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Dive into the research topics where Ajay Gupta is active.

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Featured researches published by Ajay Gupta.


Clinical Imaging | 2013

MRI perfusion in determining pseudoprogression in patients with glioblastoma

Robert J. Young; Ajay Gupta; Akash D. Shah; Jerome Graber; Timothy A. Chan; Zhigang Zhang; Weiji Shi; Kathryn Beal; Antonio Omuro

We examine the role of dynamic susceptibility contrast (DSC) magnetic resonance imaging (MRI) perfusion in differentiating pseudoprogression from progression in 20 consecutive patients with treated glioblastoma. MRI perfusion was performed, and relative cerebral blood volume (rCBV), relative peak height (rPH), and percent signal recovery (PSR) were measured. Pseudoprogression demonstrated lower median rCBV (P=.009) and rPH (P<.001), and higher PSR (P=.039) than progression. DSC MRI perfusion successfully identified pseudoprogression in patients who did not require a change in treatment despite radiographic worsening following chemoradiotherapy.


Computer Methods and Programs in Biomedicine | 2015

A comparative approach of four different image registration techniques for quantitative assessment of coronary artery calcium lesions using intravascular ultrasound

Tadashi Araki; Nobutaka Ikeda; Nilanjan Dey; Sayan Chakraborty; Luca Saba; Dinesh Kumar; Elisa Cuadrado Godia; Xiaoyi Jiang; Ajay Gupta; Petia Radeva; John R. Laird; Andrew Nicolaides; Jasjit S. Suri

In IVUS imaging, constant linear velocity and a constant angular velocity of 1800 rev/min causes displacement of the calcium in subsequent image frames. To overcome this error in intravascular ultrasound video, IVUS image frames must be registered prior to the lesion quantification. This paper presents a comprehensive comparison of four registration methods, namely: Rigid, Affine, B-Splines and Demons on five set of calcium lesion quantification parameters namely: (i) the mean lesion area, (ii) mean lesion arc, (iii) mean lesion span, (iv) mean lesion length, and (v) mean lesion distance from catheter. Using our IRB approved data of 100 patient volumes, our results shows that all four registrations showed a decrease in five calcium lesion parameters as follows: for Rigid registration, the values were: 4.92%, 5.84%, 5.89%, 5.27%, and 4.57%, respectively, for Affine registration the values were: 6.06%, 6.51%, 7.28%, 6.50%, and 5.94%, respectively, for B-Splines registration the values were: 7.35%, 8.03%, 9.54%, 8.18%, and 7.62%, respectively, and for Demons registration the five parameters were 7.32%, 8.02%, 10.11%, 7.94%, and 8.92% respectively. The relative overlap of identified lesions decreased by 5.91% in case of Rigid registration, 6.23% in case of Affine registration, 4.48% for Demons registration, whereas it increased by 3.05% in case of B-Splines registration. Rigid and Affine transformation-based registration took only 0.1936 and 0.2893 s per frame, respectively. Demons and B-Splines framework took only 0.5705 and 0.9405 s per frame, respectively, which were significantly slower than Rigid and Affine transformation based image registration.


Neuroimaging Clinics of North America | 2010

Imaging of brain tumors: functional magnetic resonance imaging and diffusion tensor imaging.

Ajay Gupta; Akash D. Shah; Robert J. Young; Andrei I. Holodny

The eloquent brain can be identified using functional MR (fMR) imaging for the gray matter and diffusion tensor (DT) imaging for the white matter. fMR imaging and DT imaging are especially important for patients with tumors near the important motor and language centers of the brain, where the normal anatomic references may be distorted by the tumor and associated edema. This article explains fMR imaging and DT imaging techniques and illustrates their clinical applications and limitations.


Clinical Neuroradiology-klinische Neuroradiologie | 2015

Pretreatment Dynamic Susceptibility Contrast MRI Perfusion in Glioblastoma: Prediction of EGFR Gene Amplification

Ajay Gupta; Robert J. Young; Akash D. Shah; A. D. Schweitzer; Jerome Graber; Weiji Shi; Zhigang Zhang; Jason T. Huse; Antonio Omuro

Background and PurposeMolecular and genetic testing is becoming increasingly relevant in GBM. We sought to determine whether dynamic susceptibility contrast (DSC) magnetic resonance imaging (MRI) perfusion imaging could predict EGFR-defined subtypes of GBM.Materials and MethodsWe retrospectively identified 106 consecutive glioblastoma (GBM) patients with known EGFR gene amplification, and a subset of 65 patients who also had known EGFRvIII gene mutation status. All patients underwent T2* DSC MRI perfusion. DSC perfusion maps and T2* signal intensity time curves were evaluated, and the following measures of tumor perfusion were recorded: (1) maximum relative cerebral blood volume (rCBV), (2) relative peak height (rPH), and (3) percent signal recovery (PSR). The imaging metrics were correlated to EGFR gene amplification and EGFRvIII mutation status using univariate analyses.ResultsEGFR amplification was present in 44 (41.5u2009%) subjects and absent in 62 (58.5u2009%). Among the 65 subjects who had undergone EGFRvIII mutation transcript analysis, 18 subjects (27.7u2009%) tested positive for the EGFRvIII mutation, whereas 47 (72.3u2009%) did not. Higher median rCBV (3.31 versus 2.62, pu2009=u20090.01) and lower PSR (0.70 versus 0.78, pu2009=u20090.03) were associated with high levels of EGFR amplification. Higher median rPH (3.68 versus 2.76, pu2009=u20090.03) was associated with EGFRvIII mutation.ConclusionDSC MRI perfusion may have a role in identifying patients with EGFR gene amplification and EGFRvIII gene mutation status, potential targets for individualized treatment protocols. Our results raise the need for further investigation for imaging biomarkers of genetically unique GBM subtypes.


American Journal of Neuroradiology | 2013

Potential role of preoperative conventional MRI including diffusion measurements in assessing epidermal growth factor receptor gene amplification status in patients with glioblastoma.

Robert J. Young; Ajay Gupta; Akash D. Shah; Jerome Graber; A. D. Schweitzer; A. Prager; Weiji Shi; Zhigang Zhang; Jason T. Huse; Antonio Omuro

BACKGROUND AND PURPOSE: Epidermal growth factor receptor amplification is a common molecular event in glioblastomas. The purpose of this study was to examine the potential usefulness of morphologic and diffusion MR imaging signs in the prediction of epidermal growth factor receptor gene amplification status in patients with glioblastoma. MATERIALS AND METHODS: We analyzed pretreatment MR imaging scans from 147 consecutive patients with newly diagnosed glioblastoma and correlated MR imaging features with tumor epidermal growth factor receptor amplification status. The following morphologic tumor MR imaging features were qualitatively assessed: 1) border sharpness, 2) cystic/necrotic change, 3) hemorrhage, 4) T2-isointense signal, 5) restricted water diffusion, 6) nodular enhancement, 7) subependymal enhancement, and 8) multifocal discontinuous enhancement. A total of 142 patients had DWI available for quantitative analysis. ADC maps were calculated, and the ADCmean, ADCmin, ADCmax, ADCROI, and ADCratio were measured. RESULTS: Epidermal growth factor receptor amplification was present in 60 patients (40.8%) and absent in 87 patients (59.2%). Restricted water diffusion correlated with epidermal growth factor receptor amplification (P = .04), whereas the other 7 morphologic MR imaging signs did not (P > .12). Quantitative DWI analysis found that all ADC measurements correlated with epidermal growth factor receptor amplification, with the highest correlations found with ADCROI (P = .0003) and ADCmean (P = .0007). CONCLUSIONS: Our results suggest a role for diffusion MR imaging in the determination of epidermal growth factor receptor amplification status in glioblastoma. Additional work is necessary to confirm these results and isolate new imaging biomarkers capable of noninvasively characterizing the molecular status of these tumors.


American Journal of Neuroradiology | 2016

Magnetic Susceptibility from Quantitative Susceptibility Mapping Can Differentiate New Enhancing from Nonenhancing Multiple Sclerosis Lesions without Gadolinium Injection

Yan Zhang; Susan A. Gauthier; Ajay Gupta; L. Tu; Joseph P. Comunale; Gloria C. Chiang; Weiwei Chen; C.A. Salustri; W. Zhu; Yi Wang

In 54 patients, new T2-weighted lesions were evaluated for enhancement on conventional T1-weighted imaging with gadolinium, and their susceptibility values were measured on quantitative susceptibility mapping. Eighty-six of 133 new lesions that were gadolinium-enhancing had relative susceptibility values significantly lower than those of nonenhancing lesions. Using susceptibility values to discriminate enhancing from nonenhancing lesions showed a sensitivity of 88.4% and specificity of 91.5%, with a cutoff value of 11.2 parts per billion for QSM. BACKGROUND AND PURPOSE: Magnetic susceptibility values of multiple sclerosis lesions increase as they change from gadolinium-enhancing to nonenhancing. Can susceptibility values measured on quantitative susceptibility mapping without gadolinium injection be used to identify the status of lesion enhancement in surveillance MR imaging used to monitor patients with MS? MATERIALS AND METHODS: In patients who had prior MR imaging and quantitative susceptibility mapping in a current MR imaging, new T2-weighted lesions were evaluated for enhancement on conventional T1-weighted imaging with gadolinium, and their susceptibility values were measured on quantitative susceptibility mapping. Receiver operating characteristic analysis was used to assess the diagnostic accuracy of using quantitative susceptibility mapping in distinguishing new gadolinium-enhancing from new nonenhancing lesions. A generalized estimating equation was used to assess differences in susceptibility values among lesion types. RESULTS: In 54 patients, we identified 86 of 133 new lesions that were gadolinium-enhancing and had relative susceptibility values significantly lower than those of nonenhancing lesions (β = −17.2; 95% CI, −20.2 to −14.2; P < .0001). Using susceptibility values to discriminate enhancing from nonenhancing lesions, we performed receiver operating characteristic analysis and found that the area under the curve was 0.95 (95% CI, 0.92–0.99). Sensitivity was measured at 88.4%, and specificity, at 91.5%, with a cutoff value of 11.2 parts per billion for quantitative susceptibility mapping–measured susceptibility. CONCLUSIONS: During routine MR imaging monitoring to detect new MS lesion activity, quantitative susceptibility mapping can be used without gadolinium injection for accurate identification of the BBB leakage status in new T2WI lesions.


Neuroradiology | 2012

Continuing the search for MR imaging biomarkers for MGMT promoter methylation status: conventional and perfusion MRI revisited

Ajay Gupta; Antonio Omuro; Akash D. Shah; Jerome Graber; Weiji Shi; Zhigang Zhang; Robert J. Young

Dear Sir: n nIt is with great interest that we read the recent investigation by Moon et al. [1] that assessed the value of preoperative imaging in the prediction of methyl-guanine methyl transferase (MGMT) promoter methylation status in 24 patients with high-grade gliomas. By evaluating preoperative computed tomography (CT), conventional magnetic resonance (MR) imaging, perfusion MR imaging, and diffusion tensor imaging (DTI), they found that MGMT promoter methylation was associated with ill-defined tumor margins, lower CT attenuation, higher apparent diffusion coefficient (ADC), and lower fractional anisotropy (FA). The remainder of the qualitative conventional MR imaging measures (ring versus nodular tumor enhancement, presence of a cystic portion, and heterogeneity of the signal intensity on the T2-weighted images) as well as perfusion MR imaging (as assessed by relative cerebral blood volume) were not found to be different between groups. Their results are relevant given the recently described prognostic significance of MGMT promoter methylation status in the survival of patients with high-grade gliomas [2, 3]. An imaging biomarker for MGMT methylation could serve as a surrogate for histopathology in those cases where pathology sampling is suboptimal, or could be of value if future preoperative treatment regimens are developed and based on presumed MGMT status. However, a major confounding factor in that study is the fact that both WHO grade III tumors and grade IV tumors were included, with a relatively small number of patients in each group. WHO grade III and IV tumors are a highly heterogeneous group in terms of histological findings, biological behavior, and radiographic characteristics. In that study, a total of 57.1% of grade III tumors were methylated versus only 41.1% in the grade IV tumors. Although this difference has not reached statistical significance, likely reflecting small sample sizes, the possibility that radiographic differences found between the methylated and unmethylated groups could at least in part reflect differences in histological grade cannot be excluded. The radiographic differences among the different types of malignant gliomas such as anaplastic oligodendrogliomas, grade III astrocytomas, and glioblastomas have been well described and cannot be ignored. The distribution of the different radiographic parameters according to tumor type and grade was not provided in that paper. n nWe would like to take this opportunity to report our experience with attempting to find MR imaging parameters that may predict MGMT promoter methylation status. We examined the preoperative MR imaging of patients with malignant glioma treated at our institution and who had the MGMT promoter methylation status determined. To improve the homogeneity of the sample, we restricted the analysis to patients with glioblastomas (WHO grade IV tumors). The cohort of 77 patients all underwent preoperative conventional MR imaging with standard sequences (axial diffusion, T1-weighted, T2-weighted, FLAIR, gradient-echo or susceptibility-weighted, and triplanar post-gadolinium T1-weighted images). We qualitatively assessed, by consensus of experienced neuroradiologists (6 and 11 years experience), the following signs: (1) enhancing border sharpness; (2) cystic/necrotic change; (3) hemorrhage; (4) T2-isointense signal; (5) diffusion restriction; (6) nodular enhancement; (7) subependymal enhancement; and (8) multifocal discontinuous enhancement. In addition, 49 of the 77 patients had T2* dynamic susceptibility contrast perfusion-weighted MR imaging, where rCBV was recorded using maximal region-of-interest (ROI) technique (in a fashion similar to the manner described by Moon et al. [1]) as well as additional perfusion metrics including peak height (PH), relative peak height (rPH), and percentage signal recovery (PSR). n nSimilar to Moon et al. [1], we found that 31 of our 77 patients (40.2%) had methylation of the MGMT promoter, compared with 46 (59.8%) with unmethylated MGMT promoter. Despite measuring additional perfusion metrics such as PH, rPH, and PSR, we also found MR perfusion-weighted imaging to have no value in predicting MGMT promoter methylation, with p values ranging from 0.66 to 0.87 (Table 1). n n n nTable 1 n nRelationship between perfusion metric and MGMT methylation status n n n nHowever, none of our conventional MR imaging signs was significantly associated with MGMT methylation promoter status, with p values ranging from 0.14 to 0.97 (Table 2). Moon et al. [1] found that ill-defined tumor margins were associated with methylation of the MGMT promoter, which could be potentially explained by the fact that some lower-grade tumors tend to have ill-defined margins and have higher frequency of MGMT promoter methylation. Moon’s findings also disagree with a study performed by Drabcyz et al. [4] in 59 patients, which found that ring enhancement was highly associated with unmethylated MGMT promoter status (p=0.006) and in an elegant texture analysis found T2-weighted texture features to be important (p<0.05). Moreover, an additional study by Eoli et al. [5] in 86 patients found that ring enhancement was associated with unmethylated MGMT status (p<0.005). Clearly, additional studies are needed to settle this question. n n n nTable 2 n nRelationship between MRI sign and MGMT methylation status n n n nWe did not perform DTI in our patients. It is interesting that Moon et al. found that reduced FA is associated with methylation of the MGMT promoter. They performed DTI by applying six different directions of orthogonal diffusion gradients. They do not specify the number of excitations (NEX) used, but we estimate that at 3 T with a commonly applied NEX=6 that this sequence required approximately 2–3 min. We have considered adding DTI as a routine sequence for preoperative imaging at our institutions, but our standard DTI protocol prescribes 15 to 33 non-collinear gradient directions that may add 5–11 min to total scan time. The authors measured ROIs in the enhancing solid portions of the tumors and obtained ratios relative to ROIs in the contralateral homologous normal-appearing brain parenchyma. This technique helps mitigate but does not completely eliminate potentially dramatic regional and anatomy-specific variations in FA. Given these limitations, incorporating DTI into routine clinical practices in all preoperative imaging of high-grade gliomas may be challenging, and further validation would be needed. n nGiven the variability of these reports, we would urge caution in attempting to predict MGMT status based on preoperative MR imaging sequences. Our cohort of 77 patients showed no significant differences after qualitative assessment of MR imaging signs. It is therefore our opinion that, despite the interesting preliminary findings of Moon et al. and previous reports, additional studies are needed to address this critical clinical question. Although the potential role of DTI or quantitative ADC measurements in predicting MGMT status is important and warrants further investigation, qualitative measures performed at the picture archive and communication system (PACS) station that do not require sophisticated time-consuming post-processing are more likely to be adopted in standard clinical practice and are therefore more valuable to practicing radiologists. Clearly, more work is needed in this area before neuroradiologists can suggest with any reasonable degree of confidence the likely MGMT status of a high-grade glioma based on standard, conventional MR imaging sequences.


Otolaryngologic Clinics of North America | 2012

Imaging Evaluation of the Parapharyngeal Space

Ajay Gupta; J. Levi Chazen; C. Douglas Phillips

The authors present imaging anatomy of the parapharyngeal space. Imaging approach is discussed in terms of the effect it has on differential diagnosis and diagnosis by the otolaryngologist. Neoplastic and congenital lesions are discussed along with other neck diseases occurring in this space.


Clinical Imaging | 2014

Sellar collision tumor involving metastatic lung cancer and pituitary adenoma: radiologic-pathologic correlation and review of the literature

Julie Sogani; Wanhua Yang; Ehud Lavi; Robert D. Zimmerman; Ajay Gupta

Collision tumors of the sella turcica involving metastases to pituitary adenomas are rare. We report a case of a collision tumor involving metastatic lung cancer with an emphasis on the neuroimaging and histopathological studies. A review of the literature including the diagnostic and management implications as well as pathogenetic mechanisms is also discussed.


Laryngoscope | 2013

Variability in the position of the retropharyngeal internal carotid artery

Ajay Gupta; Akash D. Shah; Zhigang Zhang; C. Douglas Phillips; Robert J. Young

The retropharyngeal internal carotid artery (ICA) is a well‐described arterial anomaly with important implications for patients undergoing pharyngeal approach surgical procedures. Existing clinical and imaging classification schemes for a retropharyngeal ICA take into account arterial distance to the pharyngeal mucosal wall. We describe a case of mobility of a retropharyngeal ICA between short‐interval imaging studies. The possibility of respiratory variability or other etiologies causing such changes in retropharyngeal carotid position have not been described previously. Our findings suggest that imaging findings from a single study alone may not be sufficient to confidently exclude this clinically significant arterial anomaly.

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Akash D. Shah

Memorial Sloan Kettering Cancer Center

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Robert J. Young

Memorial Sloan Kettering Cancer Center

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Zhigang Zhang

Memorial Sloan Kettering Cancer Center

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Antonio Omuro

Memorial Sloan Kettering Cancer Center

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Jerome Graber

Memorial Sloan Kettering Cancer Center

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Weiji Shi

Memorial Sloan Kettering Cancer Center

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A. D. Schweitzer

Memorial Sloan Kettering Cancer Center

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Jason T. Huse

University of Texas MD Anderson Cancer Center

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A. Prager

Memorial Sloan Kettering Cancer Center

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