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UNLABELLED: The Executive Committee of the Society of Toxicologic Pathology appointed an ad hoc working group to review the current use of the Peto model for statistical analysis of rodent carcinogenicity study data and to provide recommendations for pathologists regarding appropriate and consistent classification of neoplasms for analysis by the Peto model. In the Peto model, neoplasms that are detected as in-life observations are classified as Mortality Independent and the incidences of these neoplasms are analyzed by the onset-rate method. For neoplasms that are not detected in-life in animals that come to necropsy before the end of the treatment period, the original Peto model requires pathologists to classify neoplasms as Fatal or Incidental (Non-fatal). Each Fatal neoplasm is modeled statistically as rapidly fatal regardless of how long the neoplasm has been present in the animal, and the date of death is used as a surrogate for date of onset of Fatal neoplasms. Fatal neoplasms are analyzed by the death-rate (life-table analysis) method, while Incidental neoplasms are analyzed by the prevalence method. In practice, most neoplasms that cause death are not rapidly fatal, e.g., a slowly progressive pituitary adenoma in a rat. The Peto model does not appropriately model slowly growing or slowly progressive neoplasms that cause death. RECOMMENDATIONS: 1. For animals that die or are killed prior to scheduled sacrifice, all neoplasms should be classified into one of four categories on an animal-by-animal basis: Observed In Life (Mortality-lndependent)--Neoplasms that were observed during in-life observations and for which the day of onset (first observation) was recorded: Incidental--Neoplasms that were not observed prior to necropsy and likely did not contribute to death of the animal or bringing the animal to necropsy; Rapidly Fatal--Neoplasms that were not observed prior to necropsy, likely contributed to death or bringing an animal to necropsy, and appeared to grow and develop rapidly. For these neoplasms, the day of death would serve as a surrogate for the day of onset of the neoplasm: Not Rapidly Fatal--Neoplasms that were not observed prior to necropsy, likely contributed to death or bringing an animal to necropsy, and did not appear to grow or develop rapidly. 2. Other guidelines for pathologists interpreting carcinogenicity studies include: More than one neoplasm may be Rapidly Fatal, Not Rapidly Fatal, and/or Incidental in a single animal. An individual animal may have 2 or more Rapidly Fatal neoplasms if the pathologist believes that each neoplasm had a rapid onset and likely contributed to bringing the animal to necropsy: Each pathologist should use scientific judgment when differentiating Rapidly Fatal and Not Rapidly Fatal neoplasms. This scientific judgment is similar to that used in determining whether neoplasms contribute to the cause of death. Criteria for malignancy (tissue invasion, metastasis, necrosis, high mitotic index, anaplasia, etc.) can be helpful as guides for classifying a neoplasm as Rapidly Fatal. 3. Industry and regulatory statisticians should continue to explore alternatives to the Peto method that do not require classification of neoplasms according to their impact on the death of the animal, and should use these methods if they offer equivalent or superior analytical capabilities.
OBJECTIVE: To estimate the apparent recurrence rates of benign neoplasms and the development of malignant colorectal neoplasms over a 5-yr period in a high risk managed care population. METHODS: Using the CPT and ICD-9 CM codes, a cohort of subjects with benign neoplasms were identified with a colonoscopy in 1992 from a longitudinal claims database (MarketScan). Three groups of subjects (benign neoplasms with polypectomy, benign neoplasms without polypectomy, and no neoplasms) were evaluated. Five-year recurrence rates of benign or new malignant colorectal neoplasms were determined for the baseline benign neoplasms with polypectomy and no neoplasm groups. For the benign neoplasm without polypectomy, only rates for malignancy were evaluated. RESULTS: Of 16,293 subjects at baseline, 39.50% were diagnosed with benign and 5.50% with malignant neoplasms. The 5-yr cumulative incidence of benign neoplasms in subjects without an index neoplasm (n = 8,967) was 7.92% compared to the recurrence of 40.93% in subjects with a benign neoplasm and polypectomy (n = 4,046) at baseline (p < 0.001). The 5-yr cumulative incidence rates of malignant colorectal neoplasms in the no neoplasm (n = 8,967) and benign neoplasm groups (n = 6,438) were 1.81% and 2.55%, respectively (p < 0.005). A lower 5-yr malignancy rate was observed in benign neoplasm group with polypectomy (2.17%) compared to the benign neoplasm group without polypectomy (3.18%) (p < 0.05). CONCLUSION: The high recurrence rate of benign colorectal neoplasms and a higher incidence of colorectal cancer in subjects at high risk (history of benign colorectal neoplasm) highlight a healthcare opportunity for surveillance and/or interventions to reduce the morbidity associated with colorectal neoplasms.
Although inhibin has been shown to be a sensitive marker for ovarian sex cord-stromal and fibrous neoplasms, it may be negative in some cases. Calretinin, a mesothelial marker, has shown promise as a marker for sex cord-stromal neoplasms. The aim of this study was to evaluate and compare calretinin and inhibin as immunohistochemical markers for sex cord-stromal and fibrous neoplasms. A total of 215 ovarian neoplasms were immunostained with commercially available antibodies to calretinin and inhibin. These tumors included 87 sex cord-stromal (39 granulosa cell, 13 Sertoli-Leydig, 4 Sertoli, 9 thecomas, 14 fibrothecomas, and 8 other stromal tumors), 37 fibrous (20 fibromas, 9 adenofibromas, and 8 fibrosarcomas), 65 epithelial, 22 germ cell, and 4 miscellaneous neoplasms. The staining was evaluated on a 0-4 scale based on percentage of neoplastic cells labeling: 0 = none; 1+ = 1-25%; 2+ = 26-50%; 3+ = 51-75%; 4+ = 76-100%. Calretinin reactivity was detected in 100% of sex cord-stromal and 90% of fibrous neoplasms, including 32 that were inhibin negative (2 granulosa cell tumors, 1 Sertoli-Leydig cell tumor, 1 thecoma, 3 fibrothecomas, 16 fibromas, 6 adenofibromas, and 3 fibrosarcomas). All four calretinin-negative fibrous neoplasms were inhibin negative. Calretinin staining was also detected in 22% of epithelial neoplasms but none of the germ cell and miscellaneous neoplasms tested. Inhibin staining was detected in 92% of sex cord-stromal neoplasms, 22% of fibrous neoplasms, 2% of epithelial neoplasms, and none of the germ cell and miscellaneous neoplasms tested. Calretinin has a 97% sensitivity and 85% specificity for sex cord-stromal and fibrous neoplasms, whereas inhibin has a 71% sensitivity and 99% specificity. This study shows that both calretinin and inhibin are useful in the diagnosis of ovarian sex cord-stromal and fibrous neoplasms. Calretinin is a more sensitive but less specific immunohistochemical marker than inhibin. Calretinin is particularly useful in the diagnosis of sex cord-stromal and fibrous neoplasms that are inhibin negative. The high frequency of calretinin in fibrous neoplasms suggests that a subgroup of these neoplasms may be derived from specialized gonadal stromal cells, perhaps thecal cells.
Oncocytic neoplasms of the adrenal gland are rare. We describe the clinicopathologic and immunohistochemical findings of seven oncocytic adrenocortical neoplasms, five oncocytomas, and two oncocytic neoplasms of uncertain malignant potential. Three tumors were studied using electron microscopy. These neoplasms occurred in five women and two men (median age, 55 years) with no clinical evidence that the neoplasms were functional. The size of the neoplasms varied from 5.0 cm to 13.5 cm. Histologically, each neoplasm was composed exclusively of oncocytes. The oncocytomas had very low or absent mitotic activity and no evidence of necrosis. The two oncocytic neoplasms of uncertain malignant potential had increased mitotic activity and necrosis but no evidence of invasion or metastases. Nuclear atypia, either focal or generalized, was found in all neoplasms. Immunohistochemical studies performed using fixed, paraffin-embedded sections showed strong reactivity with the mitochondrial antibody mES-13 in all neoplasms. Four of five oncocytomas and one oncocytic neoplasm of uncertain malignant potential expressed keratin, predominantly keratin 18, as shown using the CAM 5.2 and AE3 antibodies. Two neuroendocrine-associated markers, neuron specific enolase and synaptophysin, were positive in seven and five neoplasms, respectively. However, all neoplasms were negative for the other neuroendocrine markers tested, including chromogranin A, tyrosine hydroxylase, and dopamine beta-hydroxylase, as well as for epithelial membrane antigen, S100, and p53. Using the MIB-1 (Ki-67) antibody, proliferative activity was increased in both oncocytic neoplasms of uncertain malignant potential. All six patients with available clinical follow-up data are alive without evidence disease, although the follow-up interval is relatively short (< 2 years) for the two patients with oncocytic neoplasms of uncertain malignant potential. We conclude that oncocytic adrenocortical neoplasms are nonfunctional tumors that can become large before they are detected by radiologic studies. The majority of neoplasms are benign and should not be misdiagnosed as carcinoma.
The behavior of pancreatic mucinous cystic neoplasms has long been debated. Some authors contend that histologically benign neoplasms can recur and metastasize. We reviewed the gross and microscopic findings and outcomes of 61 mucinous cystic neoplasms diagnosed at The Johns Hopkins Hospital from March 20, 1984 to July 8, 1998. Each neoplasm was placed into one of four categories based on complete histologic examination: invasive mucinous cystadenocarcinoma, mucinous cystic neoplasm with in situ carcinoma, borderline mucinous cystic neoplasm, and mucinous cystadenoma. Neoplasms in the latter three categories were included only if they were entirely resected and completely examined. Patient outcomes were obtained from hospital records and patient and physician follow-up. Twenty (33%) of the patients had invasive mucinous cystadenocarcinomas, and they had 2- and 5-year disease-specific survival rates of 67% and 33% (mean follow-up of survivors, 4.2 years), respectively. Nine (15%) patients had mucinous cystic neoplasms with in situ carcinoma (mean follow-up of survivors, 4.1 years). Five (8.2%) patients had borderline mucinous cystic neoplasms (mean follow-up of survivors, 5.6 years). Twenty-seven (44%) patients had mucinous cystadenomas (mean follow-up of survivors, 5.1 years). No mucinous cystadenoma, borderline mucinous cystic neoplasm, or mucinous cystic neoplasm with in situ carcinoma recurred or metastasized. No patient with the diagnosis of mucinous cystadenoma, borderline mucinous cystic neoplasm, or mucinous cystic neoplasm with in situ carcinoma died of disease. The difference in disease-specific survival rates between patients with invasive mucinous cystadenocarcinomas and those with noninvasive tumors was significant (p < 0.0001, log-rank test). One case, originally showing only benign histology on incisional biopsy, contained foci of invasive carcinoma on complete resection. Completely resected and entirely examined mucinous cystadenomas, borderline mucinous cystic neoplasms, and mucinous cystic neoplasms with in situ carcinoma follow benign courses. Because invasive carcinoma can be focal, failure to study an entire mucinous cystic neoplasm may result in the miscategorization of a malignant neoplasm as benign.
Intraductal papillary neoplasms of the biliary tree are unusual lesions characterized by solitary or diffuse growth along the intra- and/or extrahepatic biliary tract. Biliary papillary neoplasms bear some clinicopathologic similarity to intraductal papillary mucinous neoplasms of the pancreas. Like intraductal papillary mucinous neoplasms of the pancreas, biliary papillary neoplasms can be purely intraductal lesions or can give rise to invasive adenocarcinomas. We recently studied the genetic alterations present in a series of biliary papillary neoplasms and noted the presence of allelic shifts in some biliary tumors during allelic loss assays on chromosomes 5q and 18q. This suggested that microsatellite instability might play a role in the molecular pathogenesis of biliary papillary neoplasms. Genomic DNA was extracted from 17 intraductal papillary neoplasms, 6 associated invasive cholangiocarcinomas, and corresponding normal tissues, and microsatellite instability testing was performed using the 5 microsatellite loci recommended by the 1997 National Cancer Institute-sponsored consensus conference (D2S123, D5S346, D17S250, Bat-25, and Bat-26). High-level microsatellite instability was considered to be present when at least two of five microsatellite loci showed allelic shifts, and low-level microsatellite instability, when only one locus was shifted, as per the National Cancer Institute criteria. We also determined the methylation status of the DNA mismatch repair gene hMLH1 by bisulfite treatment of genomic DNA, followed by methylation-specific PCR. High-level microsatellite instability was present in 2 of 17 (11.8%) biliary papillary neoplasms, including 1 case of purely intraductal tumor and 1 case with both intraductal and invasive cholangiocarcinoma components. In both cases there was extensive microsatellite instability, with allelic shifts in five of five and four of five microsatellite markers, respectively. Low-level microsatellite instability was present in 6 of 17 (35.3%) biliary papillary neoplasms, including 2 cases of purely intraductal tumor and 4 cases with both intraductal and invasive cholangiocarcinoma components. Interestingly, the pattern of allelic shifts was frequently not identical between the intraductal and invasive cholangiocarcinoma components; although the same microsatellite markers were shifted, alleles of differing lengths were generated in the intraductal and invasive components of the neoplasms with high-level microsatellite instability and of two neoplasms with low-level microsatellite instability. None of the biliary papillary neoplasms (0 of 10 cases with adequate DNA for evaluation) showed methylation of hMLH1. These results indicate that microsatellite instability is a relatively frequent event in papillary neoplasms of the biliary tree but is not associated with hMLH1 promoter hypermethylation. The finding that alleles of differing lengths were frequently generated between the intraductal and invasive components of those tumors with microsatellite instability suggests that there is significant genetic heterogeneity within these neoplasms.
INTRODUCTION: Cardiac neoplasms are rare and the vast majority are metastatic in origin. Symptoms of cardiac neoplasms (primary or metastatic) usually appear late in the course of the disease and are often ignored because of the more severe effects of the primary malignant disorder or its therapy. Consequently, cardiac neoplasms, especially metastatic ones, are often not discovered until autopsy. OBJECTIVES: To assess the incidence of cardiac neoplasms at autopsy and to determine the sites of origins of metastatic cardiac neoplasms. METHODS: The pathology records from consecutive autopsies performed at the University Health Network, Toronto, Ontario, from January 1973 to May 2004 were reviewed. They showed 266 cases of neoplasms involving the heart among 11,432 consecutive autopsies. These cases were then categorized based on their system of origin and further subclassified into specific primary site categories. As well, the type of cardiac tissue affected was noted in 193 cases (72.6%). RESULTS: The 266 autopsy cases involving cardiac neoplasms represented 2.33% of the total number of autopsies. Among the 266 cases, two neoplasms were primaries, while 264 were metastatic in origin. Metastatic cardiac neoplasms most frequently metastasized from the respiratory system, followed (in order of decreasing frequency) by the hematopoietic, gastrointestinal, breast and genitourinary systems. A minority of metastatic cardiac neoplasms were found to have spread from other systems. Cardiac neoplasms most frequently involved the pericardium, followed (in order of decreasing frequency) by the myocardium, epicardium and endocardium. CONCLUSIONS: There were 132 times more metastatic cardiac neoplasms than primary cardiac neoplasms found in the present study. The most common sites of metastatic origin were the lungs, bone marrow (leukemia/multiple myeloma), breasts and lymph nodes (lymphoma). Leukemias were more prevalent in the present study than in previous studies. The pericardium was the tissue that was most frequently affected by metastatic cardiac neoplasms.
Although cystic neoplasms and lesions of the pancreas are rare, they have attracted a great deal of attention because of their potential curability. Since, in recent years, several new entities have been identified, the relative frequency of the tumors and their classification need to be reevaluated. In a series of 1454 tumorous lesions of the pancreas collected between 1971 and 2003 in our surgical pathology files and consultation files, all cystic pancreatic neoplasms and tumor-like lesions were identified and typed both histologically and immunohistochemically. There were 418 cases (29%) showing cysts with a diameter ranging between 0.5 cm and 27 cm. Most common were solid pseudopapillary neoplasms (21%) and intraductal papillary-mucinous neoplasms (18%). When only the cystic neoplasms and lesions that had been resected in a single institution were considered, intraductal papillary mucinous neoplasms were the most frequent cystic neoplasms, while solid pseudopapillary neoplasms took fifth place behind ductal adenocarcinomas with cystic features, serous cystic neoplasms and mucinous cystic neoplasms. The most frequent cystic tumor-like lesions were pancreatitis-associated pseudocysts. New and rare entities that have recently been identified are mucinous nonneoplastic cysts, acinar cell cystadenomas and cystic hamartomas. Bearing in mind that figures from referral centers such as ours may be biased regarding the relative frequency of lesions, we concluded from our data that intraductal papillary-mucinous neoplasms are the most frequently occurring pancreatic cystic neoplasms, rather than solid pseudopapillary neoplasms. It was possible to classify all cystic lesions encountered in our files or described in the literature in a new system that distinguishes between neoplastic and nonneoplastic lesions, with further subdivisions into epithelial (adenomas, borderline neoplasms and carcinomas) and nonepithelial tumors. This classification is easy to handle and enables a distinction on the basis of clinical behavior and prognosis.
OBJECTIVE: Helical CT scanners now allow sequential arterial phase and portal venous phase scans of the entire liver to be obtained during a single bolus injection of contrast material. The purpose of this study was to determine if arterial phase scans improve detection of small (< or = 1.5 cm) malignant hepatic neoplasms when compared with portal venous scans alone. MATERIALS AND METHODS: Dual-phase helical CT of the liver was done in 96 patients referred for known or suspected malignant hepatic lesions. Malignant hepatic neoplasms were detected in 38 patients (27 with at least one small neoplasm), one patient had undetected metastases, one patient had a benign hepatic neoplasm, and 56 patients had no hepatic neoplasm. Proof of individual neoplasms was based on biopsy results, surgical findings, or findings on other imaging studies (primarily follow-up CT). The absence of disease was established by surgical or autopsy findings, findings on subsequent imaging studies, or a combination of clinical and laboratory data. A total of 150 ml of 60% nonionic contrast material was infused at 5 ml/sec followed by sequential arterial phase and portal venous phase helical scans of the liver. Three radiologists retrospectively reviewed the scans. Individual lesions were measured and the conspicuity of each lesion on arterial phase and portal venous phase scans was compared. The percentage of patients in whom some malignant neoplasms were detected better on the arterial phase scan was calculated using categories based on lesion size and typical tumor vascularity. RESULTS: In 10 (37%) of 27 patients who had at least one small malignant neoplasm, lesions 1.5 cm or less in diameter were only visible or were more conspicuous on the arterial phase scan. No malignant neoplasms more than 1.5 cm in diameter were visible only on the arterial phase scan. In four (11%) of 38 cases, malignant neoplasms more than 1.5 cm in diameter were more conspicuous on the arterial phase scan. The arterial phase scans improved lesion conspicuity in nine (39%) of 23 patients who had typically hypervascular neoplasms, whereas lesion conspicuity was improved in three (20%) of 15 patients who had typically hypovascular neoplasms (p = .02). The arterial phase scan resulted in the false-positive detection of lesions in two (2%) of 96 cases. CONCLUSION: Arterial phase helical CT of the liver improves detection of some small, malignant hepatic neoplasms when performed in addition to portal venous scanning. The value is greatest in those patients who have hypervascular neoplasms.
WT-1 positivity has previously been noted in nonneoplastic endometrial stroma. In this study we examined WT-1 expression in endometrial stromal neoplasms to ascertain whether these tumors are immunoreactive and whether this antibody might be of value in the diagnosis of these lesions. We also stained cases of cellular and highly cellular leiomyomas to investigate whether WT-1 might be of value in distinguishing these from an endometrial stromal neoplasm. We compared WT-1 staining with CD10, desmin, alpha smooth muscle actin, h-caldesmon, and AE1/3, many of these antibodies being commonly used to distinguish between an endometrial stromal and a smooth muscle phenotype. Cases of ESN (n = 5), low grade ESS (n = 14), and cellular or highly cellular leiomyoma (n = 14) were stained with the aforementioned antibodies. Cases were scored on a scale of 0 to 4+, with 4+ cases exhibiting positivity of >50% of cells. Sixteen of 19 endometrial stromal neoplasms were positive with WT-1, most (14 of 16) with 4+ positivity. Staining was nuclear (5 cases), cytoplasmic (5 cases), or combined nuclear and cytoplasmic (6 cases). All endometrial stromal neoplasms exhibited 4+ staining with CD10. Staining for alpha smooth muscle actin was present in most cases (14 of 19) and desmin and h-caldesmon were positive in a smaller number of cases (8 and 2 respectively). There was 4+ positivity with desmin in only 1 case. The 2 cases that were h-caldesmon positive both exhibited 1+ staining (<5% cells positive). Six cases were positive with AE1/3, 1 with 4+ staining. Leiomyomatous neoplasms always exhibited 4+ staining with desmin and alpha smooth muscle actin and in most cases (12 of 14) with h-caldesmon. The other 2 cases exhibited 2+ positivity. Most cases (12 of 14) were positive with WT-1 (7 of 14 with 4+ staining) and CD10 (5 of 14 with 4+ positivity). One case was positive with AE1/3. We conclude that diffuse WT-1 positivity is characteristic of endometrial stromal neoplasms and that this may be of value in diagnosis. However, WT-1 is of limited use in the distinction between an endometrial stromal and a cellular leiomyomatous neoplasm because many of the latter are also positive. This study confirms the value of h-caldesmon in the distinction between an endometrial stromal neoplasm (almost always h-caldesmon negative) and a cellular leiomyomatous neoplasm (h-caldesmon positive). Although CD10 is positive in endometrial stromal neoplasms, the commonly observed immunoreactivity of cellular and highly cellular leiomyomas with this antibody limits its diagnostic usefulness. Desmin is useful as all leiomyomatous neoplasms exhibited diffuse positivity, whereas only a small number of endometrial stromal neoplasms were focally positive and only 1 case exhibited 4+ positivity. Smooth muscle actin is of limited value since most neoplasms studied were positive. The overlapping immunophenotype of endometrial stromal and leiomyomatous neoplasms may reflect the origin of both cell types from a common progenitor within the uterus.
The relative frequency of ovarian neoplasms varies according to information in different texts. In an attempt to clarify the distribution of primary ovarian neoplasms by decades of life, a 10-year retrospective review of 861 women with a postoperative diagnosis of an ovarian neoplasm was undertaken. Benign cystic teratoma was the single most common ovarian neoplasm, accounting for 44% of all neoplasms, and was 57% more frequent than benign serous tumors. Germ cell neoplasms were the most common group of benign ovarian neoplasms; epithelial neoplasms were the most common malignant neoplasm. Stromal neoplasms and neoplasms of low malignant potential were uncommon at all ages. The risk that an ovarian neoplasm was malignant increased 12-fold from ages 20-29 to 60-69. The overall risk that an ovarian neoplasm was malignant was 13% in premenopausal women and 45% in postmenopausal women.
BACKGROUND: The significance of the small distal tubular adenoma detected by sigmoidoscopy as a predictor of proximal neoplasm remains controversial. The aim of this study was to examine the prevalence of proximal neoplasms in patients with and without distal neoplasms. METHODS: This is a retrospective study of 3131 asymptomatic middle-aged men who underwent total colonoscopy. For 812 men with colorectal neoplasms characteristics of the identified neoplasms were determined. RESULTS: The prevalence of proximal neoplasms in patients with small distal tubular adenoma was 20% (92 of 461), whereas the prevalence of proximal neoplasms in patients without distal neoplasms was 11.5% (301 of 2620). The prevalence of advanced proximal neoplasms in patients with small distal tubular adenoma and without distal neoplasm was 1.3% and 0.8%, respectively. In the 29 patients with advanced proximal neoplasms, only 6 (21%) had a small distal tubular adenoma. CONCLUSIONS: The presence of small distal tubular adenomas may provide a clue to the presence of small proximal tubular adenomas. However, the majority of advanced proximal neoplasms (79%) do not have a synchronous small distal tubular adenoma. (Gastrointest Endosc 2000;52:358-61).
BACKGROUND: We investigated the incidence and imaging features of hepatic neoplasms containing normal hepatic vessels. METHODS: Among 3183 patients with various hepatic neoplasms, we found nine patients with normal hepatic vessels traversing hepatic neoplasms. The presence of mass effect on the vessel traversing hepatic neoplasms was evaluated. Other suggestive findings of neoplasms such as altered hepatic contour, portal vein thrombosis, mass effect on extratumoral vessel, and bile duct dilatation were analyzed. RESULTS: Thirteen hepatic vessels (nine hepatic veins and four portal veins) extended through hepatic neoplasms in nine patients. Undisturbed hepatic vessels within the neoplasms were found in five patients with either primary or metastatic hepatic neoplasm. In one patient with undisturbed hepatic vessels within the neoplasm, there were no associated abnormal findings such as biliary dilatation, change of hepatic contour, or any changes involving the vessels external to neoplasms. CONCLUSION: Although rare, various primary and secondary hepatic neoplasms can have normal hepatic vessels passing through them without mass effect. However, correct diagnosis in most neoplasms would be possible with careful examination of associated findings.
BACKGROUND: Accurate identification of phyllodes neoplasms without surgical intervention is difficult, reducing the ability to manage "benign" lumps non-operatively and impacting on the open benign biopsy rate. Needle core biopsy is considered to be a highly accurate technique in the diagnosis of breast carcinoma. Its accuracy in the diagnosis of phyllodes neoplasm has not been established. METHODS: A series of 3729 core biopsies performed between January 1999 and July 2005 were examined. All core biopsies followed by surgical excision were identified. Histologic concordance between core biopsy and excision specimen was analyzed. RESULTS: Twenty-three patients had phyllodes neoplasm on excisional biopsy with prior core biopsy findings as follows: phyllodes neoplasm (n=2), "equivocal" for phyllodes neoplasm (n=12), fibroadenoma (n=3), benign (n=6). The false negative rate for phyllodes neoplasm was therefore 39% (n=9/23). Of the total biopsy series, 35 patients had a core biopsy suggesting the possibility of phyllodes neoplasm. Of these, 32% (n=11) were found to be phyllodes neoplasm on excision, 3% (n=1) phyllodes neoplasm with breast carcinoma, 6% (n=2) breast carcinoma, and 3% (n=1) sarcoma. When a preference for phyllodes neoplasm (n=4) was stated on the equivocal core biopsies, excision correlated with the stated preference; this correlation also occurred in 90% (n=9/10) of core biopsies where fibroadenoma was favored. CONCLUSIONS: Needle core biopsy rarely produces a definite preoperative diagnosis of phyllodes neoplasm. A diagnosis of fibroadenoma or equivocal phyllodes neoplasm on core biopsy should not prevent excision if clinical suspicion remains.
Sixty-six cases of multiple primary neoplasms in children in Japan were collected, including 8 cases of our own. These could be divided into 19 synchronous and 47 metachronous multiple neoplasms. Metachronous or multiple primary neoplasms comprised leukemia, osteosarcoma, mesenchymal sarcoma, epithelial carcinoma and others in contrast to synchronous neoplasms which consisted of many pairs of embryonic tumors. The presumptive factors for multiple primary neoplasms suggested radiotherapy-associated cancers in 30%, radiochemotherapy-associated in 13%, chemotherapy-associated in 34%, and genetic factor-related in 36% of cases. Chromosomal analysis was performed in 12 cases. Three of 4 leukemias revealed major karyotypic abnormalities in the leukemic cells. No 13q14, deletion was detected in 5 cases with multiple primary neoplasms developed with retinoblastoma. Frequent incidence of sister chromatid exchange (SCE) was detected in cultured fibroblasts or lymphocytes from one of 3 cases of second primary neoplasms associated with chemotherapy. The time interval between both neoplasms ranged from 2 to 15 years in the majority of cases. Chemotherapy-associated multiple primary neoplasms seemed to appear more quickly than radiotherapy-associated multiple primary neoplasms. Seven children out of 459 long-term survivors of childhood cancer developed multiple primary neoplasms during the period from 5 to 20 years after diagnosis of the first tumor at the National Cancer Center Hospital, Tokyo. The relative risk was suggested to be 14 times higher than the expected incidence of childhood cancer in Japan. Refinement of treatment, long-term monitoring and protective procedures for high-risk patients against multiple primary neoplasms are therefore warranted.
Chloroprene is the 2-chloro analog of 1,3-butadiene, a potent carcinogen in laboratory animals. Following 2 years of inhalation exposure to 12.8, 32 or 80 p.p.m. chloroprene, increased incidences of lung and Harderian gland (HG) neoplasms were observed in B6C3F1 mice at all exposure concentrations. The present study was designed to characterize genetic alterations in the K- and H-ras proto-oncogenes in chloroprene-induced lung and HG neoplasms. K-ras mutations were detected in 80% of chloroprene-induced lung neoplasms (37/46) compared with only 30% in spontaneous lung neoplasms (25/82). Both K- and H-ras codon 61 A-->T transversions were identified in 100% of HG neoplasms (27/27) compared with a frequency of 56% (15/27) in spontaneous HG neoplasms. The predominant mutation in chloroprene-induced lung and HG neoplasms was an A-->T transversion at K-ras codon 61. This mutation has not been detected in spontaneous lung tumors of B6C3F1 mice and was identified in only 7% of spontaneous HG neoplasms. In lung neoplasms, greater percentages (80 and 71%) of A-->T transversions were observed at the lower exposures (12.8 and 32 p.p.m.), respectively, compared with 18% at the high exposure. In HG neoplasms, the percentage of A-->T transversions was the same at all exposure concentrations. The chloroprene-induced ras mutation spectra was similar to that seen with isoprene, where the predominant base change was an A-->T transversion at K-ras codon 61. This differed from 1,3-butadiene, where K-ras codon 13 G-->C transitions and H-ras codon 61 A-->G transitions were the predominant mutations. The major finding of K-ras A-->T transversions in lung and Harderian gland neoplasms suggests that this mutation may be important for tumor induction by this class of carcinogens.