Artificial intelligence solution to accelerate the acquisition of MRI images: Impact on the therapeutic care in oncology in radiology and radiotherapy departments.

PURPOSE: MRI is essential in the management of brain tumours. However, long waiting times reduce patient accessibility. Reducing acquisition time could improve access but at the cost of spatial resolution and diagnostic quality. A commercially available artificial intelligence (AI) solution, SubtleMR™, can increase the resolution of acquired images. The objective of this prospective study was to evaluate the impact of this algorithm that halves the acquisition time on the detectability of brain lesions in radiology and radiotherapy. MATERIAL AND METHODS: The T1/T2 MRI of 33 patients with brain metastases or meningiomas were analysed. Images acquired quickly have a matrix divided by two which halves the acquisition time. The visual quality and lesion detectability of the AI images were evaluated by radiologists and radiation oncologist as well as pixel intensity and lesions size. RESULTS: The subjective quality of the image is lower for the AI images compared to the reference images. However, the analysis of lesion detectability shows a specificity of 1 and a sensitivity of 0.92 and 0.77 for radiology and radiotherapy respectively. Undetected lesions on the IA image are lesions with a diameter less than 4mm and statistically low average gadolinium-enhancement contrast. CONCLUSION: It is possible to reduce MRI acquisition times by half using the commercial algorithm to restore the characteristics of the image and obtain good specificity and sensitivity for lesions with a diameter greater than 4mm.

RBE of kV CBCT radiation determined by Monte Carlo DNA damage simulations.

Due to the higher LET of kilovoltage (kV) radiation, there is potential for an increase in relative biological effectiveness (RBE) of absorbed doses of radiation from kV cone beam computed tomography (CBCT) sources in reference to megavoltage or Co-60 doses. This work develops a method for accurately coupling a Monte Carlo (MC) radiation transport code (PENELOPE) with the damage simulation (MCDS) to predict relative numbers of DNA double strand breaks (DSBs). The MCDS accounts for slowing down of electrons and delta ray production within the cell nucleus; however, determining the spectrum of electrons incident on the cell nucleus from photons interacting in a larger region of tissue is not trivial. PENELOPE simulations were conducted with a novel tally algorithm invoked where electrons incident on a detection material were tracked and both the incident energy and the final deposited dose were recorded. The DSB yield predicted by a set of MCDS runs of monoenergetic electrons was then looked up in a table and weighted by the specific energy of the incident electron. Our results indicate that the RBE for DSB induction is 1.1 for diagnostic x-rays with energies from 80 to 125 kVp. We found no significant change in RBE with depth or filtration. The predicted absolute DSB yields are about three times lower for cells irradiated under anoxic conditions than the yield in cells irradiated under normoxic (5%) or fully aerobic (100%) conditions. However, oxygen concentration has a negligible (± 0.02) effect on the RBE of kV CBCT x-rays.

Sci-Fri PM: Delivery - 08: Characterizing the spatially varying fluence and spectra of a kV imaging source for dose calculations.

Kilovoltage (kV) daily image-guided radiotherapy (IGRT) procedures accumulate radiation dose within the patient that is currently not routinely incorporated in the treatment plan. As part of the process of developing a patient-specific kV dose computation tool, the kV x-ray source must be characterized. We propose a simple, clinically feasible experimental characterization method using in-air dose measurements along the transverse axis. We determine half-value layer (HVL) along the transverse axis, from which we derive the HVL-specific mass-absorption coefficient, which is used to determine beam fluence. These values are interpolated over the entire field. The spectrum at each interpolation point in the field is found from HVL and accelerating potential (kVp) using third-party software Spektr. We use this method to characterize the spatially varying fluence and spectra of a Varian® On-Board Imaging® source for energies 80, 100 and 125 kVp. This characterization is used to compute dose within a heterogeneous phantom, using our previously validated in-house dose computation software, which we compare with relative dose measurements. We show that for a 10×10 cm2 field size using no added filtration, the agreement for all three energies is within 2% for the central depth-dose profile and within 2.6% for the transverse profiles. This clinically feasible experimental characterization method for kV imaging sources represents a crucial step in the development of a patient-specific dose computation tool.

Sci-Sat AM: Brachy - 06: Monte carlo DNA damage simulations of kV cbct radiation.

When performed daily, cone beam CT (CBCT) images can accumulate radiation dose to non-negligible levels. Because kV x-rays have a larger relative biological effectiveness (RBE) than its MV x-rays, the accumulated absorbed dose needs to be multiplied by an appropriate RBE to better evaluate the impact of CBCT dose in a treatment planning context. We investigated this question using PENLEOPE simulations to look in detail at the electron energy spectra produced by kV x-rays and Co-60 γ-rays in biologically motivated geometries. The electron spectra were input into the published Monte Carlo Damage Simulation (MCDS) and used to estimate the average number of double strand breaks (DSBs) per Gy per cell. Our results suggest an approximately 10% increase in the RBE for DSB induction. For the majority of treatment planning scenarios where imaging dose is only a small fraction of the total delivered dose to target volumes and organs at risk, the increase in RBE is not critical to be factored in, however for it may play a significant role in predicting the induction of secondary cancers.

Amphetamine-like stimulant cessation in an abusing patient treated with bupropion.

OBJECTIVE: Bupropion sustained release is considered to be a weak inhibitor of dopamine and serotonin reuptake. METHOD: We report the case of an amphetamine-abusing patient who self-administered bupropion. RESULTS: Since 30 years, a 52-year-old women used amphetamine derivates. She explained her need for amphetamine use in order to perform daily activities. Recently, she decided to experiment with bupropion. She abruptly stopped taking clobenzorex and simultaneously started taking bupropion (150 mg/day). The seventh day she reported a concomitant intake of clobenzorex; this induced adverse effects. Whilst taking bupropion, she described experiencing an euthymic state without any compulsion to take amphetamine drugs and was able to perform daily activities. After stopping it, no symptoms of withdrawal were reported by the patient. CONCLUSION: This observation supports an another report suggesting that bupropion may be of help in weaning from amphetamine users and should be confirmed by clinical trials.

Chromosome 1 in human colorectal tumors. Cytogenetic research on structural changes and their significance.

The significance of short and long arm anomalies of chromosome 1 was investigated in 55 colorectal tumors comprising 41 carcinomas and 14 adenomas. The tumors were at various stages of transformation from adenoma to carcinoma. Our investigation was prompted by the observation of a p32-pter deletion on the short arm of chromosome 1 in a case of benign tubulovillous adenoma with mild dysplasia, as well as by frequent reports that chromosome 1 is involved in many neoplastic processes. Long arm anomalies were found in seven of the 41 carcinomas, six of which were in stage B2, and short arm anomalies in ten carcinomas at various stages. Three of the adenomas exhibited chromosome 1 anomalies, which in one case comprised a 1p32-pter deletion only. Overall, short arm anomalies especially concerned the p32-36 region. These results suggest that the cytogenetic anomalies respectively located on the short and long arms of chromosome 1 should be considered separately. Damage to the long arm might constitute a late non-specific event, whereas damage to the p32-pter region of the short arm might be involved in triggering colorectal tumor development.

Distinct helper virus requirements for Abelson murine leukemia virus-induced pre-B- and T-cell lymphomas.

Abelson murine leukemia virus (A-MuLV) can induce pre-B- or T-cell lymphomas (thymomas) in mice depending on the route and time of injection. Previous studies have shown that the choice of the helper virus used to rescue A-MuLV greatly influences its ability to induce pre-B-cell lymphomas. In this study, we investigated the role of the helper virus in A-MuLV-induced thymomas. A-MuLV rescued with the helper Moloney MuLV, BALB/c endogenous N-tropic MuLV, and two chimeric MuLVs derived from these two parents were injected intrathymically in young adult NIH Swiss mice. All four A-MuLV pseudotypes were found to be equally efficient in the induction of thymomas, whereas drastic differences were observed in their pre-B-cell lymphomagenic potential. Thymoma induction by A-MuLV was independent of the replication potential of the helper virus in the thymus, and no helper proviral sequences could be detected in the majority of thymomas induced by A-MuLV rescued with parental BALB/c endogenous or chimeric MuLVs. In the thymomas in which helper proviruses were present, none of them were found integrated in the Ahi-1 region, a common proviral integration site found in A-MuLV-induced pre-B-cell lymphomas (Y. Poirer, C. Kozak, and P. Jolicoeur, J. Virol. 62:3985-3992, 1988). In addition, helper-free stocks of A-MuLV were found to be as lymphomagneic as other pseudotypes in inducing thymomas after intrathymic inoculation, in contrast to their inability to induce pre-B-cell lymphomas when injected intraperitoneally in newborn mice. Restriction enzyme analysis revealed one to three A-MuLV proviruses in each thymoma, indicating the oligoclonality of these tumors. Analysis of the immunoglobulin and T-cell receptor loci confirmed that the major population of cells of these primary thymomas belongs to the T-cell lineage. Together, these results indicate that the helper virus has no effect in the induction of A-MuLV-induced T-cell lymphomas, in contrast to its important role in the induction of A-MuLV-induced pre-B-cell lymphomas. Our data also revealed distinct biological requirements for transformation of these two target cells by v-abl.

Identification of a common helper provirus integration site in Abelson murine leukemia virus-induced lymphoma DNA.

Abelson murine leukemia virus induces oligoclonal pre-B lymphoma in mice. The expression of the v-abl oncogene in target cells does not appear to be sufficient for tumor induction in several mouse strains, and additional genetic events are thought to be required. We postulated that the helper Moloney murine leukemia virus might induce these events, and its potential role as an insertional mutagen was assessed by the search of a common helper provirus integration site in Abelson murine leukemia virus lymphomas. Molecular cloning of cellular sequences adjacent to Moloney proviruses enabled us to identify a cellular region, designated Ahi-1, which was found occupied by the helper proviruses in 16% of Abelson pre-B-cell lymphomas. All proviruses for which the precise integration site within Ahi-1 could be mapped were found to be in the same orientation. Ahi-1 has been mapped to mouse chromosome 10 and represents a new common proviral integration site. These data suggest that the helper virus contributes to the induction of secondary genetic events which may be important for the development of Abelson murine leukemia virus-induced pre-B-cell lymphoma.

Tubulovillous adenoma of the colon with hyperdiploidy, double-minute chromosomes, and inversion of chromosome 1.

A sessile adenoma of the left flexure of the colon was studied after surgical colectomy. Specimens were obtained for complete histologic evaluation. The tumor consisted of glandular tubes with decreased mucin production and a papillary structure on the luminal aspect. The muscularis mucosa was not involved; there was no carcinomatous focus. Cytogenetic study was carried out on 56 cells; none was normal, 77% were hyperdiploid (52-87 chromosomes), 16% were hypodiploid (18-39 chromosomes), and 7% were paradiploid. The supernumerary chromosomes were chromosomes #3, #6, #13, #19, and #20; chromosome #18 was missing in 80% of the cells. A marker for chromosome #1 resulting from a q21.1-q21.2 break with inversion of the centromere-bearing segment (pter-q21) was observed in 58% of the cells. Twenty-five percent of the cells had double minute chromosomes. Despite the histologically benign nature of the tumor, all the cells showed significant cytogenetic aberrations, some of which are considered to be markers of neoplastic transformation (polyploidy, double minutes, chromosome #1 marker).

Important role of the long terminal repeat of the helper Moloney murine leukemia virus in Abelson virus-induced lymphoma.

The helper virus has been shown to play a critical role in the development of lymphoma induced by the defective Abelson murine leukemia virus (A-MuLV). Indeed, A-MuLV pseudotyped with some viruses, such as the Moloney MuLV, has been shown to be highly lymphogenic, whereas A-MuLV pseudotyped with other viruses, such as the BALB/c endogenous N-tropic MuLV, has been shown to be devoid of lymphogenic potential (N. Rosenberg and D. Baltimore, J. Exp. Med. 147:1126-1141, 1978; C. D. Scher, J. Exp. Med. 147: 1044-1053, 1978). To map the viral DNA sequences encoding the determinant of the lymphogenic potential of Moloney MuLV when complexed with A-MuLV, we constructed chimeric helper viral DNA genomes in vitro between parental cloned infectious viral DNA genomes from Moloney MuLV and from BALB/c endogenous N-tropic MuLV. Chimeric helper MuLVs, recovered after transfection of NIH 3T3 cells were used to rescue A-MuLV, and the pseudotypes were inoculated into newborn NIH Swiss, CD-1, and SWR/J mice to test their lymphogenic potential. We found that a 0.44-kilobase-pair PstI-KpnI long terminal repeat-containing fragment from the Moloney MuLV was sufficient to confer some, but not complete, lymphogenic potential to a chimeric virus (p7M2) in NIH Swiss and SWR/J mice, but not in CD-1 mice. The addition of the 3'-end env sequences (comprising the carboxy terminus of gp70 and all p15E) to the U3 long terminal repeat sequences restored the full lymphogenic potential of the Moloney MuLV. Our data indicate that the 3'-end sequences of the helper Moloney MuLV are somehow involved in the development of lymphoma induced by A-MuLV. The same sequences have previously been found to harbor the determinant of leukemogenicity and of disease specificity of Moloney MuLV when inoculated alone.