Biomedical subjects

Neema Aghamohammadi

Publications and source records attributed to Neema Aghamohammadi.

3 recordsLinked to original sources

PubMed2006

Developmental pathways and specification of intrapulmonary stem cells.

Tissues have the capacity to maintain a homeostatic balance between wear-and-tear and regeneration. Repair of non-lethal injury also activates cell proliferation to repopulate the injured sites with appropriate cell types and to restore function. Although controversial, the source of the material appears to be at least partly from pools of unique, multipotent stem cells that reside in specialized locations referred to as "niches." Molecular interactions between the niche and the intracellular factors within stem cells are crucial in maintaining stem cell functions, particularly the balance between self-renewal and differentiation. Many of the mediators of the stem cell-niche interactions are similar or identical to those that control developmental pathways during organogenesis. In this review, we present a systematic discussion and evaluation of the relevant literature with a focused emphasis on three primary signaling pathways, WNT, SHH and BMP with potentially overlapping roles during both development and stem cell maintenance.

Humans↗

PubMed2003

Fluorescence in situ hybridization for detecting TP16 MTS1/CDK41 gene deletions in squamous cell carcinoma of the head and neck.

We have previously shown TP16 MTS1/CDK41 gene deletion in more than 50% of a cohort of squamous cell carcinoma of the head and neck (SCCHN) patients using polymerase chain reaction (PCR). We have performed fluorescence in situ hybridization (FISH) on paraffin-embedded SCCHN specimens from the same cohort to identify the deletion of TP16 MTS1/CDK41CDK41gene. Twenty normal and 19 SCCHN specimens were studied. An alpha-satellite DNA probe specific for chromosome 9 and a cosmid probe for the TP16 MTS1/CDK41CDK41gene were used. Of the 19 tumors examined by FISH, 6 had homozygous deletions, 7 were hemizygously deleted, and the remaining 6 showed no evidence of deletion of the TP16 MTS1/CDK41 gene. None of the normal specimens showed TP16 gene deletion. Data obtained from FISH highly correlated with the PCR results for the identification of TP16 MTS1/CDK41 gene deletions. Patients with deletion of the TP16 MTS1/CDK41 gene show a greater tendency toward the development of recurrence and metastasis.

Adult↗

PubMed2002

Cyclin D1 amplification and p16(MTS1/CDK4I) deletion correlate with poor prognosis in head and neck tumors.

OBJECTIVES/HYPOTHESIS: Cyclin D1, a cell cycle regulator localized to chromosome 11q13, is amplified in several human tumors including head and neck squamous cell carcinoma (HNSCC). Amplification and/or overexpression of cyclin D1 have been correlated to a poor prognosis. Deletion of the p16 gene, localized to 9p21, has also been observed in a significant proportion of HNSCC. The p16 gene regulates cyclin D1-CDK4 activity and prevents retinoblastoma tumor suppressor gene phosphorylation, thereby downregulating cellular proliferation. Detection of cyclin D1 amplification and p16 deletion using a simple and sensitive method will be valuable for the development of effective treatment modalities for head and neck cancer. STUDY DESIGN: We have used fluorescence in situ hybridization (FISH) to study cyclin D1 amplification and p16 gene deletion in head and neck tumors. Both single- and dual-color FISH were performed. METHODS: Paraffin-embedded tissues from 103 patients with HNSCC were analyzed using genomic DNA probes for cyclin D1 and p16. Dual-color FISH was performed with chromosome 11 or 9 centromeric probes as a control. Twenty-eight of these samples were analyzed for p16 expression by immunohistochemistry. RESULTS: Cyclin D1 amplification was observed in 30% (31/103) of patients, and p16 deletion in 52% (54/103). Lack of p16 expression was observed in 64% (18/28) of patients. There was a good correlation between the deletion of p16 sequences and the loss of p16 expression (P = .008). Amplification of cyclin D1 had a statistically significant association with recurrence, distant metastasis, and survival at 36 months. There was a significant association between p16 deletion and the development of distant metastases. Cyclin D1 amplification and p16 deletion together correlated with recurrence, distant metastasis, and survival. CONCLUSIONS: We demonstrate that FISH is a simple and sensitive method for detecting cyclin D1 amplification and p16 deletion in head and neck cancer. Our results suggest that these two genetic aberrations together portend a poorer outcome than either of the abnormalities alone in head and neck cancer.

Adult↗