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Dr. Justin Oh. University of British Columbia

Good evening
This video shows symptoms and treatment of pituitary tumour which is a brain tumour. Most of pituitary tumours are benign in nature.
Beatcancer rj07
Dr. Shankar lal jakhar
My self Dr.Shankar Lal JAKHAR Professor radiation oncology working in Department of oncology in Acharya Tulsi regional Cancer Treatment and research Institute. Acharya Tulsi Cancer Centre situated in the PBM Hospital in Sardar Patel medical College Bikaner Rajasthan. This cancer hospital is famous for cancer treatment in whole Rajasthan and north east India where patients of the surrounding states like Punjab, Haryana, Delhi, Uttarakhand, Uttar Pradesh and Bihar come for cancer treatment. The Centre is known for low cost and standard cancer treatment with less time. There are multiple oncology wing in the centre like radiation oncology surgical oncology medical oncology and palliative care. It’s an autonomous regional Cancer Centre. Renowned cancer doctors are working in this hospital. Dr. M R bardia, Director of Acharya tulsi regional cancer treatment and research institute, Dr. H S kumar, senior professor and former Principal & controller SP medical college, Dr. Neeti sharma, senior professor and Head of departmen, Dr. Surendra Beniwal professor medical oncology, Dr. shankar lal jakhar professor radiation oncology, Dr. Kamlesh Kumar Harsh associate professor radiation oncology, Dr. Sandeep Gupta associate professor surgical oncology, Dr. Rajendra Bothra Surgical oncology, Dr. Rajesh kumar Sinwar assistant professor radiation oncology, Dr. Guman singh assistant professor radiation oncology, Dr. Swetha Mohta assistant professor radiation oncology, Dr. Pankaj Tantia assistant professor medical oncology, Dr. Saroj sogat cancer specialist, Dr. Pramila kumari khatri cancer specialist, Dr. Mukesh Singhal cancer specialist, Dr. Punam bana cancer specialist, Dr. Sitaram Maharia cancer cancer, Dr. Rajkumar Nirban cancer specialist, Dr. Pukhraj Sad cancer specialist, Dr. Saroj dhaka cancer specialist, Dr. Ranjeet kashnia cancer specialist, Dr. Amit singh sekhawat nuclear medicine incharge, Dr. Buvnesh narayan purohit cancer specialist.
In this institute there are 2 Linear accelerator with true beam, SRT, VMAT, IGRT, IMRT, 3DcRT and electron beam treatment facility and 3 cobalt therapy machine and HDR brachytherapy machines available.

The hedgehog signaling pathway is a vital factor for embryonic development and stem cell maintenance. Dysregulation of its function results in tumor initiation and progression. The aim of this research was to establish a disease model of hedgehog-related tumorigenesis with Gorlin syndrome-derived induced pluripotent stem cells (GS-iPSCs). Induced neural progenitor cells from GS-iPSCs (GS-NPCs) show constitutive high GLI1 expression and higher sensitivity to smoothened (SMO) inhibition compared with wild-type induced neural progenitor cells (WT-NPCs). The differentiation process from iPSCs to NPCs may have similarity in gene expression to Hedgehog signal-related carcinogenesis. Therefore, GS-NPCs may be useful for screening compounds to find effective drugs to control Hedgehog signaling activity.

Summary
The hedgehog signaling pathway is a pivotal pathway for basal cell carcinoma and
medulloblastoma. Gorlin syndrome-derived induced pluripotent stem cells (iPSCs) with a heterozygous mutation of PTCH1, one of the hedgehog target genes, exhibited high GLI1 expression and enhanced sensitivity to the hedgehog pathway inhibitor after neural differentiation. These iPSCs can serve a good model of the hedgehog pathway-related tumors.

Background: The hedgehog signaling pathway is a vital factor for embryonic development and stem cell maintenance. Dysregulation of its function results in tumor initiation and progression. The aim of this research was to establish a disease model of hedgehog-related tumorigenesis with Gorlin syndrome-derived induced pluripotent stem cells (GS-iPSCs), with a heterozygous mutation of PTCH1.

Methods: We induced neural progenitor cells from GS-iPSCs with the SFEBq method. Their expression levels of the hedgehog related genes and reactions to SMO inhibitor (Vismodegib) and agonist (SAG) were evaluated by quantitative real-time PCR.

Results: Induced neural progenitor cells from GS-iPSCs showed constitutive high GLI1 expression and higher sensitivity to smoothened inhibition compared to wild-type induced neural progenitor cells.

Conclusions: Neural progenitor cells from GS-iPSCs may be useful for compounds screening to find effective drugs to control Hedgehog signaling activity.





Introduction
The hedgehog (Hh) signaling pathway plays an important role in embryogenesis and stem cell maintenance. Ectopic Hh signal up-regulation causes tumors such as basal cell carcinoma (BCC) and medulloblastoma. Hh signaling is also related to other malignancies such as breast cancer, pancreatic cancer, lung cancer, and prostate cancer6. A lot of medications have been under research to establish treatment and prevention of Hh signaling pathway-related tumors. The Hh signaling pathway can be initiated by three ligands: desert hedgehog (DHH), Indian hedgehog (IHH) or sonic hedgehog (SHH)8. These proteins bind to the 12-pass transmembrane protein receptor PTCH1. Once ligand binding occurs, the PTCH1 receptor relieves its inhibitory action on smoothened (SMO), a 7-pass transmembrane G-protein-coupled signal transduction molecule, which then activates a signaling cascade resulting in the translocation of Gli transcription factors to the nucleus. In the absence of the ligand, SMO is normally localized in vesicles. When the pathway is activated, SMO localizes to the primary cilium on the cell membrane.

Gorlin syndrome (GS) or nevoid basal cell carcinoma syndrome (NBCCS; OMIM 109400) is a rare autosomal dominantly inherited disorder that is characterized by congenital anomalies and development of tumors such as basal cell carcinoma and medulloblastoma. GS is caused by mutations in the PTCH1 gene and is transmitted as an autosomal dominant trait with complete penetrance and variable expressivity. Haploinsufficiency of PTCH1 results in constitutive activation of the Hh signaling pathway. Multiple genes that influence embryogenesis and pluripotency are oncogenes that drive the development of tumors. Additionally, some mechanisms of tumorigenesis are similar to embryonic development. GS patients frequently develop medulloblastoma at a young age compared to patients with sporadic cases, because mutation of PTCH1 causes dysregulation of the Hh signaling pathway during development of the cerebellum, which can lead to medulloblastoma.

In this study, we generated GS-iPSCs with a heterozygous mutation of PTCH1, and induced neural progenitor cells (NPCs) from GS-iPSCs. Neural progenitors from GS-iPSCs expressed GLI1, a downstream target gene of Hh signaling and exhibited sensitivity to Vismodegib, an SMO inhibitor. Induced neural progenitor cells from Gorlin syndrome iPSCs may therefore serve a good precancerous model for Hh related tumors.


KEYWORDS:
GLI1; PTCH1; hedgehog signaling pathway; induced pluripotent stem cells; vismodegib


#Gohlin syndrome #biomarker #iPSC #iPS cell

Hajime Ikehara 20161222091403

There are no limits to your wardrobe after breast cancer surgery thanks to strapless mastectomy bras.

The death of actor Chadwick Boseman is pushing colon cancer survivors to share their stories.

Aiwu Ruth He, MD, Georgetown Lombardi Comprehensive Cancer Center, Washington DC, USA, comments on future avenues in research for the diagnosis and treatment of biliary tract cancer. Specifically, Dr He comments on the potential identification of novel biomarkers which may aid in the selection of patients with biliary tract cancer who could benefit from treatment with durvalumab plus chemotherapy. Moreover, personalized therapy and fibroblast growth factor receptor (FGFR) inhibitors for the treatment of biliary tract cancer are discussed. This interview took place at the European Society for Medical Oncology World Congress on Gastrointestinal Cancer (ESMO WCGIC) 2022 in Barcelona, Spain.

In this video i talked about Acute Lymphoblastic Leukemia ( ALL ) . Its two subtypes B-ALL and T-ALL .Its confirmatory tests and its prognosis.Its association with down syndrome.