SummaryBackgroundPrevious efforts to report estimates of cancer incidence and mortality in India and its different parts include the National Cancer Registry Programme Reports, Sample Registration System cause of death findings, Cancer Incidence in Five Continents Series, and GLOBOCAN. We present a comprehensive picture of the patterns and time trends of the burden of total cancer and specific cancer types in each state of India estimated as part of the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2016 because such a systematic compilation is not readily available.MethodsWe used all accessible data from multiple sources, including 42 population-based cancer registries and the nationwide Sample Registration System of India, to estimate the incidence of 28 types of cancer in every state of India from 1990 to 2016 and the deaths and disability-adjusted life-years (DALYs) caused by them, as part of GBD 2016. We present incidence, DALYs, and death rates for all cancers together, and the trends of all types of cancers, highlighting the heterogeneity in the burden of specific types of cancers across the states of India. We also present the contribution of major risk factors to cancer DALYs in India.Findings8·3% (95% uncertainty interval [UI] 7·9–8·6) of the total deaths and 5·0% (4·6–5·5) of the total DALYs in India in 2016 were due to cancer, which was double the contribution of cancer in 1990. However, the age-standardised incidence rate of cancer did not change substantially during this period. The age-standardised cancer DALY rate had a 2·6 times variation across the states of India in 2016. The ten cancers responsible for the highest proportion of cancer DALYs in India in 2016 were stomach (9·0% of the total cancer DALYs), breast (8·2%), lung (7·5%), lip and oral cavity (7·2%), pharynx other than nasopharynx (6·8%), colon and rectum (5·8%), leukaemia (5·2%), cervical (5·2%), oesophageal (4·3%), and brain and nervous system (3·5%) cancer. Among these cancers, the age-standardised incidence rate of breast cancer increased significantly by 40·7% (95% UI 7·0–85·6) from 1990 to 2016, whereas it decreased for stomach (39·7%; 34·3–44·0), lip and oral cavity (6·4%; 0·4–18·6), cervical (39·7%; 26·5–57·3), and oesophageal cancer (31·2%; 27·9–34·9), and leukaemia (16·1%; 4·3–24·2). We found substantial inter-state heterogeneity in the age-standardised incidence rate of the different types of cancers in 2016, with a 3·3 times to 11·6 times variation for the four most frequent cancers (lip and oral, breast, lung, and stomach). Tobacco use was the leading risk factor for cancers in India to which the highest proportion (10·9%) of cancer DALYs could be attributed in 2016.InterpretationThe substantial heterogeneity in the state-level incidence rate and health loss trends of the different types of cancer in India over this 26-year period should be taken into account to strengthen infrastructure and human resources for cancer prevention and control at both the national and state levels. These efforts should focu...

The cell-cell adhesion receptor gene E-cadherin (CDH1) is expressed by epithelial cells, in which it mediates adhesion and morphogenesis. Invasive lobular carcinoma (ILC) characteristically infiltrates diffusely as single cells; by immunohistochemistry, many of these tumours lack E-cadherin expression. In the present study we investigated various ways in which loss of function of the E-cadherin gene could occur in ILCs, namely, promoter methylation, mutation and allelic loss. We analysed 22 ILCs and found 12 (55%) E-cadherinnegative samples by immunohistochemical analysis. Methylation-specific polymerase chain reaction (PCR) showed that 17/22 (77%) of these tumours had methylation of the CDH1 promoter, including 11/12 (91%) of the E-cadherin-negative tumours. All 16 exons of E-cadherin (including intron-exon boundaries) were amplified from chromosomal DNA and screened for mutations by conformation-sensitive gel electrophoresis (CSGE). Bands with altered mobility were analysed by direct sequencing. We identified five frameshift mutations, which resulted in downstream stop codons and one splice site mutation in six different tumours (29%). Loss of heterozygosity (LOH) was assessed using microsatellite markers, and 9/18 (50%) informative tumours showed LOH. We conclude that most ILCs show genetic or epigenetic changes affecting the E-cadherin gene and that many of these tumours lack E-cadherin expression. In all cases in which there was loss of expression, this was consistent with biallelic inactivation of CDH1 by promoter methylation, mutation or allelic loss in any combination. © 2001 Wiley-Liss, Inc. Key words: breast lobular carcinoma; E-cadherin; LOH; promoter methylationE-cadherin is a transmembrane glycoprotein, expressed mainly in epithelial cells, which mediates calcium-dependent cell-cell adhesion through homophilic interactions while controlling cell polarity and morphogenesis. 1 An intracellular domain interacts with the catenins, and, through these proteins, E-cadherin is linked to the cytoskeleton. 2 The gene (CDH1, HSECAD) maps to 16q22.1 and consists of 16 exons. The CDH1 promoter, originally identified by Behrens et al., 3 has a high GC-rich region that may be implicated in transcriptional regulation.Downregulation of E-cadherin levels has been associated with reduced differentiation and poorer prognosis in breast cancer, 4 -6 although this has not been an universal finding. 7 Previous studies from our own institute and other centres have documented loss of E-cadherin expression, as determined by immunohistochemistry, in around 85% or more of invasive lobular carcinomas (ILCs) and lobular carcinoma in situ (LCIS). 8,9 Such findings suggest that the absence of expression of this molecule could play an important role in determining morphology as well as in mediating the distinct pattern of invasion of this tumour. A more recent report has shown simultaneous loss of ␣-and ␤-catenin expression in E-cadherinnegative lobular breast carcinomas. 10 Reduced immunoreactivity of any of the four proteins (E-ca...

Growing teratoma syndrome is the term applied to enlarging retroperitoneal or other metastatic masses containing mature teratoma during chemotherapy for nonseminomatous germ cell tumors. Four cases of the growing teratoma syndrome are presented, the metastatic masses being in the retroperitoneal in all the cases. All these patients had enlarging retroperitoneal masses in the presence of normal serum biomarkers following chemotherapy for nonseminomatous tumors. Surgical excision was carried out in all four patients, with disease free survivals ranging from 6 to 24 months after surgery.

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