Trends in the Incidence of Non-Hodgkin’s Lymphoma in India

Non-Hodgkin’s Lymphoma is the 11th most common cause of cancer incidence. It is most frequent in highincome countries, with rates more than twice those of middle - to low – income countries. It is usually fatal, witha 5 year survival rate of less than 35 percent. It is not a single cancer, but rather a wide group of cancers(including entities such as Burkitt’s lymphoma and diffuse large B-cell lymphoma), each with a districtgeographical distribution, development path, age profile and prognosis. Non-Hodgkin’s lymphoma is increasingin incidence world wide. On this background, in this paper an attempt has been made to study the trends inNon-Hodgkin’s Lymphoma in various Indian populations in both sexes.     

Current concepts in the treatment of Ewing’s sarcoma

Current concepts in the treatment of patients with Ewing’s sarcoma are presented focusing on the role of chemotherapy, radiation therapy and surgical resection. Particular attention is given to current methods of limb salvage. Problem areas, including the pelvis, proximal femur and spine, are discussed.     

The Importance of the Pathologist’s Role in Assessment of the Quality of the Mesorectum

Total mesorectal excision (TME) is considered standard of care for rectal cancer treatment. Failure to remove the mesorectal fat envelope entirely may explain part of observed local and distant recurrences. Several studies suggest quality of the mesorectum after TME surgery as determined by pathological evaluation may influence prognosis. We aimed to determine the prognostic value of the plane of surgery as well as factors influencing the likelihood of a high-quality specimen by reviewing the literature. A pooled meta-analysis of relevant outcome data was performed where appropriate. A muscularis propria resection plane was found to increase the risk of local recurrence (RR 2.72 [95 % CI 1.36 to 5.44]) and overall recurrence (RR 2.00 [95 % CI 1.17 to 3.42]) compared to an (intra)mesorectal plane. Plane of surgery is an important factor in rectal cancer treatment and the documentation by pathologists is essential for the improvement of TME quality and patient outcome.     

Letter in Response to ‘Approach to Oligometastatic Cancer in the Elderly Patient’

Current Oncology Reports -     

Barrett’s esophagus in the patients with familial adenomatous polyposis

Familial adenomatous polyposis (FAP) is caused by germ line mutations in the APC gene. Barrett’s esophagus (BE) and Barrett’s adenocarcinoma are intestinal type lesions of the esophagus characterized by an early loss of heterozygosity at the APC locus. We hypothesized that patients with FAP are at risk for the early development of BE due to the inherited mutations in the APC gene (haploinsufficiency). Upper gastrointestinal (UGI) tract biopsies from 36 patients with FAP were reviewed to determine the incidence and characteristics of BE in these patients. Twenty-four patients were confirmed carriers of a deleterious germline APC mutation. The other 12 patients were from FAP families with known APC gene mutations and had clinical manifestations of FAP. The control group consisted of patients who did not have a personal or family history of FAP undergoing UGI endoscopic examination in our institution over a 30 month period of time. The difference in expression of Wnt pathway proteins (APC, β-catenin, E-cadherin and cyclin D1) in BE between BE⁺/FAP⁺, BE^?/FAP⁺ and age-matched BE⁺/FAP^? groups was studied using immunohistochemistry. BE was found in 6 of 36 (6/36 or 16%) patients with FAP and in 266 of 1662 patients (16%) in the control group of symptomatic patients. The average age at the first diagnosis of BE in FAP patients was 37.8 versus 57.5 years in the control group (sporadic BE). When compared to age matched BE⁺/FAP- group (7/334), patients with FAP had a significantly (p = 0.005843, odds ratio 9.2; Fisher exact test) higher incidence of BE. Both classic FAP and attenuated FAP phenotypes were associated with BE .Two types of germ line mutations in APC gene were identified in BE⁺/FAP⁺ patients: Five patients had 2-base deletion in exon 4 (426delAT) and one patient had 4-base deletion in exon 15 (3202del4). No difference in Wnt signaling pathway proteins expression was detected between BE⁺/FAP⁺ and the age matched group of patients with sporadic BE (BE⁺/FAP^?). Patients with FAP appear to have increased risk for the development of BE, which on average develops some 20 years earlier than in patients without FAP. This association needs to be taken in account when caring for the patients with FAP.     

Advances in the treatment of Waldenström’s macroglobulinemia

Waldenström’s macroglobulinemia is a distinct disorder characterized by a monoclonal immunoglobulin M paraprotein and morphological evidence of lymphoplasmacytic lymphoma. It is relatively rare, accounting for approximately 2% of all hematological malignancies. The aim of treatment for patients with Waldenström’s macroglobulinemia should be to improve the quality and duration of life with minimal side effects in the most cost-effective manner. It is not yet clear if achievement of a complete remission confers clinical benefit and it is possible that prolonging therapy to maximal response may increase toxicity without extra benefit. Plasma exchange is indicated for the acute management of patients with severe problems due to a circulating paraprotein. There are no comparative data but alkylating agent-based treatments, combination therapy or purine analogs are all suitable choices for the initial therapy of patients requiring treatment. In younger patients, in whom high-dose treatment is contemplated, there is a role for the use of rituximab; however, it should be administered with caution in patients with high levels of immunoglobulin M paraprotein or signs of hyperviscosity because of the risk of ‘flare’ in the paraprotein level and consequent adverse clinical events.     

Adult survivors of childhood cancers’ identity disclosures in the workplace

Purpose

Recent medical advances have resulted in unprecedented increases in the number and vitality of employed adult survivors. These survivors must make decisions about whether or not to disclose their identities to others. The purpose of this study was to examine the characteristics that are related to cancer survivorship disclosure in workplace settings (perceived organizational support, centrality of survivorship to one’s self-concept, and the degree to which family and friends know about one’s survivor status) and an important organizational consequence: intentions to leave one’s job.

Methods

A total of 151 adult survivors of childhood cancer completed an online survey.

Results

Extent of disclosure of one’s identity as a cancer survivor was negatively associated with turnover intentions. Furthermore, organizational support, identity centrality, and disclosure outside of work were all related to disclosure in the workplace. Relative weight analysis revealed that disclosure outside of work was the most strongly related to disclosure at work. Finally, there were indirect relations such that disclosure mediated the relations among organizational support, identity centrality, and disclosure outside of work and turnover intentions.

Conclusions

Survivors who were more open about their cancer survivor status at work had fewer intentions to leave their organizations. Importantly, although some antecedents to disclosure were personal characteristics, organizations can also encourage identity disclosure demonstrating that they are related to of work retention.

Implications for Cancer Survivors

While disclosure in the workplace is a complex decision to make, the relationship with work retention may reflect that disclosure is more likely to occur in an existing positive work environment or that disclosure itself may contribute to a positive work environment where employees tend to remain. The specific factors that trigger both disclosure and retention require further study although they are clearly related.

     

Advances in the management of patients with non-Hodgkin’s lymphoma

Non-Hodgkin’s lymphoma is the fifth most common cause of death due to cancer and has been rising at a rate of 4% per year for the last four decades. Although ‘traditional’ chemotherapy and radiotherapy have had important contributions to improving outcomes, new tools in the treatment of non-Hodgkin’s lymphoma are needed. This review describes therapeutic modalities that are currently being used or are in the process of being developed and which are based on concepts divergent from ‘traditional’ approaches to managing non-Hodgkin’s lymphoma.     

The ‘death pace’ in the CO.17 trial

In an era where the cost of care in oncology is rising, suggestions of new frameworks that may help in orienting biomarker discovery are highly desirable. We propose a different perspective for looking at survival data, which we call ‘death pace’ analysis, which focuses on the variation of the gap between survival curves over time and that may make it easier to identify subpopulations with distinct predictive molecular features. The recently published data on EJC on the impact of the primary colonic site in the CO.17 trial seem to be particularly suitable for the death pace analysis.     

Preface to the ‘UKCCCR guidelines for the Welfare of animals in experimental neoplasia’

Preface to the UKCCCR guidelines for the Welfare of animals in experimental neoplasia     

Milestones in Mission: the Work of the American Cancer Society’s Mission Delivery

Since its founding in 1913, the American Cancer Society (the Society) has played a prominent role in the fight against cancer. Through its presence in over 5,000 communities around the nation, the Society has explored and pursued innovative ideas, searched for breakthroughs, and pushed to have the nation understand the complexities of the disease. Ongoing assessment of the cancer problem, thoughtful strategic planning, and promotion of evidence-based cancer control programs are integral to the Society’s mission. This paper provides a summary of these efforts.     

TP53 - Molecular Soldier’s Mutations in Bladder Cancer in the Kashmiri Population

Purpose: We made a preliminary attempt to study mutations in exons 5-8 (the DNA binding domain) ofthe tumor suppressor gene TP53, in urinary bladder cancer patients from Kashmir. Further the relation ofclinicopathological characteristics with mutation status was asessed. Materials and Methods: The study populationconsisted of 60 patients diagnosed with transitional cell carcinomas who underwent transurethral resection and/or radical cystectomy. Mutations in 5-8 exons of TP53 gene were detected by means of single strand conformationpolymorphism (SSCP). All samples which showed different migration bands in SSCP were confirmed by DNAsequencing. Results: 19 of 60 (31.6%) bladder cancers had mutations of the TP53 gene (11 transitions and 8transversions), three were G→A transitions, two G→T transversions, three A→C transversions, five C→Ttransitions and six A→T transversions. Predominantly missense mutations (66%) were detected but no deletionsor insertions were found. Statistically significant associations (<0.05) were noted with higher tumor stage (T2 orhigher), recurrence and large tumor size (>3cm). No correlation was found between smoking and tumor gradeand the presence of TP53 mutations. Conclusions: Mutation of the TP53 gene is one of the commonest geneticchanges in human bladder cancer, also in a high risk ethnic Kashmiri population.     

Colorectal cancer: a researcher’s perspective of the molecular angel’s gone eccentric in the Vale of Kashmir

Colorectal cancer (CRC), being the most common cancer, is the major cause of mortality and morbidity worldwide. In Kashmir, CRC has been found to be the third most common gastrointestinal cancer after esophageal and gastric. The etiology of CRC involves two pathways: chromosomal instability (CIN) and microsatellite instability. CIN occurs in 80–85 % of CRC resulting in either gross changes in chromosome structure and number or point mutations in the chromosomes. Many molecular studies have been carried out on CRC in Kashmir so as to elucidate the role of tumor suppressor genes and oncogenes in modulating the carcinogenesis. We searched the various literature databases including Medline, PubMed, ASCO abstracts, and ESMO abstracts for the papers regarding colorectal cancer published in English using the terms “Kashmir,” “colorectal cancer,” “colon cancer,” “rectal cancer,” “carcinogenesis,” “epidemiology,” “genetics,” “mutation,” and “polymorphism.” Here in this review, I have shed light on the different studies carried on CRC in our Kashmiri population in an attempt to share what we know so far about the molecular carcinogenesis of CRC in Kashmir.     

What’s new in the field of prostate cancer chemoprevention?

Chemoprevention trials for several malignancies are completed, planned, or underway. Prostate cancer is one of the most common forms of cancer and understandably has received considerable recent attention as a potential target for chemoprevention. This article examines chemoprevention trials for prostate cancer, including the Prostate Cancer Prevention Trial, Selenium and Vitamin E Cancer Prevention Trial, and cyclooxygenase inhibitors in the prevention of prostate cancer.     

Contradictory concepts in the etiology and regression of kaposi’s sarcoma

The Introduction is an overview of 3 decades of works performed by Professor Ferenc Györkey? (in many cases in collaboration with the author) and aimed at the elucidation of viral participation in the etiology of arteriosclerosis, SLE, hairy cell leukemia, HD, AIDS and KS. Controversial issues surrounding the etiology, treatment and regression of KS are discussed in terms of paracrine and autocrine loops of growth factors; protooncogene-oncogene activations, immunosuppression and retro-and/or herpesviral etiology. In regressing KS lesions the roles played by Fas, Bcl-2, Bax, TNFß; apoptotic-antiapoptotic events; and antiangiogenesis agents especially that of Hu-r-IFNα are elaborated on.