Muhammad Wasif Saif

Prof. Dr. Muhammad Wasif Saif

Karmanos Cancer Institute, Detroit, Michigan, USA
orcid

Research Focus & Metrics

Academic Career Length

17Years (2010-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 March 2014 in Clinical Colorectal Cancer
Verified
Journal Article
Closed access
JCJiezhong Chen
Jiezhong Chen
AEAymen Elfiky
Aymen Elfiky
MHMei Han
Mei Han
CCChen Chen
Chen Chen
Muhammad Wasif SaifMuhammad Wasif Saif
Muhammad Wasif Saif

20 November 2012 in Pharmaceuticals
Verified
Journal Article
Open access
PDF file
ESEvangelos G. Sarris
Evangelos G. Sarris
Muhammad Wasif SaifMuhammad Wasif Saif
Muhammad Wasif Saif
KSKonstantinos Syrigos
Konstantinos Syrigos
Lung cancer is the primary cause of cancer-related mortality worldwide and although improvements in treatment have been achieved over the last few years, long-term survival rates for lung cancer patients remain poor. Therefore, there is an imperative need for molecularly targeted agents that will achieve long-term disease control. Numerous downstream molecular pathways, such as EGF/RAS/RAF/MEK/ERK and PI3K/AKT/mTOR are identified as having a key role in the pathogenesis of various forms of human cancer, including lung cancer. PI3K/AKT/mTOR signal pathway is an important intracellular signal transduction pathway with a significant role in cell proliferation, growth, survival, vesicle trafficking, glucose transport, and cytoskeletal organization. Aberrations in many primary and secondary messenger molecules of this pathway, including mutations and amplifications, are accounted for tumor cell proliferation, inhibition of apoptosis, angiogenesis, metastasis and resistance to chemotherapy-radiotherapy. In this review article, we investigate thoroughly the biological role of PI3K pathway in lung cancer and its contribution in the development of future therapeutic strategies.

7 May 2015 in Therapeutic Advances in Gastroenterology
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Journal Article
Open access
SKSaravanan K. Krishnamoorthy
Saravanan K. Krishnamoorthy
VRValerie Relias
Valerie Relias
SSSunit Sebastian
Sunit Sebastian
VJVijay Jayaraman
Vijay Jayaraman
Muhammad Wasif SaifMuhammad Wasif Saif
Muhammad Wasif Saif
Regorafenib (Stivarga, BAY 73-4506; Bayer Pharma AG, Berlin, Germany) is an oral multikinase inhibitor that targets the angiogenic tumor microenvironment and oncogenic kinases including vascular endothelial growth factor receptor 2 (VEGFR2), VEGFR1, VEGFR3, fibroblast growth factor receptor 1 (FGFR1), RAF, KIT, RET and BRAF. Its antiangiogenic effect is greater than that of its related drug, sorafenib. Regorafenib has been approved by the US Food and Drug Administration (FDA) for the treatment of metastatic colorectal cancer (mCRC) in patients who have failed treatment with fluoropyrimidine, oxaliplatin and irinotecan based chemotherapy, an anti-VEGF therapy and, if KRAS wild type, an anti-EGFR therapy. The FDA based this approval on data from the CORRECT trial, which showed the efficacy of regorafenib compared with placebo. The most common grade 3–4 adverse reactions with the drug are hand foot skin reactions (HFSR), diarrhea, hypertension and fatigue. This review discusses the efficacy data, and the incidence and management of regorafenib’s toxicities.

30 December 2019 in Pancreas (POJ)
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Journal Article
Open access
NHNausheen Hakim
Nausheen Hakim
RPRajvi Patel
Rajvi Patel
CDCraig Devoe
Craig Devoe
Muhammad Wasif SaifMuhammad Wasif Saif
Muhammad Wasif Saif
Survival rates for pancreatic cancer (PC) remain dismal. Current standard of care treatment regimens provide transient clinical benefit but eventually chemoresistance develops leading to poor outcomes. PC is a relatively chemoresistant tumor and one of the explanations for this is attributed to desmoplasia that impedes drug delivery. Based on this, stromal modifying agent such as Pegvorhyaluronidase alfa (PEGPH20) was developed and investigated in phase I-III studies. Although phase I-II studies showed promising results in patients with high hyaluronic acid (HA) expressing tumors, the phase III HALO 301 study failed to miss it’s primary endpoint and further development of PEHPH20 is halted. This failure implies that targeting desmoplasia alone is not sufficient and other intrinsic factors such as lack of significant neoantigens, low tumor mutational burden, and epithelial to mesenchymal transition may be at play. It is also important to consider that although the tumor stroma may be a physical bar-rier hampering drug delivery, it may also have protective effects in restraining tumor growth and progression. Further studies in molecular biology to better characterize the complex interaction between the microenvironment and cancer cells are warranted.

26 August 2016 in Cancer Chemotherapy and Pharmacology
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Journal Article
Closed access
PDF file
Muhammad Wasif SaifMuhammad Wasif Saif
Muhammad Wasif Saif
JKJames A. Knost
James A. Knost
ECE. Gabriela Chiorean
E. Gabriela Chiorean
SKSiva Rama Prasad Kambhampati
Siva Rama Prasad Kambhampati
DYDanni Yu
Danni Yu
BOBert H. O’neil
Bert H. O’neil

3 December 2013 in Cancer Chemotherapy and Pharmacology
Verified
Journal Article
Closed access
PDF file
Muhammad Wasif SaifMuhammad Wasif Saif
Muhammad Wasif Saif
JLJia Li
Jia Li
LLLynne Lamb
Lynne Lamb
KKKristin Kaley
Kristin Kaley
KEKyle Elligers
Kyle Elligers
YCYung-Chi Cheng
Yung-Chi Cheng