Practical Radiation Oncology (2011) 1, 208–211
www.practicalradonc.org
Teaching Case
Radiation recall associated with insulin growth factor 1R antibody Jennifer Y. Wo MD a,⁎, David P. Ryan MD b , Matthew H. Kulke MD c , Theodore S. Hong MD a a
Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts c Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts b
Received 4 November 2010; revised 14 December 2010; accepted 18 December 2010
Case report A 34-year-old white male presented to an outside hospital in March 2005 with sudden onset of persistent abdominal pain. Computed tomographic (CT) abdomen and pelvis demonstrated a 3-cm soft tissue mass contiguous with loops of small bowel. Exploratory laparotomy with simple excision revealed a 4-cm wellcircumscribed pancreatic endocrine tumor with negative surgical margins and no evidence of lymphovascular invasion. Postoperatively, he was managed expectantly with serial labs and scans. After 11 months, he developed increasing fatigue and progressive nausea and vomiting. Restaging CT scans showed the interval development of multiple small hepatic lesions, and a liver-directed biopsy confirmed metastatic pancreatic endocrine tumor. He clinically progressed on temozolomide-bevacizumab (May 2006 to June 2006), and was switched to streptomycin-doxorubicin with stable disease after 1 cycle. In an attempt to render the patient with no evidence of disease, right hepatectomy and a partial left hepatectomy was performed in August 2006 to remove more than 15 metastatic lesions with clean surgical margins.
Conflicts of interest: None. ⁎ Corresponding author. Massachusetts General Hospital, 100 Blossom St, Cox 3, Boston, MA 02114. E-mail address: [email protected] (J.Y. Wo).
He did well until September 2007 when he represented with multifocal recurrence in the primary tumor bed, peripancreatic lymph nodes, and liver. Since then, he has enrolled in numerous phase I-II studies and has been treated with multiple systemic therapy regimens including sunitinib, temsirolimus, AV-412 (an oral tyrosine kinase inhibitor), 5-fluorouracil-leukovorin, and everolimus-pasireotide. Additionally, he has received several courses of palliative radiotherapy, including to the right hip (30 Gy in 10 fractions in October 2009), left chest wall (30 Gy in 10 fractions in November 2009), L1-L3 spine (35 Gy in 15 fractions in June 2010), fluoroscopic simulation films taken at time of treatment planning depicted in Fig 1), and the right ischium (30 Gy in 10 fractions in June 2010). Most recently, in July 2010, he was enrolled into a phase II protocol evaluating the effectiveness of AMG 479, a fully humanized monoclonal antibody directed against human insulin growth factor receptor (IGF-1R), in the treatment of advanced neuroendocrine tumors. Per protocol, the patient received an intravenous bolus infusion of AMG 479 18 mg/kg on day 1 of a 3-week cycle. Fourteen days after cycle-1 administration of AMG 479, he developed a hyperpigmented, erythematous, nontender region on his lower back approximating the outline of his prior lumbar spine irradiation field, consistent with a radiation recall dermatitis (Fig 2). There was no evidence of radiation recall dermatitis within any other prior irradiation fields.
1879-8500/$ – see front matter © 2011 American Society for Radiation Oncology. Published by Elsevier Inc. All rights reserved. doi:10.1016/j.prro.2010.12.003
Practical Radiation Oncology: July-September 2011
Radiation recall with IGF 1R antibody
209
Discussion Preclinical data have suggested a potential role of the IGF-1R signaling pathway in the development of neoplasia.1 Although IGF-1R can be found frequently expressed in both normal tissues and the majority of human tumors, some IGF-1R positive tumor cells may exhibit heightened sensitivity to IGF-1R targeting, thus forming the basic rationale for targeting IGF-1R as a potential cancer therapeutic agent.2,3 AMG 479 is an investigational fully human monoclonal antibody, immunoglobulin type G1, developed to inhibit the interaction of IGF-1R with its natural ligands, IGF-1 and IGF-2, thereby preventing tumor growth and invasion. In preclinical models, AMG 479 has been found to inhibit in vitro and in vivo activation of the PI3 kinase-AKT pathway, leading to growth inhibition.4,5 Recent phase I clinical data found that AMG 479 can be administered safely at 20 mg/kg intravenously every 2 weeks with no maximal tolerated dose reached.6 Of 53 patients with advanced solid malignancies or non-Hodgkin's lymphoma, tumor responses included 1 durable complete response and 1 unconfirmed partial response in 2 patients with Ewing'sprimitive neuroectodermal tumors, and 1 partial response in a patient with neuroendocrine tumor.6 More recently, data from a small, randomized placebo-controlled phase II study among patients with metastatic pancreatic cancer, demonstrated an improvement in median overall survival from 5.9 months to 8.7 months with the addition of AMG 479 to gemcitabine compared to gemcitabine alone.7 Due to the success of these reported results, AMG 479 is now moving into phase III studies for metastatic pancreatic cancer. Reported adverse side effects associated with administration of AMG 479 include fatigue, thrombocytopenia, fever, chills, anorexia, hyperglycemia, elevated
Figure 1
Figure 2
hepatic enzymes, and an infusional rash manifested in the form of dermatitis acneiform, pruritus, maculopapular rash, or hyperhidrosis.6 To date, this is the first published report of radiation recall dermatitis associated with administration of an IGF receptor antibody. Radiation recall refers to an inflammatory reaction that develops within a previously irradiated field in response to administration of certain systemic agents. Initially reported in 1959 with actinomycin-D,8 a wide range of cytotoxic and non-cytotoxic agents have been subsequently reported as potential triggers of this reaction including taxanes,9 anthracyclines,10 alkylating agents,11 nucleoside analogs,12 anti-tuberculosis drugs and antibiotics,13 simvastatin,14 and tamoxifen.15 Radiation recall reactions typically manifest as dermatitis and can be associated with clinical manifestations of maculopapular eruptions, vesicle formation, ulceration, skin desquamation, and rarely, skin necrosis.16 Radiation recall dermatitis can be graded based on the National Cancer Institute Common Toxicity Criteria, version 2.0, with severity ranging from faint erythema or dry desquamation (grade 1) to skin necrosis or ulceration of full thickness dermis (grade 4). The frequency of radiation recall dermatitis has not been extensively studied; however, one recent retrospective study reported a frequency of 9% among 91 patients treated with palliative radiation followed by cytotoxic chemotherapy delivered within 6 months of radiation.17 Involvement of visceral organs and muscles are much less frequently reported; however, certain precipitating agents, particularly gemcitabine, have been recently implicated in triggering radiation recall myositis, optic neuritis, and lymphangitis.12,18 Other organs can also be involved as well, resulting in esophagitis, colitis, mucositis, pneumonitis, and vaginal necrosis.12,18-20 Although the exact underlying pathophysiologic etiology of radiation recall dermatitis is currently unknown, “stem-cell inadequacy” within the radiation field, 21 idiosyncratic hypersensitivity due to prior radiationinduced “trauma” manifesting as an inflammatory response,22 and increased vascular permeability have all
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been proposed as potential mechanisms.23 Defects in DNA repair and toxic drug effects have also been proposed as potential causative factors.22,24 No absolute dose threshold has been established; however, there has been some suggestion that the likelihood of developing radiation recall dermatitis may be dependent on the dose of prior irradiation and the dose of drug administered.9,25,26 Radiation dose dependence may help explain the development of radiation recall dermatitis within the L1-L3 field, treated to 35 Gy, and not within the R ischium field, treated to 30 Gy. As in this patient, radiation recall reactions typically develop in patients after the administration of the first dose of the offending pharmacologic agent. The time interval between completion of radiation therapy and development of radiation recall dermatitis can be extremely variable, ranging from 2 days8 to 25 years.27 Shorter time interval between radiation therapy and administration of the offending drug may predict for increased severity in radiation recall dermatitis.8 Patients with mild radiation recall dermatitis may be followed with close observation alone, as the reaction may regress spontaneously. However, patients with severe radiation recall dermatitis should be treated with corticosteroids and nonsteroidal anti-inflammatory agents and the offending agent should be withdrawn, often producing dramatic improvements. Attempts to re-challenge the patient with the administration of the offending agent often leads to recurrence of radiation recall dermatitis; however, successful re-challenging of the patient with dose reduction of the offending agent and pretreatment with corticosteroids have been reported.28 Physical examination finding for our patient was consistent with grade 1 radiation recall dermatitis with evidence of mild hyperpigmentation without evidence of skin desquamation. Due to the mildness of his reaction, the patient opted to continue administration of intravenous AMG 479 18 mg/kg without dose reduction or requirement of initiation of steroids or nonsteroidal antiinflammatory agents. He has now received 3 cycles of AMG 479 with persistence of his radiation recall reaction, with radiographic evidence of disease progression on his most recent follow-up scans.
Conclusion In summary, radiation recall has been reported in association with administration of numerous systemic agents; however, to date, this is the first reported case of radiation recall dermatitis associated with administration of an IGF-1R antibody. This case report suggests that biologically targeted agents may be associated with side effects classically attributed to chemotherapy. Patients with mild radiation recall dermatitis may be followed with close observation alone, as the reaction may regress spontaneously. However, patients with severe radiation
Practical Radiation Oncology: July-September 2011
recall dermatitis should be treated with corticosteroids and nonsteroidal anti-inflammatory agents and the offending agent should be withdrawn.
References 1. Pollak MN, Perdue JF, Margolese RG, Baer K, Richard M. Presence of somatomedin receptors on primary human breast and colon carcinomas. Cancer Lett. 1987;38:223-23. 2. Ellis MJ, Singer C, Hornby A, Rasmussen A, Cullen KJ. Insulin-like growth factor mediated stromal-epithelial interactions in human breast cancer. Breast Cancer Res Treat. 1994;31:249-26. 3. LeRoith D, Werner H, Neuenschwander S, Kalebic T, Helman LJ. The role of the insulin-like growth factor-I receptor in cancer. Ann N Y Acad Sci. 1995;766:402-40. 4. Beltran PJ, Mitchell P, Chung YA, et al. AMG 479, a fully human anti-insulin-like growth factor receptor type I monoclonal antibody, inhibits the growth and survival of pancreatic carcinoma cells. Mol Cancer Ther. 2009;8:10951105. 5. Moody G, Mitchell P, Cajulis E, et al. AMG 479, a fully human anti IGF-1 receptor monoclonal antibody, is efficacious against Ewing sarcoma and osteoarcoma xenografts. 19th International EORTCNCI-AACR Conference on Molecular Targets and Cancer Therapeutics; October 22-26; 2007. San Francisco, CA; Abstract A64. 6. Tolcher AW, Sarantopoulos J, Patnaik A, et al. Phase I, pharmacokinetic, and pharmacodynamic study of AMG 479, a fully human monoclonal antibody to insulin-like growth factor receptor 1. J Clin Oncol. 2009;27:5800-5807. 7. Kindler H, Richards DA, Stephenson J, et al. A placebo-controlled, randomized phase II study of conatumumab (C) or AMG 479 (A) or placebo (P) plus gemcitabine (G) in patients (pts) with metastatic pancreatic cancer (mPC) [Abstract]. J Clin Oncol. 2010;28(suppl 15):4035. 8. D'Angio GJ, Farber S, Maddock CL. Potentiation of x-ray effects by actinomycin D. Radiology. 1959;73:175-77. 9. Yeo W, Leung SF, Johnson PJ. Radiation-recall dermatitis with docetaxel: establishment of a requisite radiation threshold. Eur J Cancer. 1997;33:698-69. 10. Mayer EG, Poulter CA, Aristizabal SA. Complications of irradiation related to apparent drug potentiation by adriamycin. Int J Radiat Oncol Biol Phys. 1976;1:11791188. 11. Kellie SJ, Plowman PN, Malpas JS. Radiation recall and radiosensitization with alkylating agents. Lancet. 1987;1:11491150. 12. Jeter MD, Janne PA, Brooks S, et al. Gemcitabine-induced radiation recall. Int J Radiat Oncol Biol Phys. 2002;53:394-40. 13. Extermann M, Vogt N, Forni M, Dayer P. Radiation recall in a patient with breast cancer treated for tuberculosis. Eur J Clin Pharmacol. 1995;48:77-78. 14. Abadir R, Liebmann J. Radiation reaction recall following simvastatin therapy: a new observation. Clin Oncol (R Coll Radiol). 1995;7:325-32. 15. Parry BR. Radiation recall induced by tamoxifen. Lancet. 1992;340:49. 16. Spirig C, Omlin A, D'Addario G, et al. Radiation recall dermatitis with soft tissue necrosis following pemetrexed therapy: a case report. J Med Case Reports. 2009;3:93. 17. Kodym E, Kalinska R, Ehringfeld C, Sterbik-Lamina A, Kodym R, Hohenberg G. Frequency of radiation recall dermatitis in adult cancer patients. Onkologie. 2005;28:18-21. 18. Friedlander PA, Bansal R, Schwartz L, Wagman R, Posner J, Kemeny N. Gemcitabine-related radiation recall preferentially involves internal tissue and organs. Cancer. 2004;100:1793-79. 19. Schweitzer VG, Juillard GJ, Bajada CL, Parker RG. Radiation recall dermatitis and pneumonitis in a patient treated with paclitaxel. Cancer. 1995;76:1069-07.
Practical Radiation Oncology: July-September 2011 20. Greco FA, Brereton HD, Kent H, Zimbler H, Merrill J, Johnson RE. Adriamycin and enhanced radiation reaction in normal esophagus and skin. Ann Intern Med. 1976;85:294-29. 21. Hellman S, Botnick LE. Stem cell depletion: an explanation of the late effects of cytotoxins. Int J Radiat Oncol Biol Phys. 1977;2:181-84. 22. Camidge R, Price A. Radiation recall dermatitis may represent the Koebner phenomenon. J Clin Oncol. 2002;20:4130. 23. Camidge R, Price A. Characterizing the phenomenon of radiation recall dermatitis. Radiother Oncol. 2001;59:237-24. 24. Phillips TL, Fu KK. Quantification of combined radiation therapy and chemotherapy effects on critical normal tissues. Cancer. 1976; 37(suppl 2):1186-1200.
Radiation recall with IGF 1R antibody
211
25. Cassady JR, Richter MP, Piro AJ, Jaffe N. Radiation-adriamycin interactions: preliminary clinical observations. Cancer. 1975;36: 946-94. 26. Stelzer KJ, Griffin TW, Koh WJ. Radiation recall skin toxicity with bleomycin in a patient with Kaposi sarcoma related to acquired immune deficiency syndrome. Cancer. 1993;71:1322-32. 27. Barlési F, Tummino C, Tasei AM, Astoul P. Unsuccessful rechallenge with pemetrexed after a previous radiation recall dermatitis. Lung Cancer. 2006;54:423-42. 28. Castellano D, Hitt R, Cortés-Funes H, Romero A, Rodriguez-Peralto JL. Side effects of chemotherapy. Case 2. Radiation recall reaction induced by gemcitabine. J Clin Oncol. 2000;18:695-69.
www.practicalradonc.org
Teaching Case
Radiation recall associated with insulin growth factor 1R antibody Jennifer Y. Wo MD a,⁎, David P. Ryan MD b , Matthew H. Kulke MD c , Theodore S. Hong MD a a
Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts c Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts b
Received 4 November 2010; revised 14 December 2010; accepted 18 December 2010
Case report A 34-year-old white male presented to an outside hospital in March 2005 with sudden onset of persistent abdominal pain. Computed tomographic (CT) abdomen and pelvis demonstrated a 3-cm soft tissue mass contiguous with loops of small bowel. Exploratory laparotomy with simple excision revealed a 4-cm wellcircumscribed pancreatic endocrine tumor with negative surgical margins and no evidence of lymphovascular invasion. Postoperatively, he was managed expectantly with serial labs and scans. After 11 months, he developed increasing fatigue and progressive nausea and vomiting. Restaging CT scans showed the interval development of multiple small hepatic lesions, and a liver-directed biopsy confirmed metastatic pancreatic endocrine tumor. He clinically progressed on temozolomide-bevacizumab (May 2006 to June 2006), and was switched to streptomycin-doxorubicin with stable disease after 1 cycle. In an attempt to render the patient with no evidence of disease, right hepatectomy and a partial left hepatectomy was performed in August 2006 to remove more than 15 metastatic lesions with clean surgical margins.
Conflicts of interest: None. ⁎ Corresponding author. Massachusetts General Hospital, 100 Blossom St, Cox 3, Boston, MA 02114. E-mail address: [email protected] (J.Y. Wo).
He did well until September 2007 when he represented with multifocal recurrence in the primary tumor bed, peripancreatic lymph nodes, and liver. Since then, he has enrolled in numerous phase I-II studies and has been treated with multiple systemic therapy regimens including sunitinib, temsirolimus, AV-412 (an oral tyrosine kinase inhibitor), 5-fluorouracil-leukovorin, and everolimus-pasireotide. Additionally, he has received several courses of palliative radiotherapy, including to the right hip (30 Gy in 10 fractions in October 2009), left chest wall (30 Gy in 10 fractions in November 2009), L1-L3 spine (35 Gy in 15 fractions in June 2010), fluoroscopic simulation films taken at time of treatment planning depicted in Fig 1), and the right ischium (30 Gy in 10 fractions in June 2010). Most recently, in July 2010, he was enrolled into a phase II protocol evaluating the effectiveness of AMG 479, a fully humanized monoclonal antibody directed against human insulin growth factor receptor (IGF-1R), in the treatment of advanced neuroendocrine tumors. Per protocol, the patient received an intravenous bolus infusion of AMG 479 18 mg/kg on day 1 of a 3-week cycle. Fourteen days after cycle-1 administration of AMG 479, he developed a hyperpigmented, erythematous, nontender region on his lower back approximating the outline of his prior lumbar spine irradiation field, consistent with a radiation recall dermatitis (Fig 2). There was no evidence of radiation recall dermatitis within any other prior irradiation fields.
1879-8500/$ – see front matter © 2011 American Society for Radiation Oncology. Published by Elsevier Inc. All rights reserved. doi:10.1016/j.prro.2010.12.003
Practical Radiation Oncology: July-September 2011
Radiation recall with IGF 1R antibody
209
Discussion Preclinical data have suggested a potential role of the IGF-1R signaling pathway in the development of neoplasia.1 Although IGF-1R can be found frequently expressed in both normal tissues and the majority of human tumors, some IGF-1R positive tumor cells may exhibit heightened sensitivity to IGF-1R targeting, thus forming the basic rationale for targeting IGF-1R as a potential cancer therapeutic agent.2,3 AMG 479 is an investigational fully human monoclonal antibody, immunoglobulin type G1, developed to inhibit the interaction of IGF-1R with its natural ligands, IGF-1 and IGF-2, thereby preventing tumor growth and invasion. In preclinical models, AMG 479 has been found to inhibit in vitro and in vivo activation of the PI3 kinase-AKT pathway, leading to growth inhibition.4,5 Recent phase I clinical data found that AMG 479 can be administered safely at 20 mg/kg intravenously every 2 weeks with no maximal tolerated dose reached.6 Of 53 patients with advanced solid malignancies or non-Hodgkin's lymphoma, tumor responses included 1 durable complete response and 1 unconfirmed partial response in 2 patients with Ewing'sprimitive neuroectodermal tumors, and 1 partial response in a patient with neuroendocrine tumor.6 More recently, data from a small, randomized placebo-controlled phase II study among patients with metastatic pancreatic cancer, demonstrated an improvement in median overall survival from 5.9 months to 8.7 months with the addition of AMG 479 to gemcitabine compared to gemcitabine alone.7 Due to the success of these reported results, AMG 479 is now moving into phase III studies for metastatic pancreatic cancer. Reported adverse side effects associated with administration of AMG 479 include fatigue, thrombocytopenia, fever, chills, anorexia, hyperglycemia, elevated
Figure 1
Figure 2
hepatic enzymes, and an infusional rash manifested in the form of dermatitis acneiform, pruritus, maculopapular rash, or hyperhidrosis.6 To date, this is the first published report of radiation recall dermatitis associated with administration of an IGF receptor antibody. Radiation recall refers to an inflammatory reaction that develops within a previously irradiated field in response to administration of certain systemic agents. Initially reported in 1959 with actinomycin-D,8 a wide range of cytotoxic and non-cytotoxic agents have been subsequently reported as potential triggers of this reaction including taxanes,9 anthracyclines,10 alkylating agents,11 nucleoside analogs,12 anti-tuberculosis drugs and antibiotics,13 simvastatin,14 and tamoxifen.15 Radiation recall reactions typically manifest as dermatitis and can be associated with clinical manifestations of maculopapular eruptions, vesicle formation, ulceration, skin desquamation, and rarely, skin necrosis.16 Radiation recall dermatitis can be graded based on the National Cancer Institute Common Toxicity Criteria, version 2.0, with severity ranging from faint erythema or dry desquamation (grade 1) to skin necrosis or ulceration of full thickness dermis (grade 4). The frequency of radiation recall dermatitis has not been extensively studied; however, one recent retrospective study reported a frequency of 9% among 91 patients treated with palliative radiation followed by cytotoxic chemotherapy delivered within 6 months of radiation.17 Involvement of visceral organs and muscles are much less frequently reported; however, certain precipitating agents, particularly gemcitabine, have been recently implicated in triggering radiation recall myositis, optic neuritis, and lymphangitis.12,18 Other organs can also be involved as well, resulting in esophagitis, colitis, mucositis, pneumonitis, and vaginal necrosis.12,18-20 Although the exact underlying pathophysiologic etiology of radiation recall dermatitis is currently unknown, “stem-cell inadequacy” within the radiation field, 21 idiosyncratic hypersensitivity due to prior radiationinduced “trauma” manifesting as an inflammatory response,22 and increased vascular permeability have all
210
J.Y. Wo et al
been proposed as potential mechanisms.23 Defects in DNA repair and toxic drug effects have also been proposed as potential causative factors.22,24 No absolute dose threshold has been established; however, there has been some suggestion that the likelihood of developing radiation recall dermatitis may be dependent on the dose of prior irradiation and the dose of drug administered.9,25,26 Radiation dose dependence may help explain the development of radiation recall dermatitis within the L1-L3 field, treated to 35 Gy, and not within the R ischium field, treated to 30 Gy. As in this patient, radiation recall reactions typically develop in patients after the administration of the first dose of the offending pharmacologic agent. The time interval between completion of radiation therapy and development of radiation recall dermatitis can be extremely variable, ranging from 2 days8 to 25 years.27 Shorter time interval between radiation therapy and administration of the offending drug may predict for increased severity in radiation recall dermatitis.8 Patients with mild radiation recall dermatitis may be followed with close observation alone, as the reaction may regress spontaneously. However, patients with severe radiation recall dermatitis should be treated with corticosteroids and nonsteroidal anti-inflammatory agents and the offending agent should be withdrawn, often producing dramatic improvements. Attempts to re-challenge the patient with the administration of the offending agent often leads to recurrence of radiation recall dermatitis; however, successful re-challenging of the patient with dose reduction of the offending agent and pretreatment with corticosteroids have been reported.28 Physical examination finding for our patient was consistent with grade 1 radiation recall dermatitis with evidence of mild hyperpigmentation without evidence of skin desquamation. Due to the mildness of his reaction, the patient opted to continue administration of intravenous AMG 479 18 mg/kg without dose reduction or requirement of initiation of steroids or nonsteroidal antiinflammatory agents. He has now received 3 cycles of AMG 479 with persistence of his radiation recall reaction, with radiographic evidence of disease progression on his most recent follow-up scans.
Conclusion In summary, radiation recall has been reported in association with administration of numerous systemic agents; however, to date, this is the first reported case of radiation recall dermatitis associated with administration of an IGF-1R antibody. This case report suggests that biologically targeted agents may be associated with side effects classically attributed to chemotherapy. Patients with mild radiation recall dermatitis may be followed with close observation alone, as the reaction may regress spontaneously. However, patients with severe radiation
Practical Radiation Oncology: July-September 2011
recall dermatitis should be treated with corticosteroids and nonsteroidal anti-inflammatory agents and the offending agent should be withdrawn.
References 1. Pollak MN, Perdue JF, Margolese RG, Baer K, Richard M. Presence of somatomedin receptors on primary human breast and colon carcinomas. Cancer Lett. 1987;38:223-23. 2. Ellis MJ, Singer C, Hornby A, Rasmussen A, Cullen KJ. Insulin-like growth factor mediated stromal-epithelial interactions in human breast cancer. Breast Cancer Res Treat. 1994;31:249-26. 3. LeRoith D, Werner H, Neuenschwander S, Kalebic T, Helman LJ. The role of the insulin-like growth factor-I receptor in cancer. Ann N Y Acad Sci. 1995;766:402-40. 4. Beltran PJ, Mitchell P, Chung YA, et al. AMG 479, a fully human anti-insulin-like growth factor receptor type I monoclonal antibody, inhibits the growth and survival of pancreatic carcinoma cells. Mol Cancer Ther. 2009;8:10951105. 5. Moody G, Mitchell P, Cajulis E, et al. AMG 479, a fully human anti IGF-1 receptor monoclonal antibody, is efficacious against Ewing sarcoma and osteoarcoma xenografts. 19th International EORTCNCI-AACR Conference on Molecular Targets and Cancer Therapeutics; October 22-26; 2007. San Francisco, CA; Abstract A64. 6. Tolcher AW, Sarantopoulos J, Patnaik A, et al. Phase I, pharmacokinetic, and pharmacodynamic study of AMG 479, a fully human monoclonal antibody to insulin-like growth factor receptor 1. J Clin Oncol. 2009;27:5800-5807. 7. Kindler H, Richards DA, Stephenson J, et al. A placebo-controlled, randomized phase II study of conatumumab (C) or AMG 479 (A) or placebo (P) plus gemcitabine (G) in patients (pts) with metastatic pancreatic cancer (mPC) [Abstract]. J Clin Oncol. 2010;28(suppl 15):4035. 8. D'Angio GJ, Farber S, Maddock CL. Potentiation of x-ray effects by actinomycin D. Radiology. 1959;73:175-77. 9. Yeo W, Leung SF, Johnson PJ. Radiation-recall dermatitis with docetaxel: establishment of a requisite radiation threshold. Eur J Cancer. 1997;33:698-69. 10. Mayer EG, Poulter CA, Aristizabal SA. Complications of irradiation related to apparent drug potentiation by adriamycin. Int J Radiat Oncol Biol Phys. 1976;1:11791188. 11. Kellie SJ, Plowman PN, Malpas JS. Radiation recall and radiosensitization with alkylating agents. Lancet. 1987;1:11491150. 12. Jeter MD, Janne PA, Brooks S, et al. Gemcitabine-induced radiation recall. Int J Radiat Oncol Biol Phys. 2002;53:394-40. 13. Extermann M, Vogt N, Forni M, Dayer P. Radiation recall in a patient with breast cancer treated for tuberculosis. Eur J Clin Pharmacol. 1995;48:77-78. 14. Abadir R, Liebmann J. Radiation reaction recall following simvastatin therapy: a new observation. Clin Oncol (R Coll Radiol). 1995;7:325-32. 15. Parry BR. Radiation recall induced by tamoxifen. Lancet. 1992;340:49. 16. Spirig C, Omlin A, D'Addario G, et al. Radiation recall dermatitis with soft tissue necrosis following pemetrexed therapy: a case report. J Med Case Reports. 2009;3:93. 17. Kodym E, Kalinska R, Ehringfeld C, Sterbik-Lamina A, Kodym R, Hohenberg G. Frequency of radiation recall dermatitis in adult cancer patients. Onkologie. 2005;28:18-21. 18. Friedlander PA, Bansal R, Schwartz L, Wagman R, Posner J, Kemeny N. Gemcitabine-related radiation recall preferentially involves internal tissue and organs. Cancer. 2004;100:1793-79. 19. Schweitzer VG, Juillard GJ, Bajada CL, Parker RG. Radiation recall dermatitis and pneumonitis in a patient treated with paclitaxel. Cancer. 1995;76:1069-07.
Practical Radiation Oncology: July-September 2011 20. Greco FA, Brereton HD, Kent H, Zimbler H, Merrill J, Johnson RE. Adriamycin and enhanced radiation reaction in normal esophagus and skin. Ann Intern Med. 1976;85:294-29. 21. Hellman S, Botnick LE. Stem cell depletion: an explanation of the late effects of cytotoxins. Int J Radiat Oncol Biol Phys. 1977;2:181-84. 22. Camidge R, Price A. Radiation recall dermatitis may represent the Koebner phenomenon. J Clin Oncol. 2002;20:4130. 23. Camidge R, Price A. Characterizing the phenomenon of radiation recall dermatitis. Radiother Oncol. 2001;59:237-24. 24. Phillips TL, Fu KK. Quantification of combined radiation therapy and chemotherapy effects on critical normal tissues. Cancer. 1976; 37(suppl 2):1186-1200.
Radiation recall with IGF 1R antibody
211
25. Cassady JR, Richter MP, Piro AJ, Jaffe N. Radiation-adriamycin interactions: preliminary clinical observations. Cancer. 1975;36: 946-94. 26. Stelzer KJ, Griffin TW, Koh WJ. Radiation recall skin toxicity with bleomycin in a patient with Kaposi sarcoma related to acquired immune deficiency syndrome. Cancer. 1993;71:1322-32. 27. Barlési F, Tummino C, Tasei AM, Astoul P. Unsuccessful rechallenge with pemetrexed after a previous radiation recall dermatitis. Lung Cancer. 2006;54:423-42. 28. Castellano D, Hitt R, Cortés-Funes H, Romero A, Rodriguez-Peralto JL. Side effects of chemotherapy. Case 2. Radiation recall reaction induced by gemcitabine. J Clin Oncol. 2000;18:695-69.
