complementing group D (XPD) Lys751Gln, and O-methylguanine- DNA methyltransferase (MGMT) Leu84Phe and Val143Ile. Baseline demographic information was obtained from personal interviews and tumor characteristics and treatment were obtained from cancer registry files. Cox proportional hazards models were used to calculate hazards ratio (HR) estimates for each polymorphism in relation to the risk of developing second primary neoplasms at any site, UADT, and head and neck. HRs were also determined for associations with all-cause mortality and oral cancer specific mortality. RESULTS: A significant increased risk of second neoplasms (all sites combined, as well as for UADT sites and for head and neck squamous cell cancers) was observed among XRCC3 241Met allele homozygotes (HR 2.65-3.44, P < .02). No significant association with the development of second neoplasms was observed for the XRCC1 399Gln, XPD 751Gln, or MGMT 84Phe or 143Ile alleles. Although no associations with oral cancer-specific mortality were observed, we found a significant inverse association between all-cause mortality and possessing at least one copy of the XRCC1 399Gln allele (HR 0.68, 95% confidence interval [CI] 0.47-0.97, P = .03), as well as a suggestion of a direct association between all-cause mortality and having one copy of the XRCC3 241Met allele (HR 1.39, 95% CI 0.95-2.03, P = .09). CONCLUSIONS: Polymorphisms in the DNA repair enzyme gene XRCC3 241Met was associated with an increased risk of second neoplasms, and polymorphisms of the XRCC1 399Gln gene were associated with a decreased risk of all-cause mortality in patients with primary OSCC. These findings require confirmation in other populations before the clinical implications can be considered.

Adolescent↗
PubMed1991

Cytotoxic chemotherapy-induced second primary neoplasms: clinical aspects.

The incidence of second malignancies was assessed by retrospectively analyzing data from previous studies in well-defined and closely followed patient cohorts. After a median follow-up of more than 6 years following MOPP (mechlorethamine/vincristine/procarbazine/prednisone) chemotherapy with or without radiotherapy, 5% of patients with Hodgkin's disease developed second primaries, 60% of which were leukemias. Melphalan caused a 3% leukemia rate among 1129 patients with ovarian cancer who were followed for a median period of 4 years. No leukemia was observed among 1132 breast cancer patients treated with adjuvant CMF (cyclophosphamide/methotrexate/5-fluorouracil) after a median follow-up of 7.5 years. Long-term, comprehensive studies are needed to improve the current knowledge and the prognosis of patients with second primary neoplasms.

Antineoplastic Agents↗
PubMed2001

Second primary neoplasms in 633,964 cancer patients in Sweden, 1958-1996.

The Swedish Family-Cancer Database was used to analyze concordant (same site) and discordant (different site) second primary neoplasms in 633,964 cancer patients diagnosed from 1958 to 1996. Cases of second malignant neoplasms were extracted from the Database if the diagnosis date of the first and second cancer differed by at least 1 month. The expected numbers of cancers were obtained by applying site-, sex-, age-, period-, residence- and socioeconomic level-specific rates in the corresponding population in the Database to the appropriate person-years at risk. The standardized incidence ratio (SIRs) of a second cancer was taken to be the ratio of observed to expected numbers of second cancers. Of all cancers, 8.5% were subsequent neoplasms (8.4% for males and 8.7% for females). SIRs for both concordant and discordant subsequent cancer were elevated in patients with cancer of the upper aerodigestive tract, colon, nose, breast, other female genitals, testis, kidney, urinary, bladder, skin, nervous system, endocrine, bone, connective tissue, melanoma, lymphoma and leukemia. The risks at some concordant sites, such as nose, squamous cell skin, bone and connective tissue in both sexes, breast in males and upper aerodigestive tract and leukemia in females, were very high (>10). At discordant sites, SIRs were less than 2 but significantly increased after all but gastric and prostatic cancer. Compared with the general population, cancer patients were at a modestly increased risk for new primary cancer after cancers at many sites, calling for attention in treatment, management and prevention.

Databases, Factual↗
PubMed1999

Classic Kaposi's sarcoma as a second primary neoplasm.

Although the incidence of classic Kaposi's sarcoma (CKS) has been investigated, its occurrence following a primary neoplasm and its association with this first neoplasm need to be determined. We analyzed a series of 124 patients with a secondary CKS (8.4% of a total of 1485 incident cases) which occurred between 1961 and 1992 in the Jewish Israeli population. Data on first neoplasms and subsequent Kaposi's sarcoma were retrieved from the Israel Cancer Registry. Acquired-immune-deficiency-syndrome-related Kaposi's sarcomas were excluded from the case series. Four controls were randomly selected for each CKS case among all Cancer Registry cases free from a second neoplasm at the time of diagnosis of the CKS in the case, and matched on gender, year of birth and year of diagnosis of the first neoplasm. The average time lapse between first neoplasm and secondary CKS was 4.5 years, being shorter for prostate cancer and for hematopoietic malignancies. As compared with Israel-born Jews, the risk of a subsequent CKS was significantly increased in immigrants [odds ratio (OR) 3.0]; this risk was particularly high in immigrants from the former Soviet Union (OR 9.4) and Poland (OR 7.0). There was no clear trend with age at immigration; however, low age at immigration and a short length of stay in Israel endowed a higher risk of developing a secondary CKS, markedly among patients suffering from solid tumors as the first primary. There was an excess of secondary CKS following a non-Hodgkin's lymphoma (OR 5.3), a Hodgkin's lymphoma (OR 7.5), a leukemia (OR 5.3) or a breast cancer (OR 2.2). Cancer patients with a first primary in the lung, colon, stomach, larynx, liver, pancreas or kidney showed secondary CKS less frequently. Despite the lack of control of therapy for the first neoplasm, development of secondary CKS seems to be mediated by mechanisms similar to those for hematopoietic neoplasms and selected nonhematopoietic neoplasms, such as breast cancer. The trend toward increased risk after a short time lapse and the difference in risk among immigrants indicate that genetic susceptibility is part of the complex interplay between cellular proliferation and control systems.

Aged↗
PubMed2003

CT and MRI features of recurrent tumors and second primary neoplasms in pediatric patients with retinoblastoma.

OBJECTIVE: The aim of our study was to describe the CT and MRI findings of recurrent tumors and second primary (malignant and benign) neoplasms in patients with retinoblastoma and to evaluate imaging features to assist in distinguishing them. MATERIALS AND METHODS: Records of 445 pathologically confirmed retinoblastomas were retrospectively reviewed. Thirty-four patients with recurrent retinoblastomas and 15 patients with second primary neoplasms who underwent CT and MRI were evaluated by two radiologists with agreement by consensus. RESULTS: Invasive patterns of recurrent tumors included type A, intraocular tumor (n = 13); type B, intraorbital tumor with spread into the optic nerve shown as enlargement and marked enhancement of the optic nerve on contrast-enhanced CT or MRI (n = 6); and type C, tumor extending to the lateral aspect of the orbit and invading the brain via the sphenoidal bone (n = 2). Thirty-eight percent of patients with recurrent tumors had distant metastases (n = 7) or leptomeningeal metastases (n = 6). Leptomeningeal metastases were found only in recurrent tumors. Second primary neoplasms included osteosarcoma (n = 5), rhabdomyosarcoma (n = 5), meningioma (n = 4), and other tumors (n = 3). A significant difference was seen between the patients' ages at the time of diagnosis of recurrent tumors and second primary neoplasms (p < 0.0001). Extraorbital tumors were found more frequently among second primary neoplasms than among recurrent tumors (p < 0.001). CONCLUSION: Both recurrent tumors and second primary neoplasms in patients with retinoblastoma often show characteristic imaging features. The tumor distribution on CT and MRI may help in differentiating recurrent tumors and second primary neoplasms.

Adolescent↗
PubMed2000

Second primary neoplasms following non-Hodgkin's lymphoma in New South Wales, Australia.

The incidence of non-Hodgkin's lymphoma (NHL) has been increasing rapidly over the last three decades. The reasons for this trend are not known although increasing exposure to sunlight has been postulated. We used data from the New South Wales Central Cancer Registry to analyse second primary neoplasms following NHL diagnosed between 1972 and 1995, to identify possible common causal agents. A total of 12,452 patients contributed 54,308 person-years of follow-up during which time there were 705 second primary neoplasms compared to 592.99 expected (standardized incidence ratio (SIR = 1.19, 95% confidence interval (CI) 1.10-1.28). There were excesses of melanomas of skin (SIR = 2.38, 95% CI 1.92-2.91), lip cancer (SIR = 2.74, 95% CI 1.59-4.38), tongue cancer (SIR = 2.53, 95% CI 1.09-4.99) and bladder cancer (SIR = 1.64, 95% CI 1.19-2.21). There was also over a threefold excess in soft tissue sarcomas (SIR = 3.61, 95% CI 1.80-6.45) and in thyroid cancer (SIR = 3.42, 95% CI 1.56-6.49). The SIR for myeloid leukaemia was 0.78 (95% CI 0.28-1.69). The increases in melanoma of the skin and cancer of the lip and tongue among patients with NHL strongly suggest sunlight exposure as a shared causal agent. The increase in soft tissue sarcomas might be due to shared effects of exposure to chemicals such as phenoxy acid herbicides. The increases in bladder and thyroid cancers are likely to be explained by effects of treatment for NHL. We did not find a chemotherapy related increased risk of myeloid leukaemia among NHL patients.

Adult↗