Docality.com Logo
 
Dr. Mussop  Mohammad   image

Dr. Mussop Mohammad

6576 Westlake Ct
Troy MI 48085
248 040-0501
Medical School: Other - Unknown
Accepts Medicare: No
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: 202571
NPI: 1821339797
Taxonomy Codes:
207L00000X

Request Appointment Information

Awards & Recognitions

About Us

Practice Philosophy

Conditions

Medical Malpractice Cases

None Found

Medical Board Sanctions

None Found

Referrals

None Found

Publications

Preclinical studies of apogossypolone, a novel pan inhibitor of bcl-2 and mcl-1, synergistically potentiates cytotoxic effect of gemcitabine in pancreatic cancer cells. - Pancreas
Overexpression of antiapoptotic Bcl-2 family proteins confers resistance to conventional therapy in pancreatic cancer patients. Apogossypolone (ApoG2) is an analogue of (-)-gossypol, exhibiting binding activity with Ki values of 35 nmol/L for Bcl-2 and 25 nmol/L for Mcl-1. The present study was designed to test our hypothesis whether inactivation of Bcl-2 family of proteins using ApoG2 could sensitize pancreatic cancer cells to the cytotoxic effect of gemcitabine.Two pancreatic cancer cell lines were treated with ApoG2, gemcitabine, and their combination; cytotoxicity and apoptosis was confirmed by MTT and histone/DNA enzyme-linked immunosorbent assay. Coimmunoprecipitation experiments were performed to elucidate the mechanism of action of ApoG2. In vivo efficacy of ApoG2 was evaluated in a xenograft model to confirm its therapeutic benefit with gemcitabine.When ApoG2 was combined with gemcitabine, increased cytotoxicity and apoptosis was evident. Coimmunoprecipitation experiment revealed that ApoG2 blocks the heterodimerization of Mcl-1/Bax and Bcl-2/Bim in cells. Furthermore, administration of ApoG2 with gemcitabine resulted in a statistically higher antitumor activity compared with either ApoG2 or gemcitabine alone in a severe combined immunodeficiency mouse xenograft model.Apogossypolone, which functions as a potent pan-Bcl-2 family inhibitor, seems therapeutically promising for future translational studies including the treatment of pancreatic cancer.
Antitumor activity of gemcitabine and oxaliplatin is augmented by thymoquinone in pancreatic cancer. - Cancer research
Previous studies have shown biological activity of thymoquinone, an active compound extracted from Nigella sativa, in pancreatic cancer cells; however, preclinical animal studies are lacking. Here, we report, for the first time, the chemosensitizing effect of thymoquinone to conventional chemotherapeutic agents both in vitro and in vivo using an orthotopic model of pancreatic cancer. In vitro studies revealed that preexposure of cells with thymoquinone (25 mumol/L) for 48 h followed by gemcitabine or oxaliplatin resulted in 60% to 80% growth inhibition compared with 15% to 25% when gemcitabine or oxaliplatin was used alone. Moreover, we found that thymoquinone could potentiate the killing of pancreatic cancer cells induced by chemotherapeutic agents by down-regulation of nuclear factor-kappaB (NF-kappaB), Bcl-2 family, and NF-kappaB-dependent antiapoptotic genes (X-linked inhibitors of apoptosis, survivin, and cyclooxygenase-2). As shown previously by our laboratory, NF-kappaB gets activated on exposure of pancreatic cancer cells to conventional chemotherapeutic agents; interestingly, thymoquinone was able to down-regulate NF-kappaB in vitro, resulting in chemosensitization. In addition to in vitro results, here we show for the first time, that thymoquinone in combination with gemcitabine and/or oxaliplatin is much more effective as an antitumor agent compared with either agent alone. Most importantly, our data also showed that a specific target, such as NF-kappaB, was inactivated in animal tumors pretreated with thymoquinone followed by gemcitabine and/or oxaliplatin. These results provide strong in vivo molecular evidence in support of our hypothesis that thymoquinone could abrogate gemcitabine- or oxaliplatin-induced activation of NF-kappaB, resulting in the chemosensitization of pancreatic tumors to conventional therapeutics.
TW-37, a small-molecule inhibitor of Bcl-2, inhibits cell growth and invasion in pancreatic cancer. - International journal of cancer
Bcl-2 family of proteins plays critical roles in human cancers, including pancreatic cancer, suggesting that the discovery of specific agents targeting Bcl-2 family proteins would be extremely valuable for pancreatic cancer therapy. We have previously reported the synthesis and characterization of TW-37, which seems to be a negative regulator of Bcl-2. In this investigation, we tested our hypothesis whether TW-37 could be an effective inhibitor of cell growth, invasion and angiogenesis in pancreatic cancer cells. Using multiple cellular and molecular approaches such as MTT assay, apoptosis enzyme-linked immunosorbent assay, real-time reverse transcription-polymerase chain reaction, Western blotting, electrophoretic mobility shift assay for measuring DNA binding activity of NF-kappaB, migration, invasion and angiogenesis assays, we found that TW-37, in nanomolar concentrations, inhibited cell growth in a dose- and time-dependent manner. This was accompanied by increased apoptosis and concomitant attenuation of NF-kappaB, and downregulation of NF-kappaB downstream genes such as MMP-9 and VEGF, resulting in the inhibition of pancreatic cancer cell migration, invasion and angiogenesis in vitro and caused antitumor activity in vivo. From these results, we conclude that TW-37 is a potent inhibitor of progression of pancreatic cancer cells, which could be due to attenuation of Bcl-2 cellular signaling processes. Our findings provide evidence showing that TW-37 could act as a small-molecule Bcl-2 inhibitor on well-characterized pancreatic cancer cells in culture as well as when grown as tumor in a xenograft model. We also suggest that TW-37 could be further developed as a potential therapeutic agent for the treatment of pancreatic cancer.(c) 2008 Wiley-Liss, Inc.
Efficacy of selected natural products as therapeutic agents against cancer. - Journal of natural products
With emerging sophistication in the exploration of ocean environment, a number of marine bioactive products have been identified with promising anticancer activity. Many of these are in active phase I or phase II clinical trials or have been terminated because of adverse side effects, mainly hematological in nature. Nonetheless, the information derived has aided enormously in providing leads for laboratory synthesis with modifications in the parent structure affecting compound solubility, absorption, and toxicity, resulting in less severe toxicity while achieving maximum efficacy in smaller doses. We describe herein, a few of the compounds obtained from marine and terrestrial sources [bryostatin 1 ( 1), dolastatin 10 ( 2), auristatin PE ( 3), and combretastatin A4 ( 4)] that have been extensively investigated in our laboratory and continue to be investigated for their sensitization effects with other cytotoxic agents in several different site-specific tumors employing murine models or human subjects.

Map & Directions

6576 Westlake Ct Troy, MI 48085
View Directions In Google Maps

Nearby Doctors

6038 Mayapple Dr
Troy, MI 48085
313 344-4404
6535 Rochester Rd Ste 106
Troy, MI 48085
248 795-5557
1950 E Wattles Rd Suite 102
Troy, MI 48085
248 401-1558
6780 Rochester Rd Suite A
Troy, MI 48085
248 798-8144
44201 Dequindre Rd
Troy, MI 48085
248 645-5000
5741 Folkstone Dr
Troy, MI 48085
248 796-6246
830 Longfellow Dr
Troy, MI 48085
734 316-6143
44201 Dequindre Rd
Troy, MI 48085
248 645-5000
6535 Rochester Rd Suite 102
Troy, MI 48085
248 130-0060
44199 Dequindre Rd Ste 623
Troy, MI 48085
248 285-5707