Homi Bhabha Cancer Hospital and Research Center

Visakhapatnam andhra Pradesh, India

Homi Bhabha Cancer Hospital and Research Center

Visakhapatnam andhra Pradesh, India
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Sirohi B.,Kiran Mazumdar Shaw Cancer Center | Shrikhande S.V.,The Surgical Center | Perakath B.,Christian Medical College | Raghunandharao D.K.,Homi Bhabha Cancer Hospital and Research Center | And 10 more authors.
Indian Journal of Medical and Paediatric Oncology | Year: 2014

This document is based on consensus among the experts and best available evidence pertaining to the Indian population and is meant for practice in India. Evaluation of a patient with newly diagnosed colorectal cancer (CRC) should include essential tests: A complete colonoscopy with biopsy, imaging (for colon cancer: Contrast-enhanced computed tomography (CECT) scan of the chest, abdomen and pelvis and for rectal cancer: Magnetic resonance imaging (MRI) of the pelvis, or an endoscopic ultrasound (EUS), with a chest and abdomen CECT), complete blood counts, liver and kidney function tests, carcinoembryonic antigen (CEA) and carbohydrate antigen 19.9 (CA19.9). For patients with localized colon cancer, resection is the treatment of choice, with consideration given to adjuvant chemotherapy for the patient with stage III and high-risk Stage II cancers. In patients with early rectal cancer (T1/T2, N0) surgery is the treatment of choice. Patients with locally advanced rectal cancer (T3/T4, N1, circumferential resection margin (CRM) threatened or involved) benefit from neoadjuvant therapy. Short course radiotherapy can be given if the CRM is not threatened. Others should undergo long course chemoradiotherapy. Adjuvant therapy is given to all patients receiving neoadjuvant therapy. Patients with potentially resectable metastatic liver limited disease should undergo synchronous or staged metastatectomy, along with neoadjuvant and adjuvant chemotherapy. Nonresectable metastatic disease must be assessed for chemotherapy versus best supportive care on an individual basis. Clinical examination and serum tumor markers are recommended at each followup visit, with imaging only done when either is abnormal or rising. Colonoscopic surveillance is also recommended for these patients.


Kagita S.,Nizam's Institute of Medical Sciences | Uppalapati S.,Nizam's Institute of Medical Sciences | Gundeti S.,Nizam's Institute of Medical Sciences | Digumarti R.,Nizam's Institute of Medical Sciences | Digumarti R.,Homi Bhabha Cancer Hospital and Research Center
Japanese Journal of Clinical Oncology | Year: 2015

Objective: Altered differentiation is a common feature of haematopoietic malignancies with poor prognosis. CAAT/enhancer binding protein alpha (C/EBPα) is a key transcription factor that regulates myeloid differentiation. This study is aimed to know the prognostic value of CAAT/enhancer binding protein alpha expression and correlate its expression with response to imatinib therapy. Methods: We quantified the expression of C/EBPα gene in 126 chronic myeloid leukaemia samples (82 from newly diagnosed and 44 from imatinib-resistant patients) and 20 control samples. C/EBPα mRNA level was measured by real-time quantitative polymerase chain reaction using the ΔΔCT method. Results: C/EBPα expression level was significantly lower in the imatinib-resistant group than in the pretreatment and control group (P = 0.0398). Low CAAT/enhancer binding protein alpha levels in the imatinib-resistant group were significantly associated with advanced phase (P = 0.04), with more peripheral blasts (P = 0.0001), high BCR-ABL levels (P = 0.018) and T315I and P-loop mutations (P = 0.0002). In the pretreatment group, low expression showed association with high EUTOS risk score (P = 0.03) and possible partial cytogenetic response (P = 0.010). Conclusions: Our results suggest that lowexpression of CAAT/enhancer binding protein alpha might have a role in the response to imatinib and progression of disease in patients with chronic myeloid leukaemia. © The Author 2015.


Edathara P.M.,Osmania University | Gorre M.,Osmania University | Kagita S.,Homi Bhabha Cancer Hospital and Research Center | Vuree S.,Osmania University | And 6 more authors.
Tumor Biology | Year: 2015

Chronic myeloid leukemia (CML) is a monoclonal myeloproliferative disorder of hematopoietic stem cells (HSCs), characterized by reciprocal translocation, leading to the formation of BCR-ABL oncogene with constitutive tyrosine kinase (TK) activity. This oncogene is known to deregulate different downstream pathways which ultimately lead to cell proliferation, defective DNA repair, and inhibition of apoptosis. Fas (Fas cell surface death receptor) is a member of tumor necrosis factor (TNF) superfamily which interacts with its ligand, FasL, to initiate apoptosis. Promoter polymorphisms in Fas-FasL genes are known to influence the apoptotic signaling. Hence, the present study has been aimed to find out the association of the promoter polymorphisms in Fas and FasL genes with the development and progression of CML. Blood samples from 772 subjects (386 controls and 386 cases) were collected and genotyped for Fas-FasL gene polymorphisms through PCR-RFLP method. The association between SNPs and clinical outcome was analyzed using statistical softwares like SPSS version 20, SNPSTATs, and Haploview 2.1. The study revealed a significant association of Fas −670 G>A and FasL −844 T>C polymorphisms with the development of CML while Fas −670 AG was associated with accelerated phase. Combined risk analysis by taking the risk genotypes in cases and controls revealed a significant increase in CML risk with increase in number of risk genotypes (one risk genotype—OR 1.99 (1.44–2.76), p < 0.0001; two risk genotypes—OR 3.33 (1.91–5.81), p < 0.0001). Kaplan–Meier survival analysis of Fas −670 A>G and FasL −844 T>C showed reduced event-free survival in patients carrying the variant genotypes, Fas −670 GG, 32.363 ± 6.33, and FasL −844 CC, 33.489 ± 5.83, respectively. Our findings revealed a significant association of Fas −670 GG, FasL −844 TC, and CC genotypes with increased risk of CML. © 2015 International Society of Oncology and BioMarkers (ISOBM)


Viswanath V.,Homi Bhabha Cancer Hospital and Research Center
Journal of Pain and Palliative Care Pharmacotherapy | Year: 2015

Understanding spirituality during palliative care training is not easy. It slowly unravels itself when one starts caring for patients and meeting their caregivers. One such experience in the hospice has been described in this narrative. A person with advanced incurable cancer is initially in severe distress. Over time, he slowly comes to terms with the situation and eventually, a question from his illiterate wife - an insightful question about any last wish - brings out his desire to have certain religious rituals that were alien to his own religion. After his death, the family members concur with his last wish and also indulge in some religious rituals of their own choice. This story reaffirms that the essence of spirituality is the coexistence of harmony and humanity. © 2015 Taylor & Francis Group, LLC.


bhushann Meka P.,Osmania University | Cingeetham A.,Osmania University | Nanchari S.R.,Osmania University | Damineni S.,Indian Institute of Science | And 6 more authors.
Tumor Biology | Year: 2015

Hypoxia-inducible factor 1α (HIF-1α) is an important transcription factor that regulates different cellular responses to hypoxia. HIF-1α is rapidly degraded by von Hippel–Lindau (VHL) protein under normoxic conditions and stabilized under hypoxia. A common variant of HIF-1α (1772C>T) (rs 11549465) polymorphism, corresponding to an amino acid change from proline to serine at 582 position within the oxygen-dependent degradation domain, results in increased stability of the protein and altered transactivation of its target genes. The present study was aimed to find the association between HIF-1α (1772C>T) (rs 11549465) polymorphism and breast cancer development. For this purpose, 348 primary breast cancer patients and 320 healthy and age-matched controls were genotyped through PCR-RFLP method. The genotype frequencies were compared between patients and controls, and their influence on clinical characteristics of breast cancer patients was analyzed. Our study revealed a significant increase of TT genotype in breast cancer patients compared to controls (p = 0.038). Further, TT genotype and T allele were found to be associated with progesterone receptor (PR)-negative status (p < 0.09). None of the clinical variables revealed significant association with HIF-1α (1772C>T) (rs 11549465) polymorphism. © 2014, International Society of Oncology and BioMarkers (ISOBM).


Cingeetham A.,Osmania University | Vuree S.,Osmania University | Dunna N.R.,SASTRA University | Gorre M.,Osmania University | And 7 more authors.
Tumor Biology | Year: 2015

B-cell lymphoma 2 (BCL2) and BCL2-associated X protein (BAX) proteins are anti-apoptotic and pro-apoptotic determinants of mitochondrial-mediated apoptosis, and their relative expression determines the cell fate. The promoter polymorphisms in these genes were shown to alter the protein function or expression and exert an impact on apoptosis regulation. Deregulation in the expression of any of these genes leads to disruption of cellular homeostasis and malignant transformation. The present study was aimed to determine the association of BCL2-938C>A and BAX-248G>A promoter polymorphisms with origin and progression of acute myeloid leukemia (AML). We also have performed combined genotype analysis to evaluate the cumulative effect of risk genotypes in the AML development. These polymorphisms were genotyped by polymerase chain reaction- restriction fragment length polymorphism (PCR-RFLP) in 221 AML patients and 305 age- and sex-matched healthy controls. Our study revealed that BCL2-938CA (p = 0.018) and BAX-248GG (0.043) genotypes were significantly associated with increased risk for AML occurrence. BAX-248A allele had shown decreased risk for AML. The combined analysis had shown that BCL2-938CA+AA-BAX-248GG group had a 1.63-fold (95 % CI: 1.08–2.45, p = 0.02) increased risk for AML. None of the clinical variables had shown any significant association with both polymorphisms. With respect to complete remission (CR) rate, BAX-248GG genotype (p = 0.002) and G allele (p = 0.009) had conferred significant risk for complete remission failure. Although the log rank test was not significant, survival analysis had shown a trend where BCL2-938CA genotype, and BAX-248GG had reduced median disease-free survival (DFS) of 9 and 10 months, respectively. In conclusion, BCL2-938C>A and BAX-248G>A gene polymorphisms might contribute to the origin of AML. Moreover, influence of BAX-248GG genotype on CR and DFS rate suggests that the BAX-248G>A polymorphism can serve as marker for poor prognosis in AML. © 2015, International Society of Oncology and BioMarkers (ISOBM).


PubMed | Homi Bhabha Cancer Hospital and Research Center, Institute of Oncology Regional Cancer Center, SASTRA University and Osmania University
Type: Comparative Study | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2015

B-cell lymphoma 2 (BCL2) and BCL2-associated X protein (BAX) proteins are anti-apoptotic and pro-apoptotic determinants of mitochondrial-mediated apoptosis, and their relative expression determines the cell fate. The promoter polymorphisms in these genes were shown to alter the protein function or expression and exert an impact on apoptosis regulation. Deregulation in the expression of any of these genes leads to disruption of cellular homeostasis and malignant transformation. The present study was aimed to determine the association of BCL2-938C>A and BAX-248G>A promoter polymorphisms with origin and progression of acute myeloid leukemia (AML). We also have performed combined genotype analysis to evaluate the cumulative effect of risk genotypes in the AML development. These polymorphisms were genotyped by polymerase chain reaction- restriction fragment length polymorphism (PCR-RFLP) in 221 AML patients and 305 age- and sex-matched healthy controls. Our study revealed that BCL2-938CA (p=0.018) and BAX-248GG (0.043) genotypes were significantly associated with increased risk for AML occurrence. BAX-248A allele had shown decreased risk for AML. The combined analysis had shown that BCL2-938CA+AA-BAX-248GG group had a 1.63-fold (95 % CI: 1.08-2.45, p=0.02) increased risk for AML. None of the clinical variables had shown any significant association with both polymorphisms. With respect to complete remission (CR) rate, BAX-248GG genotype (p=0.002) and G allele (p=0.009) had conferred significant risk for complete remission failure. Although the log rank test was not significant, survival analysis had shown a trend where BCL2-938CA genotype, and BAX-248GG had reduced median disease-free survival (DFS) of 9 and 10 months, respectively. In conclusion, BCL2-938C>A and BAX-248G>A gene polymorphisms might contribute to the origin of AML. Moreover, influence of BAX-248GG genotype on CR and DFS rate suggests that the BAX-248G>A polymorphism can serve as marker for poor prognosis in AML.


PubMed | Homi Bhabha Cancer Hospital and Research Center and Osmania University
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016

Chronic myeloid leukemia (CML) is a monoclonal myeloproliferative disorder of hematopoietic stem cells (HSCs), characterized by reciprocal translocation, leading to the formation of BCR-ABL oncogene with constitutive tyrosine kinase (TK) activity. This oncogene is known to deregulate different downstream pathways which ultimately lead to cell proliferation, defective DNA repair, and inhibition of apoptosis. Fas (Fas cell surface death receptor) is a member of tumor necrosis factor (TNF) superfamily which interacts with its ligand, FasL, to initiate apoptosis. Promoter polymorphisms in Fas-FasL genes are known to influence the apoptotic signaling. Hence, the present study has been aimed to find out the association of the promoter polymorphisms in Fas and FasL genes with the development and progression of CML. Blood samples from 772 subjects (386 controls and 386 cases) were collected and genotyped for Fas-FasL gene polymorphisms through PCR-RFLP method. The association between SNPs and clinical outcome was analyzed using statistical softwares like SPSS version 20, SNPSTATs, and Haploview 2.1. The study revealed a significant association of Fas -670 G>A and FasL -844 T>C polymorphisms with the development of CML while Fas -670 AG was associated with accelerated phase. Combined risk analysis by taking the risk genotypes in cases and controls revealed a significant increase in CML risk with increase in number of risk genotypes (one risk genotype-OR 1.99 (1.44-2.76), p<0.0001; two risk genotypes-OR 3.33 (1.91-5.81), p<0.0001). Kaplan-Meier survival analysis of Fas -670 A>G and FasL -844 T>C showed reduced event-free survival in patients carrying the variant genotypes, Fas -670 GG, 32.3636.33, and FasL -844 CC, 33.4895.83, respectively. Our findings revealed a significant association of Fas -670 GG, FasL -844 TC, and CC genotypes with increased risk of CML.


PubMed | Ms Ramaiah Medical College, Chaitanya Medical Center, Mahatma Gandhi Cancer Hospital and Research Center and Homi Bhabha Cancer Hospital and Research Center
Type: Journal Article | Journal: Indian journal of medical and paediatric oncology : official journal of Indian Society of Medical & Paediatric Oncology | Year: 2016

Isolated skeletal metastasis in endometrial carcinoma at recurrence is very rare. We report a 52-year-old woman diagnosed to have FIGO Stage 1b, Grade 1 endometrioid adenocarcinoma, presenting with isolated distal humerus metastasis, 2 years after surgery and adjuvant radiotherapy for primary disease. Imaging, bone scintigraphy, and cytology confirmed the diagnosis of poorly differentiated metastatic adenocarcinoma. She was treated with local radiotherapy followed by six cycles of paclitaxel and carboplatin chemotherapy along with zoledronic acid, monthly. She is symptom-free after the treatment and at a first follow-up visit after 3 months.

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