New York Medical College - Department of Neurosurgery, Neurosurgery Residency Information
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Latest Medical News & Research

Dr. Micheal LaBagnara, NS5, won The Resident Research award
site publish date: 7/2/2014

Michael Labagnara MD, PGY V, received the Resident Research Award for his outstanding presentation at the New York State Neurological Society Annual Meeting held on June 6th, 2014. He presented his research entitled "Characterization of Glioblastoma Multiforme Cancer Stem Cells by PTEN and its Downstream Signaling Pathways: Potential Targets of Therapy", done under the mentorship of Dr. Meena Jhanwar-Uniyal, Associate Professor, Department of Neurosurgery.

Dr. LaBagnara was recognized in New York Medical College's weekly Newsletter In Touch, for this accomplishment. Click here to see the article.

New York Medical College Research and News

PGY V Resident, Micheal LaBagnara, M.D., has won The Anna Samartzis Research Excellence Award
site publish date: 2/28/2014

PGY V Resident, Micheal LaBagnara, M.D., has won The Anna Samartzis Research Excellence Award for Best Basic Science Research Paper at the 11th Annual Louis R.M Del Guercio Surgical Research Day hosted by New York Medical College on December 18th, 2013 for his work on Glioblastoma Cancer Stem Cells. Congratulations and keep up the good work!

New York Medical College Research and News

NYMC Department of Neurosurgery Jayson Neil, M.D., and Dr. Jhanwar Presenting at Chicago AACR and Florida AANS Meetings
site publish date: 3/29/2012

We are pleased to announce that the current research resident Jayson Neil MD will be presenting his research with Dr. Jhanwar in April at both the AACR meeting in Chicago and the AANS meeting in Florida!

New York Medical College Research and News

NYMC Department of Neurosurgery Web Site Updates
site publish date: 5/2/2011

Our web site is going through some updates. We recently created a department calendar page, a social announcements page, as well as five new CVs to our faculty page. Over the next few months we will be adding new content to these sections as well as new CVs to our faculty page.

New York Medical College Research and News

Mutant Human Tumor Suppressor p53 Modulates the Activation of Mitogen-Activated Protein Kinase and Nuclear Factor-kB, But Not C-Jun N-Terminal Kinase and Activated Protein-1
by: Meena Jhanwar-Uniyal et al
site publish date: 2/27/2011

Introduction: The tumor suppressor p53 is a transcription factor that is expressed in all cells. In tumors, the inactivation of p53 by mutation is common and alters the normal p53 signaling pathway(s). p53 regulates cell growth by halting the cell-cycle at the G1 stage in order to repair DNA damage or trigger programmed cell death, apoptosis. p53 can lead to cell-cycle arrest or induce senescence. Transcription of p53 protects cells from DNA damaging agents, including gradiation, chemotherapeutic drugs, and oncogenic stress induced by activated oncogenes, such as myc or Ras. Cells lacking functional p53 are resistant to chemotherapy, and recent studies have shown that the restoration of p53 decreases the incidence of spontaneous tumors [1–3]. Furthermore, the activation of mitogen-activated protein kinase (MAPK) requires functional p53 [4]. In normal human diploid fibroblast cells, MAPK activation in response to DNA-damaging agents occurs only in the presence of functional p53 [4], indicating a reciprocal interaction between p53 signaling pathways with MAPK pathways. Such an interaction requires functional Ras and Raf. Lee et al. [4] established that p53 could activate MAPK pathways, perhaps through transcriptional activation of target genes [5,6]. They have alsoshownthat theMAPKcascade can integrate the p53-induced responses, and may augment permanent growth arrest by sufficient upregulation of either p53 or MAPK pathways. Furthermore, the extracellular-signal regulated kinases 1/2 (ERK1/2) can induce p21CIP expression by both p53-dependent and p53-independent pathways [7]. These suggest that MAPK signaling pathways relay, amplify, and integrate signals from a diverse range of extracellular stimuli, and hence control the genomic and physiological responses of cells.

Click here to read full article.

New York Medical College Research and News

BRCA1 IN CANCER, CELL CYCLE AND GENOMIC STABILITY
by: Meena Jhanwar-Uniyal et al
site publish date: 2/27/2011

Introduction: 2.1. Mutation spectrum of BRCA1-associated tumors The American Cancer Society estimated that a total of 203,500 new cases of breast cancer (out of 647,400 estimated cancers at all sites) would occur among US women in the year 2002 and assesses the probability that one in eight American women would develop breast cancer during their lifespan (American Cancer Society Facts and Figures, 2002). Taken together, cancers of the breast and ovaries constitute almost one fourth of all cancer-related mortality in this country. BRCA-1 and BRCA-2 genes (1,2,3) are known to be associated with early onset familial breast and ovarian cancer. Patients with a strong hereditary component account for only 5% of all breast cancers occurring in the Unites States (4,5); nevertheless, identification of genes responsible for hereditary cancers is important, as such genes have been shown to play a critical role in the much more common form of "sporadic" tumors (6) in a variety of cancers. The role of the BRCA1 gene in sporadic breast cancer, however is not well defined, as mutations of these two genes in tumors with loss of heterozygosity (LOH) for BRCA1 and 2 are very rare (6). As reviewed by Szabo and King (1995) (4), BRCA1 and BRCA2 combined contribute to only 6-10% of breast and ovarian cancer regardless of the family history. In addition, approximately 30% of high-risk families do not exhibit mutations in either BRCA1 and BRCA2 genes. Such observations are consistent with the fact that there may be other genes that may predispose individuals to breast cancer. A limited number of recurring mutations (BRCA1 185delAG, 5382insC; BRCA2 617delT) in the BRCA 1 and 2 genes account for a substantial fraction of the breast cancer burden in the Jewish population (4,7).

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New York Medical College Research and News

Assessment of angiogenesis by CD105 and nestin expression in peritumor tissue of glioblastoma
by: Meena Jhanwar-Uniyal et al
site publish date: 12/3/2010

Introduction: Tumor growth and metastasis require adequate vascularization. Glioblastoma (GBM) is among the most vascularized tumors. Different mechanisms have been proposed in determining the vasculature characteristics (1). Specifically, a model of tumor progression defining the relationship between angiogenesis and the development of pseudopalisading necrosis, which represents a peculiar histopathological feature of GBM, has been suggested (2). According to this model, vascular occlusion, provoked by infiltrating tumor cells, induces hypoxia with a central necrosis surrounded by neoplastic elements which, in turn, produce hypoxia-inducible factors responsible for exuberant angiogenesis. In regions adjacent to hypoxia, this response creates microvascular proliferation (2), that typically appears as glomeruloid tufts (1). Microvessel morphology also depends on tumor size and in larger neoplasias appears chaotic (3), with angiogenic activity that is very high next to the tumor margin and decreases towards the center of the tumor (4,5). Vascular glomeruli have also been observed in the white matter surrounding the tumor but less frequently in the cortex. The number, caliber and wall thickness mean values of vessels in peritumor white matter are significantly higher than those of the normal brain (6). The area adjacent to the tumor margin, where the angiogenic response has been observed, represents the invasion front into the neighboring tissue. In this area, differences in the level of various molecules involved in enhanced cell proliferation, edema and invasiveness have been observed (7-11).

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New York Medical College Research and News

Gene expression profiling of metastatic brain cancer
by: Meena Jhanwar-Uniyal et al
site publish date: 12/29/2010

Introduction: Metastasis, the process by which cells break free from a primary tumor, enter the bloodstream or lymphatic system, and spread to distant sites within the body, remains a major cause of morbidity and mortality in many malignant neoplasms. Breast, lung, and ovarian cancer patients may develop metastatic lesions in the brain, often associated with a poor prognosis given that the highly specialized and delicate microenvironment of the brain is disrupted. To metastasize to the brain, cancer cells must attach to microvessel endothelial cells and invade the blood-brain barrier (BBB). After passing through the BBB, a cell clone must attach to an area where angiogenesis can take place. The metastatic phenotype characterizes cells with the ability to migrate from the primary tumor, survive in the circulation, pass through the BBB, invade distant tissue, and form blood vessels needed for growth and proliferation.

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New York Medical College Research and News

Stem Cell Marker Nestin and c-Jun NH2-Terminal Kinases in Tumor and PeritumorAreas of GlioblastomaMultiforme: Possible Prognostic Implications
by: Meena Jhanwar-Uniyal et al
site publish date: 12/3/2010

Purpose: It has been hypothesized that brain tumors are derived from stem cell or transiently dividing precursor transformation. Furthermore, c-Jun NH2-terminal kinases (JNKs) have been involved in gliomagenesis. This study analyzes stem cell marker nestin and JNK expression in glioblastoma multiforme (GBM) and peritumor tissue and assesses their possible prognostic implications.

Conclusions: Nestin and JNK expression indicates that peritumor tissue, independently of the presence of neoplastic cells, may present signs of transformation. Moreover, pJNK/nestin and (pJNK/tJNK)/nestin ratios in that tissue seem to have some prognostic implications in GBM patients.

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New York Medical College Research and News

Polo-like kinase 1 regulates RhoA during cytokinesis exit in human cells
by: M. Jhanwar-Uniyal et al
site publish date: 12/3/2010

Objective: Both RhoA (Rho1) and polo-like kinase 1 (Plk1) are implicated in the regulation of cytokinesis, a cellular process that marks the division of cytoplasm of a parent cell into daughter cells after nuclear division. Cytokinesis failure is often accompanied by the generation of cells with an unstable tetraploid content, which predisposes it to chromosomal instability and oncogenic transformation. Several studies using lower eukaryotic systems demonstrate that RhoA and Plk1 are essential for mitotic progression and cytokinesis.

Conclusion: Co-immunoprecipitation reveals that RhoA and Plk1 physically interact and that their interaction appears to be enhanced during mitosis. Given the role of RhoA and Plk1 in cytokinesis, our findings suggest that regulated activation of RhoA is important for cytokinesis and that Plk1 may alter activation of RhoA during mitotic cytokinesis.

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