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J Isola

Publications and source records attributed to J Isola.

At least 37 records · Page 2Linked to original sources
PubMed2001

The visibility of cancer on previous mammograms in retrospective review.

AIM: To study how many tumours were visible in restrospect on mammograms originally reported as normal or benign in patients coming to surgery with proven breast cancer. The effect of making the pre--operative mammogram available was also assessed. MATERIALS AND METHODS: Three hundred and twenty initial mammograms of consecutive new breast cancer cases were analysed by a group of radiologists in the knowledge that all patients were later diagnosed with breast cancer. The films were read twice, first without and then with the later (pre-operative) mammograms available. The parenchymal density in the location of the tumour was classified as fatty, mixed or dense, and the tumours were classified as visible or not visible. The reasons for the invisibility of the tumour in the earlier examination were analysed. RESULTS: Fourteen per cent (45) of cancers were retrospectively visible in earlier mammograms without the pre-operative mammograms having been shown, and 29% (95) when pre-operative mammograms were shown. Breast parenchymal density decreased with age and the visibility of tumours increased with age. When considered simultaneously, the effect of age (over 55 vs under 55) was greater (OR = 2.9) than the effect of density (fatty vs others) (OR = 1.5). The most common reasons for non-detection were that the lesion was overlooked (55%), diagnosed as benign (33%) or was visible only in one projection (26%). Growing density was the most common (37%) feature of those lesions originally overlooked or regarded as benign. CONCLUSIONS: Tumours are commonly visible in retrospect, but few of them exhibit specific signs of cancer, and are recognized only if they grow or otherwise change. It is not possible to differentiate most of them from normal parenchymal densities. Saarenmaa, I. (2001). Clinical Radiology56, 40-43.

Adult↗
PubMed2001

Lumpectomy with or without postoperative radiotherapy for breast cancer with favourable prognostic features: results of a randomized study.

The aim of this trial was to study the value of adding post-operative radiotherapy to lumpectomy in a subgroup of breast cancer patients with favourable patient-, tumour-, and treatment-related prognostic features. 152 women aged over 40 with unifocal breast cancer seen in preoperative mammography were randomly assigned to lumpectomy alone (no-XRT group) or to lumpectomy followed by radiotherapy to the ipsilateral breast (50 Gy given within 5 weeks, XRT group). All cancers were required to be invasive node-negative, smaller than 2 cm in diameter and well or moderately differentiated, to contain no extensive intraductal component, to be progesterone receptor-positive, DNA diploid, have S-phase fraction </=7 and be excised with at least 1 cm margin. During a mean follow-up time of 6.7 years, 13 (18.1%) cancers recurred locally in the no-XRT and 6 (7.5%) in the XRT group (P = 0.03). There was no difference between the groups in the ultimate breast preservation rate (95.0% vs. 94.4% in XRT and no-XRT, respectively, P = 0.88), distant metastasis-free survival (P = 0.36), or 5-year cancer-specific survival (97.1% in XRT and 98.6 in no-XRT). Radiation therapy given after lumpectomy reduces the frequency of ipsilateral breast recurrences even in women with small breast cancer with several favourable clinical and biological features. However, the breast preservation rate may not increase due to more frequent use of salvage mastectomies in patients treated with postoperative radiotherapy.

Adult↗
PubMed2001

Validity of radiological examinations of patients with breast cancer in different age groups in a population based study.

By studying which radiological examinations had been performed before breast cancer operations the aim was to assess, how much benefit ultrasonography (US) and fine or core needle biopsy (FNAB, CNB) gave in addition to mammography, and whether the sensitivity of these examinations varied with the age of the patient. There were 659 consecutive histologically and six cytologically verified breast cancer cases included in the study. Information on mammography, US and FNAB findings were retrieved from the original patient files and classified as malignant or benign. The sensitivity (Se) of these was compared in three age groups (26-49, 50-59 and 60-92). Seventeen (3%) tumours had operations without any radiological examination and 73 (11%) without cytological or histological verification. The sensitivity of mammography (Se=0.92) was statistically significantly higher than the sensitivity of FNAB (Se=0.85, P=0.002) or US (Se=0.86, P=0.003). The sensitivity of mammography increased with age; US sensitivity was slightly higher amongst younger than older patients; the sensitivity of FNAB did not depend on the age of the patient. The sensitivity using a cutoff level of class 5 for mammography was higher (50% typical malignant findings) than for US (45%) or FNAB (30%). Among cases with benign mammographic finding (classes 1-2), the US finding was malignant (classes 3-5) in 4% and FNAB was malignant in 7%. Mammography is a reliable method of breast examination especially for women over 50 years of age. Ultrasonography is beneficial, particularly in younger women, but it is mainly performed as a complementary examination to a mammography and therefore could not be evaluated as an independent examination. FNAB and CNB results were not related to the age of the patient.

Journal Article↗
PubMed2001

5q11, 8p11, and 10q22 are recurrent chromosomal breakpoints in prostate cancer cell lines.

Prostate cancer cell lines have been widely used as model systems characterizing pathogenetic, functional, and therapeutic aspects of prostate cancer development. However, their chromosomal compositions are poorly characterized. In this study, five prostate cancer cell lines-TSU-Pr1, JCA-1, NCI-H660, ALVA-31, and PPC-1-were investigated by G-banding, comparative genomic hybridization (CGH), and spectral karyotyping. The results were combined with our previous findings in the prostate cancer cell lines PC-3, DU145, and LNCaP. By comparative genomic hybridization (CGH), the most frequent losses were observed at 13q, 8p, 9p, and 4q, whereas gains were most commonly seen at 8q, 10q, and 18p. The composite karyotypes were characterized by multiple numerical and structural chromosomal aberrations. Recurrent breakpoints at 5q11, 8p11, and 10q22 were observed to participate in deletion and translocation events in five of the cell lines, suggesting the importance of tumor suppressor and/or oncogenes in these regions. ALVA-31 and PPC-1 shared nine identical derivative chromosomes, two of which have also been detected in PC-3. In addition, the identification of the same homozygous deletion at D10S541 and of an identical TP53 gene mutation in all three cell lines suggests a common origin of these cell lines.

Chromosome Breakage↗
PubMed2001

Predictors of biological aggressiveness of prostate specific antigen screening detected prostate cancer.

PURPOSE: It is not known whether screening of asymptomatic men with prostate specific antigen (PSA) decreases the mortality of prostate cancer. We evaluated the extent to which PSA screening identifies clinically significant prostate cancer by analyzing markers of biological aggressiveness. MATERIALS AND METHODS: We compared prostate cancer in 56 patients in the screening and 21 in the randomized control arm of a population based cohort of 8,975 men 55 to 67 years old participating in the Finnish arm of the European Randomized Study of Screening for Prostate Cancer to 47 clinically detected organ confined, 30 clinically detected metastatic and 16 latent prostate tumors identified at autopsy in 46 consecutive subjects. Biological aggressiveness was determined by histological grading using the Gleason and Mostofi scales, tumor proliferation rate by Ki-67 immunostaining, p53 over expression by immunostaining and aneuploidy by fluorescence in situ hybridization using formalin fixed, paraffin embedded tumor specimens. RESULTS: A total of 56 neoplasms were detected in 2,781 men (2%) who participated in PSA screening and 21 were detected in 5,975 nonscreened controls (0.35%) during the study period. Disease in nonscreened controls more often involved a high tumor proliferation rate (p = 0.004) and p53 over expression (p = 0.015) than screening detected disease. At least 1 feature of biological aggressiveness was present in 19% of latent, 34% of screening detected, 51% of clinically detected and organ confined, 62% of randomized control and 87% of metastasis cases. Of the screening detected tumors defined as biologically aggressive 74% were identified at organ confined stages pT1-2N0M0. CONCLUSIONS: PSA screening detects a significant number of biologically aggressive cancers at an early clinical stage, implying that screening may decrease mortality.

Aged↗
PubMed2000

MYB oncogene amplification in hereditary BRCA1 breast cancer.

Comparative genomic hybridization analysis has demonstrated that breast tumors from BRCA1 and BRCA2 germ-line mutation carriers contain a large number of chromosomal copy number gains and losses. A high regional copy number gain at 6q22-q24 was observed in one BRCA1 tumor, and fluorescence in situ hybridization analysis indicated a strong amplification of the MYB oncogene (15 copies of MYB compared with 1 copy of chromosome 6 centromere). Fluorescence in situ hybridization analysis revealed amplification of MYB in 5 (29%) of 17 BRCA1 breast tumors, whereas none of 8 BRCA2 tumors and 13 breast cancer cell lines, and only 2 of 100 sporadic breast tumors exhibited altered MYB copy numbers. Gene amplification resulted in mRNA overexpression as determined by Northern blot and cDNA microarray analysis, and protein overexpression by immunohistochemical staining. We conclude that MYB amplification is infrequent in sporadic breast cancer but common in breast tumors from BRCA1 mutation carriers, suggesting a role of this cell cycle regulator and transcription factor in the progression of some BRCA1 tumors. However, we cannot rule out the significance of other genes in the 6q22-q24 amplicon.

Blotting, Northern↗
PubMed2000

Germline BRCA1 and HMLH1 mutations in a family with male and female breast carcinoma.

Hereditary non-polyposis colorectal cancer (HNPCC) is an autosomal dominant disease, predisposing to the development of colorectal cancer and other tumor types such as endometrial, small bowel, stomach, ovary and urinary tract carcinoma, while most investigators find no association between HNPCC and cancer of the breast. We have identified hMLH1 mutations in 2 Amsterdam-criteria HNPCC families where both male and female gene carriers were affected with breast cancer. To investigate whether these breast cancers were caused by other genetic factors, we analyzed the 2 breast cancer susceptibility genes BRCA1 and BRCA2. In one family we did not find any mutation in the breast cancer genes, while in the other, a BRCA1 mutation segregated in the breast cancer cases. Hereditary breast cancer, and in particular BRCA1 tumors, display discrete histo-pathological and immunohistological characteristics. The tumor from a woman with both hMLH1 mutations and a BRCA1 mutation exhibited typical BRCA1 histology, e.g., grade 3 invasive ductal carcinoma with dense lymphocytic infiltration, and immunohistology, estrogen receptor (ER) negative, progesterone receptor (PgR) negative, strongly p53 positive, c-erbB-2 negative and highly Ki67 positive (>50% stained cells). The histology of the breast tumor from the man with both one hMLH1 mutation and a BRCA1 mutation was a grade 2 invasive ductal carcinoma without any special BRCA1 features. Immunohistology was also different. This might merely reflect a true difference in male breast tumor progression vs. female. We cannot exclude that the combined effect of BRCA1 and hMLH1 dysfunction has a bearing on tumor progression.

Adaptor Proteins, Signal Transducing↗
PubMed2000

Chromosomal alterations in 15 breast cancer cell lines by comparative genomic hybridization and spectral karyotyping.

Breast cancer cell lines have been widely used as models in functional and therapeutical studies, but their chromosomal alterations are not well known. We characterized the chromosomal aberrations in 15 commonly used human breast carcinoma cell lines (BT-474, BT-549, CAMA-1, DU4475, MCF7, MDA-MB-134, MDA-MB-157, MDA-MB-361, MDA-MB-436, MPE600, SK-BR-3, T-47D, UACC-812, UACC-893, and ZR-75-1) by comparative genomic hybridization (CGH) and spectral karyotyping (SKY). By CGH the most frequent gains were detected at 1q, 8q, 20q, 7, 11q13, 17q, 9q, and 16p, whereas losses were most common at 8p, 11q14-qter, 18q, and Xq. SKY revealed a multitude of structural and numerical chromosomal aberrations. Simple translocations, typically consisting of entire translocated chromosome arms, were the most common structural aberrations. Complex marker chromosomes included material from up to seven different chromosomes. Evidence for a cytogenetic aberration not previously described in breast cancer, the isoderivative chromosome, was found in two cell lines. Translocations t(8;11), t(12;16), t(1;16), and t(15;17) were frequently found, although the resulting derivative chromosomes and their breakpoints were strikingly dissimilar. The chromosomes most frequently involved in translocations were 8, 1, 17, 16, and 20. An excellent correlation was found between the number of translocation events found by SKY in the individual cell lines, and the copy number gains and losses detected by CGH, indicating that the majority of translocations are unbalanced. Genes Chromosomes Cancer 28:308-317, 2000.

Breast Neoplasms↗
PubMed2000

Patterns of chromosomal imbalances in parathyroid carcinomas.

In this study we have characterized chromosomal imbalances in a panel of 29 parathyroid carcinomas using comparative genomic hybridization (CGH). The most frequently detected imbalances were losses of 1p and 13q that were seen in >40% of the cases. The commonly occurring regions of loss were assigned to 1p21-p22 (41%), 13q14-q31 (41%), 9p21-pter (28%), 6q22-q24 (24%), and 4q24 (21%), whereas gains preferentially involved 19p (45%), Xc-q13 (28%), 9q33-qter (24%), 1q31-q32 (21%) and 16p (21%). The distribution of CGH alterations supports the idea of a progression of genetic events in the development of parathyroid carcinoma, where gains of Xq and 1q would represent relatively early events that are followed by loss of 13q, 9p, and 1p, and by gain of 19p. A sex-dependent distribution was also evident for two of the common alterations with preferential gain of 1q in female cases and of Xq in male cases. When the CGH profiles for the 29 carcinomas were compared with our previously published results for sporadic parathyroid adenomas, highly significant differences were revealed. Loss of 1p, 4q, and 13q as well as gains of 1q, 9q, 16p, 19p and Xq were significantly more common in the carcinomas than in the adenomas. In contrast, loss of the 11q13 region, which is the most common CGH abnormality in sporadic adenomas, was not detected in any of the carcinomas. Taken together, the findings identify several candidate locations for tumor suppressor genes and oncogenes that are potentially involved in parathyroid carcinogenesis.

Adenoma↗
PubMed2000

Estrogen receptor beta is coexpressed with ERalpha and PR and associated with nodal status, grade, and proliferation rate in breast cancer.

The role of estrogen (ER) and progesterone receptors (PR) in breast cancer is well established. Identification of the second human estrogen receptor, the estrogen receptor beta (ERbeta), prompted us to evaluate its role in breast cancer. We studied the expression of ERbeta by immunohistochemistry and mRNA in situ hybridization in 92 primary breast cancers and studied its association with ERalpha, PR, and various other clinicopathological factors. Sixty percent of tumors were defined as ERbeta-positive (nuclear staining in >20% of the cancer cells). Normal ductal epithelium and 5 of 7 intraductal cancers were also found to express ERbeta. Three-fourths of the ERalpha- and PR-positive tumors were positive for ERbeta, whereas ERalpha and PR were positive in 87% and 67% of ERbeta-positive tumors, respectively. ERbeta was associated with negative axillary node status (P < 0.0001), low grade (P = 0.0003), low S-phase fraction (P = 0.0003), and premenopausal status (P = 0.04). In conclusion, the coexpression of ERbeta with ERalpha and PR as well as its association with the other indicators of low biological aggressiveness of breast cancer suggest that ERbeta-positive tumors are likely to respond to hormonal therapy. The independent predictive value of ERbeta remains to be established.

Adult↗
PubMed2000

Chromogenic in situ hybridization: a practical alternative for fluorescence in situ hybridization to detect HER-2/neu oncogene amplification in archival breast cancer samples.

Determination of HER-2/neu oncogene amplification has become necessary for selection of breast cancer patients for trastuzumab (Herceptin) therapy. Fluorescence in situ hybridization (FISH) is currently regarded as a gold standard method for detecting HER-2/neu amplification, but it is not very practical for routine histopathological laboratories. We evaluated a new modification of in situ hybridization, the chromogenic in situ hybridization (CISH), which enables detection of HER-2/neu gene copies with conventional peroxidase reaction. Archival formalin-fixed paraffin-embedded tumor tissue sections were pretreated (by heating in a microwave oven and using enzyme digestion) and hybridized with a digoxigenin-labeled DNA probe. The probe was detected with anti-digoxigenin fluorescein, anti-fluorescein peroxidase, and diaminobenzidine. Gene copies visualized by CISH could be easily distinguished with a x40 objective in hematoxylin-stained tissue sections. HER-2/neu amplification typically appeared as large peroxidase-positive intranuclear gene copy clusters. CISH and FISH (according to Vysis, made from frozen pulverized tumor samples) correlated well in a series of 157 breast cancers (kappa coefficient, 0.81). The few different classifications were mostly because of low-level amplifications by FISH that were negative by CISH and immunohistochemistry with monoclonal antibody CB-11. We conclude that CISH, using conventional bright-field microscopy in evaluation, is a useful alternative for determination of HER-2/neu amplification in paraffin-embedded tumor samples, especially for confirming the immunohistochemical staining results.

Archives↗
PubMed2000

Amplification and deletion of topoisomerase IIalpha associate with ErbB-2 amplification and affect sensitivity to topoisomerase II inhibitor doxorubicin in breast cancer.

Topoisomerase IIalpha (topoIIalpha) is a key enzyme in DNA replication and a molecular target for many anti-cancer drugs called topoII inhibitors. The topoIIalpha gene is located at chromosome band 17q12-q21, close to the ErbB-2 oncogene (HER-2/neu), which is the most commonly amplified oncogene in breast cancer. Because of the physical proximity to ErbB-2, copy number aberrations may also occur in the topoIIalpha gene. These topoIIalpha gene copy number aberrations may be related to the altered chemosensitivity to topoII inhibitors that breast cancers with ErbB-2 amplification are known to have. We used fluorescence in situ hybridization to study copy number aberrations of both topoIIalpha and ErbB-2 in nine breast cancer cell lines and in 97 clinical breast tumors, which were selected for the study according to their ErbB-2 status by Southern blotting. TopoIIalpha-protein expression was studied with Western blot and sensitivity to doxorubicin (a topoII inhibitor) with a 96-well clonogenic in vitro assay. Two of the five cell lines with ErbB-2 gene amplification (SK-BR-3 and UACC-812) showed amplification of topoIIalpha. In MDA-361 cells, ErbB-2 amplification (14 copies/cell) was associated with a physical deletion of topoIIalpha (four copies of chromosome 17 centromere and two copies of topoIIalpha). The topoIIalpha amplification in UACC-812 cells was associated with 5.9-fold-increased topoIIalpha protein expression and 2.5-fold-increased sensitivity to the topoII inhibitor, doxorubicin, whereas the deletion in MDA-361 leads to decreased protein expression (45% of control) and a 2.4-fold-increased chemoresistance in vitro. Of 57 ErbB-2-amplified primary breast carcinomas, 25 (44%) showed ErbB-2-topoIIalpha coamplification and 24 (42%) showed a physical deletion of the topoIIalpha gene. No topoIIalpha copy number aberrations were found in 40 primary tumors without ErbB-2 amplification. TopoIIalpha gene amplification and deletion are common in ErbB-2-amplified breast cancer and are associated with increased or decreased sensitivity to topoII inhibitors in vitro, respectively. These findings may explain the altered chemosensitivity to topoII inhibitors reported in ErbB-2-amplified breast cancers.

Antigens, Neoplasm↗
PubMed2000

High topoisomerase IIalpha expression associates with high proliferation rate and and poor prognosis in oligodendrogliomas.

The role of molecular markers predicting the prognosis and the selection of patients for further adjuvant therapies is not well established in oligodendroglioma patients. A potential prognostic as well as a therapeutically predictive factor, topoisomerase IIalpha (topoIIalpha), is a molecular target for certain cytotoxic drugs. Its expression has been shown to correlate with the prognosis in a number of different cancers and with the chemosensitivity of cancer cells in vitro. The expression of topoIIalpha was evaluated immunohistochemically in 59 oligodendrogliomas and in 29 mixed gliomas with a predominating oligodendroglioma component by the use of a tissue microarray technique. In the gliomas, the percentage of topoIIalpha immunopositive cells protein expression varied from 0.0 to 49.1% (5.2 +/- 8.3%, mean+/- SD). In oligoastrocytomas, the mean topoIIalpha score was significantly higher in the oligodendroglioma than in the astrocytoma component of the tumour (5.37 +/- 5.58% vs. 1.89 +/- 2.49%, P = 0.018). A significant association was found between the high proportion of topoIIalpha positive cells and high grade of the tumour (P < 0.0001), high tumour proliferation rate (P < 0.0001), p53 overexpression (P = 0.01) and high expression of tumour suppressing retinoblastoma protein (P = 0.023). TopoIIalpha expression was not associated with the age or sex of patient, and the rate of apoptosis. TopoIIalpha expression associated highly significantly with patient prognosis; a significantly higher proportion of patients with low rather than with high topoIIalpha score was alive at the end of the 5-year follow-up (P = 0.03). Cox analysis was used to demonstrate that topoIIalpha had an independent prognostic value for survival (P = 0.034). In conclusion, high topoIIalpha expression characterizes oligodendrogliomas and oligoastrocytomas which are poorly differentiated, have high proliferation rate, and has prognostic value for overall survival of these patients. Therefore, topoIIalpha may be a useful marker for better targeted selection of poor prognosis oligodendroglioma patients for adjuvant therapy.

Adolescent↗
PubMed2000

Direct eye visualization of Cy5 fluorescence for immunocytochemistry and in situ hybridization.

Cyanine 5.18 (or Cy5) is a fluorochrome emitting in the long-red/far-red range, usually regarded as unsuitable for direct observation by the human eye. We describe here the optimization of a direct visualization approach to Cy5 labeling, based on a standard fluorescence microscope with mercury light excitation and applicable to both immunocytochemistry and fluorescent in situ hybridization. Crucial factors were (a) an excitation path in the microscope not absorbing light in the orange-red range, up to 640 nm, (b) a 588-640-nm excitation filter range, distinctly below the excitation optimum for Cy5, (c) a 650-700-nm emission filter range, transmitting the low-wavelength portion of Cy5 emission, and (d) high-efficiency filter set components allowing a narrow gap between excitation and emission ranges without visible cross-talk of excitation light in the emission path.

Animals↗
PubMed2000

Mapping the amplification of EIF3S3 in breast and prostate cancer.

Gain of chromosome arm 8q is a frequent genetic alteration in breast and prostate cancer. Two amplified subregions, 8q21 and 8q23-24, have been identified with comparative genomic hybridization (CGH). We have recently demonstrated that the EIF3S3 (eIF3-p40) gene, located at 8q23, is often amplified and overexpressed in both breast and prostate cancer. Here, we used fluorescence in situ hybridization (FISH) to map the amplified region around EIF3S3 in primary breast cancers and cell lines. The size of the common highly amplified region was about 2.5 Mb between the markers D8S1668 and WI-7959. Next, we analyzed the expression of all expressed sequence tags (ESTs) located within and near this region by RNA slot blot hybridization. In addition to EIF3S3, three anonymous ESTs and EXT1 were found to be highly expressed in cancer cell lines with the amplification at 8q23-q24. However, the anonymous ESTs were located outside the minimal highly amplified region and EXT1 was overexpressed only in one of the cancer cell lines with 8q amplification. Since EIF3S3 was the only consistently overexpressed gene located in the minimal highly amplified region, it is the strongest candidate target gene for 8q23-q24 amplification.

Bacteriophages↗
PubMed1999

Amplification and overexpression of p40 subunit of eukaryotic translation initiation factor 3 in breast and prostate cancer.

Amplification at the long arm of chromosome 8 occurs in a large fraction of breast and prostate cancers. To clone the target genes for this amplification, we used suppression subtraction hybridization to identify overexpressed genes in the breast cancer cell line SK-Br-3, which harbors amplification at 8q (8q21 and 8q23-q24). A differentially expressed gene identified by SSH, the p40 subunit of eukaryotic translation initiation factor 3 (eIF3), was localized to 8q23 and found to be highly amplified and overexpressed in the breast and prostate cancer cell lines studied. High-level amplification of eIF3-p40 was found in 30% of hormone-refractory prostate tumors and in 18% of untreated primary breast tumors. In the vast majority of the cases, p40 and c-myc were amplified with equal copy numbers. Tumors with higher copy numbers of p40 than c-myc were also found. Expression of p40 mRNA was analyzed with in situ hybridization. The amplification of eIF3-p40 gene was associated with overexpression of its mRNA, as expected for a functional target gene of the amplification. These results imply that genomic aberrations of translation initiation factors, such as eIF3-p40, may contribute to the pathogenesis of breast and prostate cancer.

Blotting, Northern↗
PubMed1999

The visibility of cancer on earlier mammograms in a population-based screening programme.

The aim of this study was to examine how frequently the later-round screen-detected and interval breast cancers were visible in earlier screening mammograms by retrospective review and to compare their radiological and clinicopathological features with those diagnosed by primary screening. In a population-based mammography screening programme 63,731 women aged 50-59 years were invited and 56,158 examinations were carried out in the period 1987-1992 in the Tampere area in Finland. A total of 276 breast cancers were detected, of which 131 were diagnosed on later screening rounds or were interval cancers. A retrospective review of previous screening mammograms was carried out in 130 cases by the radiologist who diagnosed the breast cancer and thus knew the exact location of the tumour, no blinded review was carried out. 43 (33%) cancers were visible, 84 (65%) were not visible and 3 (2%) not included on the mammogram in a retrospective review. Later round screen-detected cancers were statistically significantly more often visible in earlier screening mammograms (43%) than interval cancers (19%) (P = 0.002). Tumours missed by screening mammography but which were visible on retrospective review were often histologically well-differentiated and were more often diagnosed in the subsequent screening round than by clinical diagnosis as interval cancers. If all retrospectively visible interval cancers had been diagnosed by screening 19% (10/54) of the interval cancers could have been avoided. If all retrospectively visible cancers had been diagnosed at the time of false-negative screening or assessment 65% (84/130) of all patients would have benefitted from an earlier diagnosis compared with the actual figure of 31% (41/130).

Breast Neoplasms↗