The cellular apoptosis susceptibility (CSE1L/CAS) protein is highly expressed in cancer, and its expression is positively correlated with high cancer stage, high cancer grade, and worse outcomes of patients. CSE1L (or CAS) regulates chemotherapeutic drug-induced cancer cell apoptosis and may play important roles in mediating the cytotoxicities of chemotherapeutic drugs against cancer cells in cancer chemotherapy. CSE1L was originally regarded as a proliferation-associated protein and was thought to regulate the proliferation of cancer cells in cancer progression. However, the results of experimental studies showed that enhanced CSE1L expression is unable to increase proliferation of cancer cells and CSE1L regulates invasion and metastasis but not proliferation of cancer cells. Recent studies revealed that CSE1L is a secretory protein, and there is a higher prevalence of secretory CSE1L in the sera of patients with metastatic cancer. Therefore, CSE1L may be a useful serological marker for screening, diagnosis and prognosis, assessment of therapeutic responses, and monitoring for recurrence of cancer. In this paper, we review the expression of CSE1L in cancer and discuss why CSE1L regulates the invasion and metastasis rather than the proliferation of cancer.

Background: Invasiveness and metastasis are the most common characteristics of non small cell lung cancer (NSCLC) and causes of tumour-related morbidity and mortality. Mitogen-activated protein kinases (MAPKs) signalling pathways have been shown to play critical roles in tumorigenesis. However, the precise pathological role(s) of mitogen-activated protein kinase phosphatase-1 (MKP-1) in different cancers has been controversial such that the up-regulation of MKP-1 in different cancers does not always correlate to a better prognosis. In this study, we showed that the induction of MKP-1 lead to a significant retardation of proliferation and metastasis in NSCLC cells. We also established that rosiglitazone (a PPARγ agonist) elevated MKP-1 expression level in NSCLC cells and inhibited tumour metastasis. Methods: Both wildtype and dominant negative forms of MKP-1 were constitutively expressed in NSCLC cell line H441GL. The migration and invasion abilities of these cells were examined in vitro. MKP-1 modulating agents such as rosiglitazone and triptolide were used to demonstrate MKP-1's role in tumorigenesis. Bioluminescent imaging was utilized to study tumorigenesis of MKP-1 over-expressing H441GL cells and anti-metastatic effect of rosiglitazone. Results: Over-expression of MKP-1 reduced NSCLC cell proliferation rate as well as cell invasive and migratory abilities, evident by the reduced expression levels of MMP-2 and CXCR4. Mice inoculated with MKP-1 over-expressing H441 cells did not develop NSCLC while their control wildtype H441 inoculated littermates developed NSCLC and bone metastasis. Pharmacologically, rosiglitazone, a peroxisome proliferator activated receptor-γ (PPARγ) agonist appeared to induce MKP-1 expression while reduce MMP-2 and CXCR4 expression. H441GL-inoculated mice receiving daily oral rosiglitazone treatment demonstrated a significant inhibition of bone metastasis when compared to mice receiving sham treatment. We found that rosiglitazone treatment impeded the ability of cell migration and invasion in vitro. Cells pre-treated with triptolide (a MKP-1 inhibitor), reversed rosiglitazone-mediated cell invasion and migration. Conclusion: The induction of MKP-1 could significantly suppress the proliferative and metastatic abilities of NSCLC both in vitro and in vivo. Therefore, MKP-1 could be considered as a potential therapeutic target in NSCLC therapy and PPARγ agonists could be explored for combined chemotherapy.

Aim To evaluate the significance of bilateral fluorodeoxyglucose (FDG) uptake in the thyroid glands. Methods Bilateral thyroid FDG uptake, defined as visualization of thyroid glands, was found in 66 (3.4%) of 1925 subjects who underwent our FDG PET cancer-screening program. Additionally, 16 of the 41 patients with Graves' disease and hyperthyroidism (GD_H) and six of the 20 subjects with Graves' disease and euthyroidism (GD_E), who had FDG uptake in thyroid glands, were enrolled in this study. Results Among the 66 subjects, 22 were normal variant, 39 subjects had chronic thyroiditis (35 subjects presented with diffuse goitre and four with multinodular goitre), and five subjects had multinodular goitre (MNG) without chronic thyroiditis. Fourteen of 22 (63.6%) of the subjects with the normal variant had a visual uptake intensity less than that of the liver, while 30 of 39 (76.9%) of the subjects with chronic thyroiditis and 14 of 22 (63.6%) of the subjects with Graves' disease had visual uptake intensity greater than or equal to liver uptake. Two of the five subjects with MNG with focally intense uptake were proven to have thyroid carcinoma. Bilateral loser uptake in thyroids associated with thymus and symmetrical skeletal muscle uptake were found in GD_H. The standard uptake value (SUV) (mean±SD) in subjects with chronic thyroiditis (2.76±1.24) were higher, while those with GD_H (1.59±0.36) were lower than that of the normal variant (1.99±0.63). Subjects with hypothyroidism (3.04±1.39) had higher SUV levels than those subjects with euthyroidism (2.44±1.11). In addition, patients with GD_H had lower levels than those with GD_E (2.0±0.38). Conclusion (1) Bilateral thyroidal uptake of FDG can be found in normal variants and subjects with various thyroid disorders, showing varieties of uptake patterns. (2) Diffuse intense uptake and higher SUV levels are a clue to a diagnosis of chronic thyroiditis, especially for those with hypothyroidism. (3) Focally intense uptake suggests the possibility of a thyroid carcinoma. (4) Sparse uptake associated with the thymus and symmetrical skeletal muscle uptake and lower SUV level raise the possibility of Graves' disease with hyperthyroidism.

Saliva plays an important role in supporting upper gastrointestinal tract function and oral well-being. Salivary dysfunction mainly manifests with a decrease in salivary flow. Among varieties of quantitative methods, salivary scintigraphy is a relatively noninvasive, well-tolerated, reproducible, and objective approach for functional evaluation of salivary disorders, yet the lack of precise quantitative reference values and no standardized protocol limit its generalized utilization. In this article, we review the scintigraphic performance between the visual analysis and quantitative methods in predicting Sjögren’s syndrome and verify the potential aspects of the application in interpreting different disease entities and phases of functional salivary disorders.

Background: The discovery of asynchronous or synchronous double or multiple malignancies in patients is not uncommon. The co-occurrence of second primary malignancy (SPM) could be randomly occurring or association with risk factors such as environmental, genetic predisposition and therapy-related. Materials and methods: We retrieved ∼782 million claim records consisting of 10.8 million males and 10.6 million females from Taiwan’s National Health Insurance, which were collected for a period of 3 years (January 2000–December 2002). All the patient records were stratified by gender and ages at a 20-year interval with SPMs and specific groups. Interestingness or Q -value was used to measure strength of the disease–disease associations. Results: A total of 9423 thyroid cancer (female: 7483, male: 1940), 276 184 SPM (female: 141 023, male: 135 161) and 861 co-occurrence cases (female: 583, male: 278) were recorded. The co-occurrence incidence rate of head and neck, breast, digestive system and lung was 1.93%, 1.59%, 1.44% and 1.18%, respectively. Malignancy of salivary glands, laryngx, sarcoma, lymphoid tissue, mouth, central nervous system and lungs found Q -value >10. Malignancies with intermediate Q -values (5.0–9.9) were observed in nasopharynx, kidney and ureter, breast, stomach and skin. Prostate, leukemia, urinary bladder, ovary, colon, liver and uterine cervix cancer have lower Q -values (1.0–4.9). Conclusion: Co-occurrence ratio of thyroid cancer and SPM was high, occurred in all organ systems. We postulated that the aggressive use of modern diagnostic modalities, aggressive radioiodine treatment, pre-existing molecular oncogen mutations, and thyroid hormone for simultaneously supple-mentary and suppressive therapies were responsible.