From daemon Mon Apr 5 13:32:03 1999 Received: (from daemon@localhost) by net.bio.net (8.9.1a/8.9.1) id KAA26433; Mon, 5 Apr 1999 10:41:17 -0700 (PDT) Message-Id: <199904051741.KAA26433@net.bio.net> To: radoncjc@net.bio.net Date: Mon, 5 Apr 1999 07:31:21 -1000 Reply-To: radoncjc@net.bio.net From: Brian J Goldsmith Subject: April 1999 Internet Radiation Oncology Journal Club (IROJC) April 1999 Internet Radiation Oncology Journal Club (IROJC) ------------------------------------------------------- Posting of references for review and discussion ------------------------------------------------------- The 47th collection of references suggested for attention and discussion by the IROJC's Board of Editors: Sarah Donaldson, M.D. Editor, Pediatric Radiation Oncology Robert Foote, M.D. Editor, Head and Neck / Skin Radiation Oncology Abram Recht, M.D. Editor, Breast Radiation Oncology Rich Hoppe, M.D. Editor, Reticuloendothelial System Radiation Oncology Perry Grigsby, M.D. Editor, Gynecological Radiation Oncology Andrew Turrisi, M.D. Editor, Lung and Mediastinum Radiation Oncology Joel Tepper, M.D. Editor, Gastrointestinal and Soft Tissue Sarcoma Radiation Oncology Mack Roach, M.D. Editor, Genitourinary Radiation Oncology David Larson, M.D. Ph.D. Editor, Central Nervous System Radiation Oncology Rod Withers, M.D., D.Sc. Editor, Radiobiology Jim Purdy, Ph.D. Editor, Radiation Oncology Physics and Dosimetry ----------------------------------------------------- You're encouraged to critically review this set of references and respond by posting your comments to the IROJC readership at radoncjc@net.bio.net. Comments should be in compliance with IROJC commentary rules (see below). In the month that follows this posting of references, submitted comments will be delivered to the e-mail boxes of the IROJC readership, with the goal of stimulating a professional discussion of these references and their subjects. ------------------------------------------------------------ ARCHIVED IROJC POSTINGS and commentary are available on the World Wide Web! Look for them on http://www.bio.net/ Click on the "Access the BIOSCI/bionet Newsgroups" hyperlink, and then go to "RADIATION-ONCOLOGY/Prototype". Or directly access the RADIATION-ONCOLOGY folder at http://www.bio.net/hypermail/RADIATION-ONCOLOGY/ There's also a freeWAIS search tool at the website, for searching archived postings for keywords or phrases! ------------------------------------------------------------ Commentary Rules: (1) Please cite the subject category in the header of your e-mail message, e.g., Subject: CNS 4/99. (2) Address the readership at large - not the Editor who suggested the reference. The Editor is under no obligation to respond to questions posed by the IROJC readership. (3) The Editor's selection is not necessarily an endorsement of the authors' conclusions. In fact, articles may be selected for criticism. (4) Comments posted to the Internet are public. Professional wording is prudent. (5) Comment only on journal articles that you have read recently, and please keep comments specific. (6) In order to minimize confusion, limit comments to the current month's list of references. (7) Please sign all comments and questions to the IROJC. By identifying yourself, you promote a more collegial and friendly environment! (8) Address to the Moderator (bjg@mhpcc.edu) private questions and comments which are not intended for IROJC posting and public reading. ****************** Peds: Donaldson 4/99 AU: Suryanarayan K, Shuster JJ, Donaldson SS, Hutchison RE, Murphy SB, Link MP. TI: Treatment of localized primary non-Hodgkin's lymphoma of bone in children: a Pediatric Oncology Group study. SO: J Clin Oncol 1999 Feb;17(2):456-9. URL: http://www.jco.org/abs17_2/v17n2p456.html Abstract: PURPOSE: The treatment of primary lymphoma of bone (PLB) in children has traditionally included radiotherapy to the primary site; more recently, it has included systemic chemotherapy. Because of concern about the untoward effects of treatment in a disease that is curable, we attempted to determine whether radiotherapy can be safely excluded from treatment. PATIENTS AND METHODS: The results of three consecutive Pediatric Oncology Group (POG) studies were examined to determine the impact on outcome of radiotherapy as adjunctive treatment in children and adolescents receiving chemotherapy for early-stage primary lymphoma of bone. RESULTS: From 1983 to 1997, 31 patients with localized PLB were entered onto POG studies of early-stage non-Hodgkin's lymphoma (NHL). Between 1983 and 1986, seven patients were treated with 8 months of chemotherapy with irradiation (XRT) of the primary site. After 1986, patients were treated without XRT; four received 8 months of chemotherapy, and 20 received 9 weeks of chemotherapy. Primary sites were the femur (nine), tibia (eight), mandible (five), mastoid (one), maxilla (one), zygomatic arch (one), rib (one), clavicle (one), scapula (one), ulna (one), talus (one), and calcaneous (one). Histologic classification revealed 21 cases of large cell lymphoma, five cases of lymphoblastic lymphoma, two cases of small, noncleaved-cell lymphoma, and three cases of NHL that could not be classified further. One patient relapsed at a distant site 22 months after completion of therapy. There have been no deaths. CONCLUSION: Localized PLB is curable in most children and adolescents with a 9-week chemotherapy regimen of modest intensity, and radiotherapy is an unnecessary adjunct. Editor's comments: Traditionally localized lymphoma of bone has been treated with primary radiotherapy. Through a series of well conducted studies, the Pediatric Oncology Group has shown that children with Non-Hodgkin's Lymphoma fare extremely well with risk adapted chemotherapy, and that radiotherapy does not contribute to local control, event free survival or survival. This study takes this observation even further by studying children with primary lymphoma of bone treated with multi-agent chemotherapy showing excellent outcome without using local radiotherapy. Here is another example of successful tailoring of therapy, minimizing potential complications of therapy without compromising survival. Such an observation requires the collaborative efforts of a cooperative group as these tumors are quite rare. ****************** Head/Neck/Skin: Foote 4/99 No Reference Selected. ****************** GYN: Grigsby 4/99 AU: Peters WA, Liu PY, Barrett R, Gordon W, Stock R, Berek JF, DiSaia PJ, Souhami L, Grigsby P, Alberts DS. TI: Cisplatin, 5-Fluorouracil plus radiation therapy are superior to radiation therapy as adjunctive therapy in high-risk, early-stage carcinoma of the cervix after radical hysterectomy and pelvic lymphadenectomy: report of a phase III inter-group study. SO: SGO 30th Annual Meeting Abstract #1. URL: http://www.sgo.org/meetings/30annual/abstracts/1.html Abstract: OBJECTIVE: To determine if the addition of chemotherapy (CT) to pelvic radiation therapy (RT) will improve the survival of early-stage, high-risk patients with cervical carcinoma. METHODS: Patients with clinical stage IA2, IB and IIA carcinoma of the cervix, initially treated with radical hysterectomy and pelvic lymphadenectomy, and who had positive pelvic lymph nodes and/or positive margins and/or microscopic involvement of the parametrium, were eligible for this study. Patients were randomized to receive radiation therapy or radiation therapy plus chemotherapy. Patients in each group received 4,930 cGY in 29 fractions to a standard pelvic field. Chemotherapy consisted of bolus cisplatin 70 mg/m2 and 96-hour infusion of 5-FU 1,000 mg/m2/day x 4D q.3w. for four total cycles, with the first and second cycles given concurrent to radiation therapy. RESULTS: Between 1991 and 1996, 268 patients were entered into the study. 241 are currently evaluable (126 RT+CT and 115 RT). Progression-free (P equals 0.01) and overall survival (Pequals 0.01) are significantly improved in the patients receiving CT. The hazard ratio for overall survival in the RT-only arm vs the RT+CT-arm is 2.02. The projected progression-free survivals at four years are 63% with RT and 81% with RT+CT. Grade 3/4 hemtologic and gastrointestinal toxicity were more frequent in the RT+CT group. There were no toxicity related deaths in either group. CONCLUSIONS: The addition of chemotherapy to radiation therapy significantly improves progression-free and overall survival for high-risk, early-stage patients who undergo radical hysterectomy and pelvic lymphadenectomy for carcinoma of the cervix. ****************** GI / Soft Tissue Sarcoma: Tepper 4/99 AU: Minsky BD, Neuberg D, Kelsen DP, Pisansky TM, Ginsberg RJ, Pajak T, Salter M, Benson AB 3rd. TI: Final report of Intergroup Trial 0122 (ECOG PE-289, RTOG 90-12): Phase II trial of neoadjuvant chemotherapy plus concurrent chemotherapy and high-dose radiation for squamous cell carcinoma of the esophagus. SO: Int J Radiat Oncol Biol Phys 1999 Feb 1;43(3):517-23. Abstract: PURPOSE: To determine the outcome of neoadjuvant chemotherapy followed by concurrent chemotherapy plus high-dose radiation therapy in patients with local/regional squamous cell carcinoma of the esophagus. METHODS AND MATERIALS: Forty-five patients with clinical Stage T1-4N0-1M0 squamous cell carcinoma were entered on a prospective single-arm study, of which 38 were eligible. Patients received 3 monthly cycles of 5-FU (1000 mg/m2/24 h x 5 days) and cisplatin (100 mg/m2 day 1; neoadjuvant segment) followed by 2 additional monthly cycles of 5-FU (1000 mg/m2/24 h x 5 days) and cisplatin (75 mg/m2 day 1) plus concurrent 6480 cGy (combined modality segment). The median follow-up in surviving patients was 59 months. RESULTS: For the 38 eligible patients, the primary tumor response rate was 47% complete, 8% partial, and 3% stable disease. The first site of clinical failure was 39% local/regional and 24% distant. For the total patient group, there were 6 deaths during treatment, of which 9% (4/45) were treatment related. The median survival was 20 months. Actuarial survival at 3 years was 30%, and at 5 years, 20%. CONCLUSION: This intensive neoadjuvant approach does not appear to offer a benefit compared with conventional doses and techniques of combined modality therapy. However, high dose radiation (6480 cGy) appears to be tolerable, and is being tested further in Intergroup Trial INT 0123. Editor's comments: This article was picked for the journal club discussion not so much for what was explicity stated in the article, but rather for the implications of the data. First of all, it is important to note that this aggressive regimen of neoadjuvant chemotherapy followed by concurrent chemoradiation therapy was toxic and lends further support to the concept, demonstrated clearly in Kelsen's recent NEJM medicine paper, that upfront chemotherapy is not of value in the treatment of esophageal cancer. Perhaps as important for the radiation oncologist are the clues that this paper provides on failure rates after high doses of radiation/chemo therapy. The failure rates presented in the paper were the failures of all patients, including those patients who were ineligible for evaluation for response because they died during treatment, went off study etc. However, if one evaluates only those patients who were assessed for response, the local failure rate in those 28 patients was 10/28 local only, and 5/28 local plus distant for a local failure rate of 15/28 (54%). What is important about this is that it suggests that pushing the radiation dose to 6,400 cGy, even when given with concurrent chemotherapy, is very unlikely to impact substantially on the high local failure rates that have been consistently reported with non-surgical therapy of this disease. Thus, although the high mortality rate seen in this trial makes this approach (neoadjuvant chemotherapy) clearly unacceptable, it also speaks against the routine use of non-surgical therapy of this disease. I think it unlikely that most radiation oncologists would view it acceptable (and not add adjuvant radiation therapy) in a disease managed with surgery alone where the local failure rate was greater than 50%. We must be sure to look at the shortcomings of our non-surgical approaches and evaluate the morbidity of local recurrence in esophageal cancer compared to the morbidity of surgery. To do this, we will need good data on quality of life which is generally not available for this disease. ****************** CNS: Larson 4/99 AU: Prados MD, Edwards MS, Chang SM, Russo C, Davis R, Rabbitt J, Page M, Lamborn K, Wara WM. TI: Hyperfractionated craniospinal radiation therapy for primitive neuroectodermal tumors: results of a Phase II study. SO: Int J Radiat Oncol Biol Phys 1999 Jan 15;43(2):279-85. Abstract: PURPOSE: To report the results of a Phase II study of hyperfractionated craniospinal radiation therapy, with and without adjuvant chemotherapy for primitive neuroectodermal brain tumors (PNETs) and malignant ependymomas. METHODS AND MATERIALS: Newly diagnosed PNET or malignant ependymomas were treated with hyperfractionated craniospinal radiation therapy. The primary tumor site was treated to a dose of 72 Gy, with 30 Gy given to the rest of the craniospinal axis. The fraction size was 1.0 Gy, given twice a day. Patients with poor risk factors also received adjuvant chemotherapy with CCNU, cisplatin, and vincristine. Patients had follow-up for survival, time to tumor progression, and patterns of relapse. RESULTS: A total of 39 patients (21 males/18 females) were treated between March 12, 1990 and October 29, 1992. The median age was 16 years (range 3-59 years). Tumor types included 25 medulloblastomas, 5 pineoblastomas, 5 cerebral PNETs, 1 spinal cord PNET, and 3 malignant ependymomas. Twenty cases were staged as poor-risk and received adjuvant chemotherapy following radiation. Three-year progression-free survival (PFS) was 60% and 63% for poor-risk and good-risk patients, respectively. Overall 3-year survival for these groups was 70% and 79%, respectively. For the 25 patients with medulloblastoma, there were 16 good-risk and 9 poor-risk patients. Three-year PFSs were 63% and 56%, respectively. The 5-year survival for good-risk medulloblastoma was 69% with 43.7% of these patients having failures outside the primary site. CONCLUSIONS: Survival in patients with good-risk medulloblastoma was no better than that seen in previous studies with single-fraction radiation, and the rate of failure outside the primary site is excessive. Those with poor-risk features had comparable survival to that seen in patients with good risk factors, but these patients were treated with chemotherapy, and the role that hyperfractionated radiation played in their outcome is uncertain. Editor's comments: This paper discusses the role of hyperfractionated craniospinal radiotherapy for tumors arising from the pineal region, cerebellum, or cerebrum, of the following histopathologic types: pineoblastoma, medulloblastoma, PNET, anaplastic ependymoma. The results, obtained in a Phase II study, demonstrate the feasibility of hyperfractionation. However, progression-free survival was not demonstrated to offer any progression-free survival advantage. Probably standard fractionation schemes are best used for patients with these tumors (unless enrolled on a study). ****************** Physics/Dosimetry: Purdy 4/99 AU: Stroom JC, de Boer HC, Huizenga H, Visser AG. TI: Inclusion of geometrical uncertainties in radiotherapy treatment planning by means of coverage probability. SO: Int J Radiat Oncol Biol Phys 1999 Mar 1;43(4):905-19. Abstract: PURPOSE: Following the ICRU-50 recommendations, geometrical uncertainties in tumor position during radiotherapy treatments are generally included in the treatment planning by adding a margin to the clinical target volume (CTV) to yield the planning target volume (PTV). We have developed a method for automatic calculation of this margin. METHODS AND MATERIALS: Geometrical uncertainties of a specific patient group can normally be characterized by the standard deviation of the distribution of systematic deviations in the patient group (Sigma) and by the average standard deviation of the distribution of random deviations (sigma). The CTV of a patient to be planned can be represented in a 3D matrix in the treatment room coordinate system with voxel values one inside and zero outside the CTV. Convolution of this matrix with the appropriate probability distributions for translations and rotations yields a matrix with coverage probabilities (CPs) which is defined as the probability for each point to be covered by the CTV. The PTV can then be chosen as a volume corresponding to a certain iso-probability level. Separate calculations are performed for systematic and random deviations. Iso-probability volumes are selected in such a way that a high percentage of the CTV volume (on average greater than 99%) receives a high dose (greater than 95%). The consequences of systematic deviations on the dose distribution in the CTV can be estimated by calculation of dose histograms of the CP matrix for systematic deviations, resulting in a so-called dose probability histogram (DPH). A DPH represents the average dose volume histogram (DVH) for all systematic deviations in the patient group. The consequences of random deviations can be calculated by convolution of the dose distribution with the probability distributions for random deviations. Using the convolved dose matrix in the DPH calculation yields full information about the influence of geometrical uncertainties on the dose in the CTV. RESULTS: The model is demonstrated to be fast and accurate for a prostate, cervix, and lung cancer case. A CTV-to-PTV margin size which ensures at least 95% dose to (on average) 99% of the CTV, appears to be equal to about 2Sigma + 0.7sigma for three all cases. Because rotational deviations are included, the resulting margins can be anisotropic, as shown for the prostate cancer case. CONCLUSION: A method has been developed for calculation of CTV-to-PTV margins based on the assumption that the CTV should be adequately irradiated with a high probability. ****************** Breast: Recht 4/99 AU: Fisher B, Costantino JP, Wickerham DL, Redmond CK, Kavanah M, Cronin WM, Vogel V, Robidoux A, Dimitrov N, Atkins J, Daly M, Wieand S, Tan-Chiu E, Ford L, Wolmark N. TI: Tamoxifen for prevention of breast cancer: report of the National Surgical Adjuvant Breast and Bowel Project P-1 Study. SO: J Natl Cancer Inst 1998 Sep 16;90(18):1371-88. URL: http://jnci.oupjournals.org/cgi/content/abstract/90/18/1371 Abstract: BACKGROUND: The finding of a decrease in contralateral breast cancer incidence following tamoxifen administration for adjuvant therapy led to the concept that the drug might play a role in breast cancer prevention. To test this hypothesis, the National Surgical Adjuvant Breast and Bowel Project initiated the Breast Cancer Prevention Trial (P-1) in 1992. METHODS: Women (N equals 13388) at increased risk for breast cancer because they 1) were 60 years of age or older, 2) were 35-59 years of age with a 5-year predicted risk for breast cancer of at least 1.66%, or 3) had a history of lobular carcinoma in situ were randomly assigned to receive placebo (n equals 6707) or 20 mg/day tamoxifen (n equals 6681) for 5 years. Gail's algorithm, based on a multivariate logistic regression model using combinations of risk factors, was used to estimate the probability (risk) of occurrence of breast cancer over time. RESULTS: Tamoxifen reduced the risk of invasive breast cancer by 49% (two-sided P less than .00001), with cumulative incidence through 69 months of follow-up of 43.4 versus 22.0 per 1000 women in the placebo and tamoxifen groups, respectively. The decreased risk occurred in women aged 49 years or younger (44%), 50-59 years (51%), and 60 years or older (55%); risk was also reduced in women with a history of lobular carcinoma in situ (56%) or atypical hyperplasia (86%) and in those with any category of predicted 5-year risk. Tamoxifen reduced the risk of noninvasive breast cancer by 50% (two-sided P less than .002). Tamoxifen reduced the occurrence of estrogen receptor-positive tumors by 69%, but no difference in the occurrence of estrogen receptor-negative tumors was seen. Tamoxifen administration did not alter the average annual rate of ischemic heart disease; however, a reduction in hip, radius (Colles'), and spine fractures was observed. The rate of endometrial cancer was increased in the tamoxifen group (risk ratio equals 2.53; 95% confidence interval equals 1.35-4.97); this increased risk occurred predominantly in women aged 50 years or older. All endometrial cancers in the tamoxifen group were stage I (localized disease); no endometrial cancer deaths have occurred in this group. No liver cancers or increase in colon, rectal, ovarian, or other tumors was observed in the tamoxifen group. The rates of stroke, pulmonary embolism, and deep-vein thrombosis were elevated in the tamoxifen group; these events occurred more frequently in women aged 50 years or older. CONCLUSIONS: Tamoxifen decreases the incidence of invasive and noninvasive breast cancer. Despite side effects resulting from administration of tamoxifen, its use as a breast cancer preventive agent is appropriate in many women at increased risk for the disease. Editor's comments: The use of chemopreventive agents in patients who are at substantial risk of developing breast cancer has been an area in which we have had only indirect evidence in the past, from studies of patients who already had a breast cancer who were receiving tamoxifen as a treatment modality. The NSABP P-1 trial is the largest of the 3 randomized trials reported to date examining this issue for patients who never had breast cancer. However, the results of these 3 trials do not agree. (See the reports of the Milan and British trials in the Lancet 1998, vol. 352, at pp.93-97 and 98-101, respectively.) Possible reasons for this have been discussed by a number of authors; I would suggest the excellent editorial by Kathleen Pritchard (Lancet 1998;352:80-82) as the best of these. The flaws of the Milan and British trials, and the much larger sample size of the P-1 trial, suggest that the truth probably lies closer to the latter results than to the former. Still, the relatively short follow-up in the P-1 trial makes it still uncertain whether the results will continue to be the same with time (although the data from the Oxford Overview on reduction in the risk of contralateral cancers suggests that they will hold up). This is particularly important because of the lack of observed difference so far in breast cancer mortality rates between the treatment and control arms. In the absence of such a difference, discussions with patients about whether to use tamoxifen as a preventive agent tend to come down to the "peace of mind" factor - that is, does the possibility of avoiding another breast cancer outweigh the potential morbidity (and even mortality) from tamoxifen? So far, neither patients nor doctors at my institution seem to have made up their minds on this. ****************** RES: Hoppe 4/99 AU: Diehl V, Sextro M, Franklin J, Hansmann ML, Harris N, Jaffe E, Poppema S, Harris M, Franssila K, van Krieken J, Marafioti T, Anagnostopoulos I, Stein H. TI: Clinical presentation, course, and prognostic factors in lymphocyte-predominant Hodgkin's disease and lymphocyte-rich classical Hodgkin's disease: report from the European Task Force on Lymphoma Project on Lymphocyte-Predominant Hodgkin's Disease. SO: J Clin Oncol 1999 Mar;17(3):776-83. URL: http://www.jco.org/abs17_3/v17n3p776.html Abstract: PURPOSE: Recent studies have suggested that lymphocyte-predominant Hodgkin's disease (LPHD) is both clinically and pathologically distinct from other forms of Hodgkin's disease, including classical Hodgkin's disease (CHD). However, large-scale clinical studies were lacking. This multicenter, retrospective study investigated the clinical characteristics and course of LPHD patients and lymphocyte-rich classical Hodgkin's disease (LRCHD) patients classified according to morphologic and immunophenotypic criteria. MATERIALS AND METHODS: Clinical data and biopsy material of all available cases initially submitted as LPHD were collected from 17 European and American centers, stained, and reclassified by expert pathologists. RESULTS: The 426 assessable cases were reclassified as LPHD (51%), LRCHD (27%), CHD (5%), non-Hodgkin's lymphoma (3%), and reactive lesion (3%); 11% of cases were not assessable. Patients with LPHD and LRCHD were predominantly male, with early-stage disease and few risk factors. Patients with LRCHD were significantly older. Survival and failure-free survival rates with adequate therapy were similar for patients with LPHD and LRCHD, and were stage-dependent and not significantly better than stage-comparable results for CHD (German trial data). Twenty-seven percent of relapsing LPHD patients had multiple relapses, which is significantly more than the 5% of relapsing LRCHD patients who had multiple relapses. Lymphocyte-predominant Hodgkin's disease patients had significantly superior survival after relapse compared with LRCHD or CHD patients; however, this was partly due to the younger average age of LPHD patients. CONCLUSION: The two subgroups of LPHD and LRCHD bore a close clinical resemblance that was distinct from CHD; the course was similar to that of comparable nodular sclerosis and mixed cellularity patients. Thorough staging is necessary to detect advanced disease in LPHD and LRCHD patients. The question of how to treat such patients, either by reducing treatment intensity or following a "watch and wait" approach, remains unanswered. Editor's comments: This study is a multi-institutional one that includes 334 cases that were initially called LPHD and in which material was available for path review and phenotyping studies. Morphologically, all satisfied the criteria of LP by the pathology panel, but phenotyping identified characteristics of classical HD (CD30 or CD15 positive, but CD20 negative vs. CD20 positive and CD30, CD15 negative for LP) in 115 of these 334 cases. These cases are called "lymphocyte-rich classical HD (LRCHD)". In the LP group, there was reportedly no impact of architecture (nodular v. diffuse v. nodular-and-diffuse). For LP vs. LRCHD, there was also little clinical difference. LPHD pts were a bit younger and had a bit lower likelihood of mediastinal disease, other characteristics were similar. The only outcome difference was "Survival after relapse", which was worse in the LRCHD group, but partially attributable to age. In addition, LP patients were more likely to have experienced multiple relapses over time. LPHD is associated with a high risk of secondary nHL's in some series. In this report, there were 2 fatal cases of nHL each in the LP and LRCHD groups, and an additional 4 non-fatal cases in the LP group. This overall risk of 2.9% (median follow-up 6.8 years) (vs. 1.7% in the LRCHD group) does not seem extraordinarily high. LPHD and LRCHD may mark differently, but they share a similar clinical presentation and outcome. ****************** Lung/Mediastinum: Turrisi 4/99 No Reference Selected ****************** GU: Roach 4/99 No Reference Selected ****************** Radiobiology: Withers 4/99 No Reference Selected ****************** Brian J. Goldsmith, M.D. Moderator, IROJC