METHODS: Seventy formalin-fixed paraffin-embedded cases previously diagnosed as primary lung squamous cell carcinoma (n = 35) and lung adenocarcinoma (n = 35) from January 2008 to December 2016 were retrieved. The results of tumour cell immunoreactivity for p40 and p63 antibodies in lung squamous cell carcinoma and lung adenocarcinoma were compared.
RESULTS: p40 was expressed in 27 cases of lung squamous cell carcinoma (77.1%). All cases of lung adenocarcinoma (35/35, 100%) were negative for p40. p63 expression was positive in 30 cases of lung squamous cell carcinoma (85.7%) and 13 cases of lung adenocarcinoma (37.1%). Reactivity for both p40 and p63 in lung squamous cell carcinoma was strong and diffuse, whereas variable reactivity was observed in lung adenocarcinoma.
CONCLUSIONS: p40 is an excellent marker for distinguishing lung squamous cell carcinoma from adenocarcinoma, and p40 expression is equivalent to p63 expression in lung squamous cell carcinoma.
Methods: A total of 100 formalin-fixed paraffin-embedded urothelial carcinoma tissues were selected from the Department of Pathology, Hospital Kuala Lumpur and the protein expression of ISL1 and LHX5 was determined using immunohistochemistry.
Results: Positive expression of ISL1 and LHX5 was detected in 94% and 98% of the samples, respectively. There were no distinct LHX5 expression patterns associated with different cancer stages, but the proportion of high-expressing tumours was higher in high-grade tumours. In addition, there was a significant association between the expression of LHX5 and tumour grade. The proportion of tumours expressing high levels of ISL1 was found to be highest in later stage tumours.
Conclusion: The high percentage of tumours expressing both these genes suggests that ISL1 and LHX5 play an important role in bladder tumourigenesis across multiple stages.
Methodology: Adult female Wistar rats were time-mated and grouped into three categories: (a) control-given 0.1 mL of normal saline, (b) low-dose nicotine-given 6.88 mg/ kg/d/0.05 mL, and (c) high-dose nicotine-given 13.76 mg/kg/d/0.1 mL in two divided doses. Treatment was given intraperitoneally from gestational days 2 to 6. On postnatal day 15 (P15), the pups were separated from their mothers, anaesthetised and sacrificed, followed by intracardial perfusion with 4% paraformaldehyde. PFC was excised from the brain and processed for tissue histology, histochemistry, and morphology of brain cells.
Results: Gestational nicotine exposure during the first week of gestation in rats significantly reduced birth weights in nicotine-treated groups compared with control; it, however, accelerated body weights, altered neuronal morphology, and elevated astrocytic count significantly, while oligodendroglial count was slightly increased in the PFC of juvenile rats examined at P15.
Conclusion: These alterations revealed that gestational nicotine exposure before the commencement of the cellular processes involved in brain development negatively affects neurodevelopment, and this could result in neurological dysfunctions in later life.