Letters to Editor
Chronic myeloid leukemia in acute lymphoblastic leukemia survivor: A case report
Sir, Secondary chronic myeloid leukemia (CML) is a rare phenomenon. The only risk factor described for CML is radiation.[1] There have been case reports in literature where survivors of various malignancies develop CML after a latent period.[2,3] The significance of this observation is largely unknown though many patients are exposed to radiation therapy as part of treatment programmes. Mr. G was 24-year-old in 1984 when he was diagnosed to have acute lymphoblastic leukemia (ALL), FAB L1 subtype. The immunophenotype and cytogenetic details were not available those days. He received multiagent chemotherapy which included vincristine, daunorubicin, L‑Asparaginase, cytarabine, cyclophosphamide, multiple doses of intrathecal methotrexate and 10 months of oral maintenance with methotrexate and 6 mercaptopurine. Patient was given 24 Gy of cranial radiation also. He was kept under regular follow up. Seventeen years later, he presented to us with bone pains. Clinically, he did not have anemia or peripheral lymphadenopathy. Spleen could not be appreciated. His investigations were as follows: Hb – 10.9 g/dl, Total count – 64600/ mm 3, Platelet count – 2.04 lakhs/m 3. Peripheral smear showed immature myeloid cells and hence a bone marrow aspiration was done which was suggestive of myeloid hyperplasia [Figure 1]. BCR – ABL qualitative test was positive. After making a diagnosis of CML, he has been initiated on Imatinib and is doing well. The cytogenetic response assessment is not yet made. Secondary CML in ALL survivors is very rare with only two cases reported so far on literature review. In a cohort of 2169 ALL survivors in St Judes hospital, only two patients had CML.[4] The reasons for secondary CML in ALL survivors are purely hypothetical. It may be that more and more pediatric and adolescent ALL patients are getting cured and surviving to face second cancers like CML which typically occurs at a later age. For our patient, definitely the cranial irradiation might have contributed for the second event. Drugs like alkylating agents and topoisomerase inhibitors are held responsible for therapy related acute myeloid leukemia (t‑AML), but not for CML. A Children’s Cancer Group analysis demonstrated that the cumulative incidence of developing a second neoplasm was 1.19% at 10 years for ALL survivors.[5] However, higher incidence upto 10.5% has been noticed with 30 year follow up study by Hijiya et al.[4] With cure rates of ALL
Recurrent sinonasal teratocarcinosarcoma with intracranial extension: Case report
Sir, Sinonasal teratocarcinosarcoma (SNTCS) is a rare and aggressive malignant tumor. As the name implies, it 398
Figure 1: Bonemarrow picture demonstrating myeloid cell hyperplasia
nearing 90%, we should be more stringent on long term follow up. Cyriac S, Philip A, Ganesan P, Kannan K, Sagar TG Department of Medical Oncology, Cancer Institute (WIA), Chennai, India
Correspondence to:
Dr. Sanju Cyriac, E‑mail: [email protected]
References 1. Druker BJ, Lee SJ. Chronic leukemias. Section1: Chronic Myelogenous Leukemia. In: DeVita, Vincent T. Lawrence, Theodore S, Rosenberg, Steven A, editors. Devita, Hellman and Rosenberg’s Cancer: Principles and Practice of Oncology, 8th ed. New York: Lippincott Williams and Wilkins; 2008. p. 2268. 2. Ramanarayanan J, Dunford LM, Baer MR, Sait SN, Lawrence W, McCarthy PL. Chronic myeloid leukemia after treatment of lymphoid malignancies: Response to imatinib mesylate and favorable outcomes in three patients. Leuk Res 2006;30:701‑5. 3. Waldman D, Weintraub M, Freeman A, Neumann Y, Rechavi G, Toren A. Favorable early response of secondary chronic myeloid leukemia to imatinib. Am J Hematol 2004;75:217‑9. 4. Hijiya N, Hudson MM, Lensing S, Zacher M, Onciu M, Behm FG, et al. Cumulative Incidence of Secondary Neoplasms as a First Event After Childhood Acute Lymphoblastic Leukemia. JAMA 2007;297:1207‑15. 5. Bhatia S, Sather HN, Pabustan OB, Trigg ME, Gaynon PS, Robison LL. Low incidence of second neoplasms among children diagnosed with acute lymphoblastic leukemia after 1983. Blood 2002;99:4257‑64. Access this article online Quick Response Code:
Website: www.indianjcancer.com DOI: 10.4103/0019-509X.146783 PMID: *****
arises from the sinonasal tract and is characterized by the presence of benign and malignant epithelial, mesenchymal and neural components. Common sites of involvement of SNTCS are nasal cavities and paranasal sinuses. The tumor is often misdiagnosed due to rarity, the complex phenotypic composition and inadequate biopsy specimen. Indian Journal of Cancer | July–September 2014 | Volume 51 | Issue 3
Letters to Editor
treatment with surgical resection or radiation therapy with 45‑70 Gy with or without concurrent chemotherapy or a combination of both. [3] Chemotherapy is rarely effective in this condition, but adjuvant multi‑drug chemotherapy with cisplatin, etoposide and ifosfamide had shown good results. [4] Despite aggressive efforts, the prognosis is still poor. The local recurrence after excision is high with reported 3 and 5 year survival rates at about 30% and 20%, respectively.[5] In an analysis by Sobani et al., recurrence was found in 42.68% of the cases with a mean recurrence time of 21.3 months in patients followed‑up for a mean period of 76.1 months.[6] Figure 1: Before chemotherapy
a
b
c
d
Figure 2(a): Low magnification reveals nests of primitive neuroectodermal tumor cells (H and E, original magnification ×200). (b) Tumor cells showing extensive skeletal muscle differentiation evident as eosinophilic strap cells (H and E, original magnification ×200). (c) The primitive neuro-ectodermal component shows immunoreactivity for synaptophysin (indirect peroxidase, original magnification ×400). (d) The skeletal muscle differentiation is highlighted by immunoreactivity to desmin (indirect peroxidase, original magnification ×200)
A 44‑year‑old male patient presented with the complaints of epistaxis, nasal blockage for month duration. He underwent left craniotomy excision of the mass at local place 10‑month back. The histopathology report was suggestive of a SNTCS. He also received adjuvant radiotherapy 60 Gy/5 weeks at local place. After a disease free interval of 5 months, he presented to our hospital with recurrence of nasal blockage and epistaxis and mass protruding from the left nostril for a month. On examination, there was a soft‑tissue mass protruding out of the left nasal cavity [Figure 1]. Histopathology report was confirmed at our hospital and was compatible with SNTCS [Figure 2]. Whole body positron emission tomography‑computed tomography scan was done, which showed an enhancing soft‑tissue mass involving the nasal cavity, the ethmoid sinus, destroying the cribriform plate of ethmoid, posteriorly extending into the nasopharynx. The mass superiorly involved the frontal sinus, destroying the posterior wall, to enter into the frontal lobe. In view of extensive disease, which was declared unresectable by our surgical team, the patient was started on 3 weekly chemotherapy with ifosfamide and doxorubicin with a palliative intent. After two cycles of chemotherapy, there was a significant symptomatic benefit. The mass had shrunk; epistaxis and nasal blockage had resolved [Figure 3]. However, his disease was still unresectable. This highlights that this tumor may be chemoresponsive and chemotherapy can be integrated in the management of these patients in either neoadjuvant, adjuvant or palliative setting. A multi‑modality treatment approach is required in these patients with aggressive therapy and close follow‑up. Joshi A, Dhumal SB, Manickam DR, Noronha V, Bal M1, Patil VM, Prabhash K Department of Medical Oncology, and 1Pathology, Tata Memorial Hospital, Mumbai, Maharashtra, India Correspondence to: Dr. Kumar Prabhash, [email protected]
Figure 3: After chemotherapy
References
First described by Shanmugaratnam et al. [1] in 1983 as teratoid carcinosarcoma the term “Teratocarcinosarcoma” was given by Heffner and Hyams in 1984. [2] The cornerstones for the management of SNTCS include local
1. Shanmugaratnam K, Kunaratnam N, Chia KB, Chiang GS, Sinniah R. Teratoid carcinosarcoma of the paranasal sinuses. Pathology 1983;15:413‑9. 2. Heffner DK, Hyams VJ. Teratocarcinosarcoma (malignant teratoma?) of the nasal cavity and paranasal sinuses A clinicopathologic study of 20 cases. Cancer 1984;53:2140‑54.
Indian Journal of Cancer | July–September 2014 | Volume 51 | Issue 3
399
Letters to Editor 3. Fukuoka K, Hirokawa M, Shimizu M, Shirabe T, Manabe T, Hirai M, et al. Teratocarcinosarcoma of the nasal cavity. Report of a case showing favorable prognosis. APMIS 2000;108:553‑7. 4. Nitsche M, Hermann RM, Christiansen H, Berger J, Pradier O. Rationale for individualized therapy in Sinonasal Teratocarcinosarcoma (SNTC): Case report. Onkologie 2005;28:653‑6. 5. Sharma HS, Abdullah JM, Othman NH, Muhamad M. Teratocarcinosarcoma of the nasal cavity and ethmoid. J Laryngol Otol 1998;112:682‑6. 6. S o b a n i Z A , A k h t a r S , J u n a i d M , S a l a h u d d i n I . S i n o n a s a l teratocarcinosarcoma. J Pak Med Assoc 2012;62:633‑5.
Access this article online Quick Response Code:
Website: www.indianjcancer.com DOI: 10.4103/0019-509X.146785 PMID: *********
Response to oral metronomic chemotherapy in carcinoma of the Buccal Mucosa: A case report
Sir, Metronomic chemotherapy is the continuous use of fractionated doses, far below the maximum tolerated dose, of chemotherapeutic agents acting on different targets in the tumor micro‑environment. [1] In palliative and resource constraint settings, we have used oral metronomic chemotherapy with methotrexate and celecoxib in metastatic, inoperable recurrent and locally advanced head and neck cancers with promising results.[2,3] However, rarely do we get a rapid and complete clinical response. Here, we present such a case. A 66‑year‑old male, chronic tobacco chewer and known case of hypertension (HTN), coronary artery disease (CAD) with atrial fibrillation (AF) and history of cerebrovascular accident presented to our hospital in December 2013, with complaints of nonhealing ulcerative lesion over right lower lip extending to buccal mucosa since 8 months. He was symptomatic for pain in the lesion with mild dysphagia and discharge from the wound. Clinically there was a 5 cm × 4 cm ulcero‑proliferative growth in right buccal mucosa involving lower lip, angle of mouth, adjoining part of the skin and upper lip. Computed tomography scan showed a plaque‑like lesion measuring 20 mm in maximum thickness involving right buccal mucosa‑buccinator complex, extending from the maxillary alveolus inferiorly up to the mandibular attachment. The retromolartrigone region and the gingival mucosa were involved with the infiltration of the skin. A right level IB lymph node was seen. Biopsy confirmed a well‑differentiated squamous cell carcinoma. Patient was staged as T4a N1 M0 – TNM stage IV (A) in view of skin involvement. Patient was planned for surgery, but he developed AF during anesthesia induction. In view of persistent AF, HTN, CAD and American Society of Anesthesiology III risk for anesthesia, patient was deemed unfit for surgery. Radiotherapy could not be given in view of skin ulceration and extensive disease. Hence, he was referred for palliative chemotherapy. Patient presented to medical oncology outpatient department in April 2014 with progressive disease. His performance status as per Eastern Cooperative Oncology Group scale was 2. Echocardiography done in January 2014 showed concentric left ventricular hypertrophy, no regional wall motion abnormalities and 60% ejection fraction. Electrocardiogram showed AF with 400
a
b
Figure 1: (a) Before chemotherapy (b) after chemotherapy
controlled ventricular rate. Patient was on metoprolol, olmesartan, hydrochlorthiazide, rosuvastatin, aspirin and warfarin. In view of multiple comorbidities, old age, reluctance for regular follow‑up and risks of intravenous chemotherapy, patient was given oral methotrexate 15 mg/ m 2 weekly and 200 mg celecoxib twice a day with palliative intent. The risk of cardiotoxicity with celecoxib was explained. He was called for a reassessment after 1‑month. After 1‑month, clinically the lesion over right buccal mucosa involving the angle of mouth and lips had completely resolved [Figure1 a and b]. The earlier symptoms of pain, discharge and dysphagia had completely resolved. Radiologically there was a partial response. The present case highlights the fact that oral metronomic chemotherapy with methotrexate and celecoxib is an effective alternative to primary systemic chemotherapy with dramatic response in some cases of head and neck cancer. Prospective randomized trials are needed to validate the encouraging response rates and minimal side effects of this schedule. In developing countries like India, this treatment strategy can be effective where most patients cannot afford costly drugs.[4] Joshi A, Agarwala V, Noronha V, Dhumal S, Juvekar S1, Prabhash K Department of Medical Oncology and Radiodiagnosis1, Tata Memorial Hospital, Parel, Mumbai, Maharashtra, India
Correspondence to:
Dr.Kumar Prabhash, E‑mail: [email protected]
References 1. Pasquier E, Kavallaris M, André N. Metronomic chemotherapy: New rationale for new directions. Nat Rev Clin Oncol 2010;7:455‑65. 2. Pai PS, Vaidya AD, Prabhash K, Banavali SD. Oral metronomic scheduling of anticancer therapy‑based treatment compared to existing standard of care in locally advanced oral squamous cell cancers: A matched‑pair analysis. Indian J Cancer 2013;50:135‑41. 3. Patil V, Noronha V, Krishna V, Joshi A, Prabhash K. Oral metronomic Indian Journal of Cancer | July–September 2014 | Volume 51 | Issue 3
Copyright of Indian Journal of Cancer is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
Chronic myeloid leukemia in acute lymphoblastic leukemia survivor: A case report
Sir, Secondary chronic myeloid leukemia (CML) is a rare phenomenon. The only risk factor described for CML is radiation.[1] There have been case reports in literature where survivors of various malignancies develop CML after a latent period.[2,3] The significance of this observation is largely unknown though many patients are exposed to radiation therapy as part of treatment programmes. Mr. G was 24-year-old in 1984 when he was diagnosed to have acute lymphoblastic leukemia (ALL), FAB L1 subtype. The immunophenotype and cytogenetic details were not available those days. He received multiagent chemotherapy which included vincristine, daunorubicin, L‑Asparaginase, cytarabine, cyclophosphamide, multiple doses of intrathecal methotrexate and 10 months of oral maintenance with methotrexate and 6 mercaptopurine. Patient was given 24 Gy of cranial radiation also. He was kept under regular follow up. Seventeen years later, he presented to us with bone pains. Clinically, he did not have anemia or peripheral lymphadenopathy. Spleen could not be appreciated. His investigations were as follows: Hb – 10.9 g/dl, Total count – 64600/ mm 3, Platelet count – 2.04 lakhs/m 3. Peripheral smear showed immature myeloid cells and hence a bone marrow aspiration was done which was suggestive of myeloid hyperplasia [Figure 1]. BCR – ABL qualitative test was positive. After making a diagnosis of CML, he has been initiated on Imatinib and is doing well. The cytogenetic response assessment is not yet made. Secondary CML in ALL survivors is very rare with only two cases reported so far on literature review. In a cohort of 2169 ALL survivors in St Judes hospital, only two patients had CML.[4] The reasons for secondary CML in ALL survivors are purely hypothetical. It may be that more and more pediatric and adolescent ALL patients are getting cured and surviving to face second cancers like CML which typically occurs at a later age. For our patient, definitely the cranial irradiation might have contributed for the second event. Drugs like alkylating agents and topoisomerase inhibitors are held responsible for therapy related acute myeloid leukemia (t‑AML), but not for CML. A Children’s Cancer Group analysis demonstrated that the cumulative incidence of developing a second neoplasm was 1.19% at 10 years for ALL survivors.[5] However, higher incidence upto 10.5% has been noticed with 30 year follow up study by Hijiya et al.[4] With cure rates of ALL
Recurrent sinonasal teratocarcinosarcoma with intracranial extension: Case report
Sir, Sinonasal teratocarcinosarcoma (SNTCS) is a rare and aggressive malignant tumor. As the name implies, it 398
Figure 1: Bonemarrow picture demonstrating myeloid cell hyperplasia
nearing 90%, we should be more stringent on long term follow up. Cyriac S, Philip A, Ganesan P, Kannan K, Sagar TG Department of Medical Oncology, Cancer Institute (WIA), Chennai, India
Correspondence to:
Dr. Sanju Cyriac, E‑mail: [email protected]
References 1. Druker BJ, Lee SJ. Chronic leukemias. Section1: Chronic Myelogenous Leukemia. In: DeVita, Vincent T. Lawrence, Theodore S, Rosenberg, Steven A, editors. Devita, Hellman and Rosenberg’s Cancer: Principles and Practice of Oncology, 8th ed. New York: Lippincott Williams and Wilkins; 2008. p. 2268. 2. Ramanarayanan J, Dunford LM, Baer MR, Sait SN, Lawrence W, McCarthy PL. Chronic myeloid leukemia after treatment of lymphoid malignancies: Response to imatinib mesylate and favorable outcomes in three patients. Leuk Res 2006;30:701‑5. 3. Waldman D, Weintraub M, Freeman A, Neumann Y, Rechavi G, Toren A. Favorable early response of secondary chronic myeloid leukemia to imatinib. Am J Hematol 2004;75:217‑9. 4. Hijiya N, Hudson MM, Lensing S, Zacher M, Onciu M, Behm FG, et al. Cumulative Incidence of Secondary Neoplasms as a First Event After Childhood Acute Lymphoblastic Leukemia. JAMA 2007;297:1207‑15. 5. Bhatia S, Sather HN, Pabustan OB, Trigg ME, Gaynon PS, Robison LL. Low incidence of second neoplasms among children diagnosed with acute lymphoblastic leukemia after 1983. Blood 2002;99:4257‑64. Access this article online Quick Response Code:
Website: www.indianjcancer.com DOI: 10.4103/0019-509X.146783 PMID: *****
arises from the sinonasal tract and is characterized by the presence of benign and malignant epithelial, mesenchymal and neural components. Common sites of involvement of SNTCS are nasal cavities and paranasal sinuses. The tumor is often misdiagnosed due to rarity, the complex phenotypic composition and inadequate biopsy specimen. Indian Journal of Cancer | July–September 2014 | Volume 51 | Issue 3
Letters to Editor
treatment with surgical resection or radiation therapy with 45‑70 Gy with or without concurrent chemotherapy or a combination of both. [3] Chemotherapy is rarely effective in this condition, but adjuvant multi‑drug chemotherapy with cisplatin, etoposide and ifosfamide had shown good results. [4] Despite aggressive efforts, the prognosis is still poor. The local recurrence after excision is high with reported 3 and 5 year survival rates at about 30% and 20%, respectively.[5] In an analysis by Sobani et al., recurrence was found in 42.68% of the cases with a mean recurrence time of 21.3 months in patients followed‑up for a mean period of 76.1 months.[6] Figure 1: Before chemotherapy
a
b
c
d
Figure 2(a): Low magnification reveals nests of primitive neuroectodermal tumor cells (H and E, original magnification ×200). (b) Tumor cells showing extensive skeletal muscle differentiation evident as eosinophilic strap cells (H and E, original magnification ×200). (c) The primitive neuro-ectodermal component shows immunoreactivity for synaptophysin (indirect peroxidase, original magnification ×400). (d) The skeletal muscle differentiation is highlighted by immunoreactivity to desmin (indirect peroxidase, original magnification ×200)
A 44‑year‑old male patient presented with the complaints of epistaxis, nasal blockage for month duration. He underwent left craniotomy excision of the mass at local place 10‑month back. The histopathology report was suggestive of a SNTCS. He also received adjuvant radiotherapy 60 Gy/5 weeks at local place. After a disease free interval of 5 months, he presented to our hospital with recurrence of nasal blockage and epistaxis and mass protruding from the left nostril for a month. On examination, there was a soft‑tissue mass protruding out of the left nasal cavity [Figure 1]. Histopathology report was confirmed at our hospital and was compatible with SNTCS [Figure 2]. Whole body positron emission tomography‑computed tomography scan was done, which showed an enhancing soft‑tissue mass involving the nasal cavity, the ethmoid sinus, destroying the cribriform plate of ethmoid, posteriorly extending into the nasopharynx. The mass superiorly involved the frontal sinus, destroying the posterior wall, to enter into the frontal lobe. In view of extensive disease, which was declared unresectable by our surgical team, the patient was started on 3 weekly chemotherapy with ifosfamide and doxorubicin with a palliative intent. After two cycles of chemotherapy, there was a significant symptomatic benefit. The mass had shrunk; epistaxis and nasal blockage had resolved [Figure 3]. However, his disease was still unresectable. This highlights that this tumor may be chemoresponsive and chemotherapy can be integrated in the management of these patients in either neoadjuvant, adjuvant or palliative setting. A multi‑modality treatment approach is required in these patients with aggressive therapy and close follow‑up. Joshi A, Dhumal SB, Manickam DR, Noronha V, Bal M1, Patil VM, Prabhash K Department of Medical Oncology, and 1Pathology, Tata Memorial Hospital, Mumbai, Maharashtra, India Correspondence to: Dr. Kumar Prabhash, [email protected]
Figure 3: After chemotherapy
References
First described by Shanmugaratnam et al. [1] in 1983 as teratoid carcinosarcoma the term “Teratocarcinosarcoma” was given by Heffner and Hyams in 1984. [2] The cornerstones for the management of SNTCS include local
1. Shanmugaratnam K, Kunaratnam N, Chia KB, Chiang GS, Sinniah R. Teratoid carcinosarcoma of the paranasal sinuses. Pathology 1983;15:413‑9. 2. Heffner DK, Hyams VJ. Teratocarcinosarcoma (malignant teratoma?) of the nasal cavity and paranasal sinuses A clinicopathologic study of 20 cases. Cancer 1984;53:2140‑54.
Indian Journal of Cancer | July–September 2014 | Volume 51 | Issue 3
399
Letters to Editor 3. Fukuoka K, Hirokawa M, Shimizu M, Shirabe T, Manabe T, Hirai M, et al. Teratocarcinosarcoma of the nasal cavity. Report of a case showing favorable prognosis. APMIS 2000;108:553‑7. 4. Nitsche M, Hermann RM, Christiansen H, Berger J, Pradier O. Rationale for individualized therapy in Sinonasal Teratocarcinosarcoma (SNTC): Case report. Onkologie 2005;28:653‑6. 5. Sharma HS, Abdullah JM, Othman NH, Muhamad M. Teratocarcinosarcoma of the nasal cavity and ethmoid. J Laryngol Otol 1998;112:682‑6. 6. S o b a n i Z A , A k h t a r S , J u n a i d M , S a l a h u d d i n I . S i n o n a s a l teratocarcinosarcoma. J Pak Med Assoc 2012;62:633‑5.
Access this article online Quick Response Code:
Website: www.indianjcancer.com DOI: 10.4103/0019-509X.146785 PMID: *********
Response to oral metronomic chemotherapy in carcinoma of the Buccal Mucosa: A case report
Sir, Metronomic chemotherapy is the continuous use of fractionated doses, far below the maximum tolerated dose, of chemotherapeutic agents acting on different targets in the tumor micro‑environment. [1] In palliative and resource constraint settings, we have used oral metronomic chemotherapy with methotrexate and celecoxib in metastatic, inoperable recurrent and locally advanced head and neck cancers with promising results.[2,3] However, rarely do we get a rapid and complete clinical response. Here, we present such a case. A 66‑year‑old male, chronic tobacco chewer and known case of hypertension (HTN), coronary artery disease (CAD) with atrial fibrillation (AF) and history of cerebrovascular accident presented to our hospital in December 2013, with complaints of nonhealing ulcerative lesion over right lower lip extending to buccal mucosa since 8 months. He was symptomatic for pain in the lesion with mild dysphagia and discharge from the wound. Clinically there was a 5 cm × 4 cm ulcero‑proliferative growth in right buccal mucosa involving lower lip, angle of mouth, adjoining part of the skin and upper lip. Computed tomography scan showed a plaque‑like lesion measuring 20 mm in maximum thickness involving right buccal mucosa‑buccinator complex, extending from the maxillary alveolus inferiorly up to the mandibular attachment. The retromolartrigone region and the gingival mucosa were involved with the infiltration of the skin. A right level IB lymph node was seen. Biopsy confirmed a well‑differentiated squamous cell carcinoma. Patient was staged as T4a N1 M0 – TNM stage IV (A) in view of skin involvement. Patient was planned for surgery, but he developed AF during anesthesia induction. In view of persistent AF, HTN, CAD and American Society of Anesthesiology III risk for anesthesia, patient was deemed unfit for surgery. Radiotherapy could not be given in view of skin ulceration and extensive disease. Hence, he was referred for palliative chemotherapy. Patient presented to medical oncology outpatient department in April 2014 with progressive disease. His performance status as per Eastern Cooperative Oncology Group scale was 2. Echocardiography done in January 2014 showed concentric left ventricular hypertrophy, no regional wall motion abnormalities and 60% ejection fraction. Electrocardiogram showed AF with 400
a
b
Figure 1: (a) Before chemotherapy (b) after chemotherapy
controlled ventricular rate. Patient was on metoprolol, olmesartan, hydrochlorthiazide, rosuvastatin, aspirin and warfarin. In view of multiple comorbidities, old age, reluctance for regular follow‑up and risks of intravenous chemotherapy, patient was given oral methotrexate 15 mg/ m 2 weekly and 200 mg celecoxib twice a day with palliative intent. The risk of cardiotoxicity with celecoxib was explained. He was called for a reassessment after 1‑month. After 1‑month, clinically the lesion over right buccal mucosa involving the angle of mouth and lips had completely resolved [Figure1 a and b]. The earlier symptoms of pain, discharge and dysphagia had completely resolved. Radiologically there was a partial response. The present case highlights the fact that oral metronomic chemotherapy with methotrexate and celecoxib is an effective alternative to primary systemic chemotherapy with dramatic response in some cases of head and neck cancer. Prospective randomized trials are needed to validate the encouraging response rates and minimal side effects of this schedule. In developing countries like India, this treatment strategy can be effective where most patients cannot afford costly drugs.[4] Joshi A, Agarwala V, Noronha V, Dhumal S, Juvekar S1, Prabhash K Department of Medical Oncology and Radiodiagnosis1, Tata Memorial Hospital, Parel, Mumbai, Maharashtra, India
Correspondence to:
Dr.Kumar Prabhash, E‑mail: [email protected]
References 1. Pasquier E, Kavallaris M, André N. Metronomic chemotherapy: New rationale for new directions. Nat Rev Clin Oncol 2010;7:455‑65. 2. Pai PS, Vaidya AD, Prabhash K, Banavali SD. Oral metronomic scheduling of anticancer therapy‑based treatment compared to existing standard of care in locally advanced oral squamous cell cancers: A matched‑pair analysis. Indian J Cancer 2013;50:135‑41. 3. Patil V, Noronha V, Krishna V, Joshi A, Prabhash K. Oral metronomic Indian Journal of Cancer | July–September 2014 | Volume 51 | Issue 3
Copyright of Indian Journal of Cancer is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
