The Intersection Among Torts, Science, Corporate Law, Insurance & Bankruptcy

“Genetic predisposition found for noise-induced hearing loss”

Posted in Litigation Industry, Science

A torrent of genetic data continues to flow out of studies of diseases and conditions. Any manufacturer, insurer,  or other entity seriously involved with risk and litigation needs to – at least – create a mechanism to ensure continuing, systematic knowledge of scientific developments relevant to products sold or risks insured.  Persons working in the area should be developing at least a working knowledge of how and why molecular knowledge can or plainly will cause material changes for some but not all risks and potential mass tort situations.  One means to gain knowledge is to attend conferences focused on molecular science and tort litigation. One upcoming session is on Friday, May 1 in Charleston, South Carolina. Almost all of the speakers are either real scientists or lawyers who really “get” the implications of molecular knowledge. See here for all the specifics on HarrisMartin’s DNA and Molecular Evidence in Toxic Torts Conference: The Time of Genomics Is Here

The point is highlighted by a new report on a condition that – at least to me – did not seem likely to possibly have genetic variables. But, an April 16, 2015 article in ScienceDaily brings news about  condition that is 1) often in litigation, and 2) is some evidence of possible genetic susceptibility. The article explains: “In a new genome-wide association study, an international team led by Keck Medicine of the University of Southern California (USC) neuroscientists has found evidence that some people may be more genetically susceptible to noise-induced hearing loss than others. …The study, “Genome-wide association study identifies Nox3 as a critical gene for susceptibility to noise-induced hearing loss,” appears in the April 16 edition of PLOS Genetics, a peer-reviewed scientific journal.”

Journal Reference:

  1. Joel Lavinsky, Amanda L. Crow, Calvin Pan, Juemei Wang, Ksenia A. Aaron, Maria K. Ho, Qingzhong Li, Pehzman Salehide, Anthony Myint, Maya Monges-Hernadez, Eleazar Eskin, Hooman Allayee, Aldons J. Lusis, Rick A. Friedman. Genome-Wide Association Study Identifies Nox3 as a Critical Gene for Susceptibility to Noise-Induced Hearing Loss. PLOS Genetics, 2015; 11 (4): e1005094 DOI: 10.1371/journal.pgen.1005094

Be Careful What You Ask For – Once Again, The Chevron Ecuador Version of Asking to Litigate Outside the United States

Posted in Litigation Industry

Time and again, US companies argue that the US courts cannot and should not take jurisdiction over disputes with some but not all of their roots in events outside the US. Chevron followed that tactic in seeking to push the Ecuador pollution litigation from the US to Ecuador. But after the courts in Ecuador ruled, Chevron deemed the ruling corrupt and waged jihad agains the plaintiff’s lawyers, litigation funders and many others involved in the litigation.  (For those wanting more background, Michael Goldhaber has constantly provided a nuanced, intelligent assessment of the issues. His Kindle book –  Crude Awakening - is especially helpful and inexpensive.)

The “be careful” moment arose again last week. Specifically, once again Chevron faced questions about its long ago request to litigate in Ecuador instead of the US, combined with further examination of its views and actions as to Ecuador’s courts and its related invocation of an arbitration process. Michael Goldhaber recounts part of the moment as follows in an April 23, 2014 article at AmLaw’s Litigation Daily. The reference to “Wesley” is to Judge Wesley of the 2d Circuit:

“The more consequential drama came after Wesley pressed Olson on why Chevron didn’t exhaust its local remedies by invoking Ecuador’s Collusion Protection Act. Here’s where the argument went off the rails. Devoted Chevronologists may follow along in the transcript, beginning on page 49.

After some diversion, Olson answered that relief in Ecuador would be worthless, as Ecuador’s system had been corrupted “right from the beginning.” With those unnecessary words, Olson set a trap for himself.

Wesley pounced: “Then why did you go there?” he asked with intensity. Meaning: if Ecuador was corrupt “right from the beginning,” then why did Chevron’s predecessor Texaco spend the decade from 1993 to 2002 telling the U.S. courts that Ecuador was not corrupt, and begging to move the case there?

For those who find these issues of note, read more:

NIH Research Budgets, Newt Gingrich, and Emily Beazley – It Is Irresponsible to Fail to Double Budgets for Awful Diseases

Posted in Cancer, Science
Near the home of Emily Beazley

Near the home of Emily Beazley (photo courtesy of Daily Southtown/Chicago Tribune)


A stem cell transplant has failed for 12 year old Emily Beazley, and so non-Hodgkin lymphoma is killing her in its vicious, painful way. Emily lives on the southwest side of Chicago near where my daughters have gone to high school. Her story is now headline news in the Daily Southtown, the Chicago Tribune and many local media outlets. My younger daughter’s high school soccer team, the high school (Marist) and countless others are doing what they can to provide financial and emotional support for Emily and her family, but it’s far from enough. The journey for Emily and her family is chronicled on a Caring Bridge page for Emily’s Entourage, and a Facebook page. A recent YouTube video will leave anyone in tears. More support is needed, but can only address symptoms and will not address the root problem of finding out the “how and why” of this and other awful diseases.

How to get to the root problem of finding the “how and why” of diseases? One part of the answer lies in national investment in research against awful diseases. Newt Gingrich recently ripped Congress for across the board budget cuts that have badly hurt budgets for research through the National Institutes of Health. Newt is correct in saying “it is irresponsible” to fail to DOUBLE  federal research budgets for awful diseases.  Everyone should be calling their legislators and demanding expanded federal budgets for disease research. Research matters because we are now in an age of molecular science at which researchers are finding treatments and answers we could not dream of only a year or two ago. We are making progress against blood cancers, but so much more is needed for that and all of the other awful diseases. Every year, the US death toll from cancer equals the population of Vermont.  Diseases are the world’s most effective terrorists, and we should spend far more on disease research than we do on homeland security.

Imagine being a member of Emil’s family. “She’s in so much pain right now,” Nadia said. “I’m her mom and I’m supposed to fix her and I just can’t do anything.”

Some Sort of Encouraging News Regarding Immunotherapy to Treat Mesothelioma and Other Awful Tumors

Posted in Asbestos, Cancer, Cancer Research

The ongoing annual AACR meeting this week included some sort of encouraging (but far from final) news on using immunotherapy to counter mesothelioma and other awful tumors (pancreatic and ovarian tumors). The news is from an abstract for a paper focused on a research project using immunotherapy to treat tumors that express a protein known as mesothelin. The abstract is pasted below. In essence it says the safety issues are probably manageable and there are some small signs of possible efficacy.

The point of immunotherapy is to stop tumors from successfully “hiding” from the immune system. Once the immune system can “see” the tumors, it sometimes can mount a successful attack on the tumors. Some times the reaction is too much and produces a “cytokine storm” that can be fatal. However, researchers and physicians are learning how to avoid the storms usiing surgery to reduce the tumor bulk, and various other tools, including chemotherapies and steroids. For more specifics, see this April 2, 2014 open access article in Nature, by Heidi Ledford:  “Cancer treatment: The killer within
The immune system can be a powerful weapon against cancer — but researchers are still grappling with how to control it.”

Abstract Number: CT105
Presentation Title: Safety and feasibility of chimeric antigen receptor modified T cells directed against mesothelin (CART-meso) in patients with mesothelin expressing cancers
Presentation Time: Sunday, Apr 19, 2015, 1:35 PM – 1:55 PM
Location: Terrace Ballroom I (400 Level), Pennsylvania Convention Center
Author Block: Janos L. Tanyi, Andrew R. Haas, Gregory L. Beatty, Mark A. Morgan, Caitlin J. Stashwick, Mark H. O’Hara, David L. Porter, Marcela V. Maus, Bruce L. Levine, Simon F. Lacey, Anne Marie Nelson, Maureen McGarvey, Naseem DS Kerr, Gabriela Plesa, Carl H. June. Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA
Abstract Body: A phase I study to evaluate the safety and feasibility of an intravenous infusion of autologous T cells transduced to express a chimeric antigen receptor directed against mesothelin (CART-meso) in patients with mesothelin expressing tumors is being conducted at the University of Pennsylvania. Here we report on the first five patients treated with CART-meso T cell infusion.
Five patients with recurrent advanced stage cancers (two serous ovarian, two epithelial mesothelioma, and one pancreatic) who had received 4-12 prior regimens, were treated with a single infusion of CART-meso cells. Apheresed autologous T cells were transduced with a lentiviral vector expressing the CAR construct composed of an extracellular anti-mesothelin single chain variable fragment derived from mouse monoclonal antibody (SS1) fused to the intracellular signaling domains of 4-1BB (CD137) and TCRzeta. Each patient received a single dose of 1-3 x 10^7 CART-meso cells/m2. No lymphodepletion with chemotherapy was given prior to infusion.
All subjects enrolled were successfully infused and there were no acute adverse events (AE) with infusion. To date, Grade 4 AEs have included sepsis(1), anemia(1), pleural effusions(1), tachypnea(1), dyspnea(1), and aspiration(1) and Grade 3 AEs have included sepsis(1), leukocytosis(2), DIC(1), tachycardia(1), dyspnea(1), hypotension(1), dusky extremities(1), fatigue(1), ascites(1), peritonitis(1), elevated LFTs(1), portal vein hypertension(1), and acute kidney injury(1). After infusion, CART-meso T cells were transiently detectable by PCR in the peripheral blood in all patients up to Day 21-28 after infusion. CART-meso cells were found to traffic to tumor sites within the peritoneum and liver, as well as to off-tumor on-target sites such as pericardial fluid, but without clinical toxicity of pericarditis. Expansion of CART-meso cells was also observed in the pleural fluid of one patient who had a known malignant pleural effusion. Cytokine profiling of the peripheral blood revealed elevations of IL-6 and VEGF with significant elevations seen in the one patient with malignant pleural effusion. No elevations in TNFα or IFNγ were found. Anti-tumor efficacy is suggested by the clearing of malignant cells in the pleural fluid of one patient on Day 21 and Day 26 after infusion, as well as radiological and clinical evidence of stable to decreased burden of disease in one patient. Patient follow-up for 1-3 months post infusion has revealed no evidence of long-term toxicities to date.
These interim results suggest that intravenous infusion of CART-meso T cells without lymphodepletion is feasible and safe. In these five patients with metastatic mesothelin expressing cancers, the infusion was well tolerated with no off-tumor on-target toxicities. Laboratory and clinical findings suggest infused T cells are effective and functional. (emphasis added)

Cancers Triggered in Less than 1 Year? Learn More at the Friday May 1 – HarrisMartin’s DNA and Molecular Evidence in Toxic Torts Conference: The Time of Genomics Is Here

Posted in Causation - Cancer, Litigation Industry

Genetics and epigenetic issues continue to knock open doors in toxic tort litigation. An example? A recent federal MDL ruling rejected defense Daubert motions seeking to strike expert opinions that were based on the concept of a cancer arising less than 1 year. How could that happen? Think epigenetic actions that “turn on” a cell receptor and leave it generating proteins at full throttle, and putting the cell into an agitated state in which it more easily transforms into a malignant cell.

I will be covering those issues and more on a panel with Lenn Murelle, a smart scientist who runs a company known as Venebio Group.  Lenn  “gets” molecular science and toxic tort litigation.

2:15 p.m. – 3:15 p.m.

Molecular Epidemiology, Epigenetics, and Nutrigenomics Bioscience – Intersections with Toxic Tort Claims

• Molecular Epidemiology and Toxic Tort Intersections
• What is Happening in the Human Body with the Increases in Obesity?
• Mesothelioma – Seeing the Intersections with BAP1 Mutation and Epigenetic Factors
• Epigenetics and Multi-Generational Toxic Tort Claims

Edward L. Murrelle, MSPH, Ph.D., Co-Founder and CEO, Venebio Group, LLC, Richmond, VA
Kirk T. Hartley, LSP Group LLC

Other panels also include real scientists who are at the front edge and also “get” the changes that will transform litigation over the next 20 years. For example, Len van Zyl and his company (ArrayXpress) are way ahead of most and actually are doing genomic testing in toxic tort cases.

9:00 a.m. – 10:00 a.m.

The Rapid Evolution of Law With Quantitative Precision Science

Len van Zyl, Ph.D., CEO and CSO, ArrayXpress, Inc., Raleigh, NC
Michael Zapata III, Executive Chairman, ArrayXpress, Inc., Raleigh, NC

10:00 a.m. – 10:45 a.m.

Understanding The Application of Epidemiology to the Science of Genomics

David G. Hoel, Ph.D., Exponent, Inc., Alexandria, VA

11:00 a.m. – 12:00 p.m.

The Role of Medical Toxicology and Ethical Issues

D. Mark Jackson, Bassi Edlin Huie & Blum LLP, San Francisco
John B. Sullivan, M.D., MBA, University of Arizona, Department of Emergency Medicine/Medical Toxicology Division, Tucson, AZ (Retired)

Go here to see the rest of the agenda and register:  HarrisMartin’s DNA and Molecular Evidence in Toxic Torts Conference: The Time of Genomics Is Here

Epignetics and Inflammation – “Cancer Feedback Loop Discovery” – A New Example of Molecular Analysis of Causes of Cancer – Today at AACR

Posted in Cancer, Epigenetics, Science

Molecular science continues to race forward in explaining the processes that generate the various processes we label as cancers. As an example, read the following new press release from the University of Pittsburgh about a presentation on Tuesday April 21, 2015 at the annual AACR meeting. While reading, do not get hung up on the specifics. Instead, simply consider the level of detail uncovered by the researchers as highlighted by the text in bullets. Then think about your favorite toxin or product, and the questions you could be asking.


“Inflammation-Cancer Feedback Loop Discovery is a Step Toward Better Cancer Drugs
PHILADELPHIA, April 20, 2015 – New findings hidden within the complex machinery behind the vicious cycle of chronic inflammation and cancer are presented today by researchers from the University of Pittsburgh Cancer Institute, partner with UPMC CancerCenter, at the American Association for Cancer Research (AACR) Annual Meeting in Philadelphia.

The research is funded by the National Institutes of Health (NIH) and Fondazione RiMED, of Palermo, Italy.

Inflammation is an important immune system tool that helps the body rid itself of foreign invaders, such as bacteria. However, chronic inflammation can fuel tumor growth by facilitating formation of cancer blood vessels, supplying nutrients and setting cancerous cells free to colonize other parts of the body.

The basic research into the specific mechanisms promoting cancer inflammation is a critical step in the development of drugs that could interrupt this process.

“In the last 20 years we’ve recognized that chronic inflammation and cancer are connected – long-term inflammation leads to the development of dysplasia and tumor progression,” said lead author Sandra Cascio, Ph.D., a research associate in Pitt’s Department of Immunology. “Recently, scientists have provided detailed insights into molecules and cellular pathways linking inflammation and cancer. In our study, we found a new mechanism that had previously escaped us.”

The mechanism is driven by a complex of MUC1, a molecule long studied in the laboratory of senior author and Pitt immunologist Olivera Finn, Ph.D., and p65, a molecule belonging to a protein complex family known to be activated in inflammation.

  • Dr. Cascio, in collaboration with Dr. Finn, looked for MUC1/p65-mediated epigenetic modifications affecting inflammatory genes. Epigenetics refers to outside factors that modify the activity of a gene, but do not cause a more obvious genetic mutation. Sure enough, the researchers discovered that this complex, which they found specifically in cancer cells, was causing DNA to be transcribed differently than expected.
  • “Normally MUC1 is covered in sugar molecules, like leaves cover a tree in spring,” said Dr. Cascio. “When it is made by a tumor, it lacks sugar and is more like a tree in fall. Our research shows that this form of MUC1 associates with p65 and regulates transcription of pro-inflammatory cytokine genes in tumor cells. This leads to the recruitment of inflammatory cells into the tumor site. Inflammatory cells, including macrophages, produce additional cytokines that enhance the activity of MUC1 and p65, establishing a continuous positive feedback loop, or a vicious circle, resulting in tumor progression.”
  • In order to pinpoint this altered pro-inflammatory mechanism in cancer cells, Dr. Cascio and her team combed through more than 20 types of epigenetic modifications and 300 factors that allow for the remodeling of chromatin, which are macromolecules in cells that control gene expression and DNA replication.
  • Specifically, the researchers found that MUC1 and p65 involve an enzyme called the Enhancer of Zeste homolog 2, or EzH2, known to induce epigenetic modifications, in order to prompt chromatin remodeling on cytokine gene promoters.

“Developing drugs that could keep these genes from being improperly turned on and off could interrupt this cancer-inflammation process and stop the tumor growth and spread,” said Dr. Cascio. “It’s a promising avenue for future exploration.”

Joshua Sciurba, B.S., of Pitt at the time of this research, also participated in this work.

This research was funded by Fondazione RiMED and NIH National Cancer Institute grant CA56103.” (italics and bullets added)

Anti-PD-1 Therapy Shows Some Promise for Treating Pleural Mesothelioma

Posted in Asbestos, Cancer, Cancer Research

The ongoing annual AACR meeting this week included some fairly encouraging clinical trial news for treatment of pleural mesothelioma. One portion of the news arises from a 25 person clinical trial at the University of Pennsylvania. Of those 25 persons, 28% (7) obtained an apparent regression of the tumor and another 48% (12) obtained “stable disease.” The treatment involves a PD-1 inhibitor, which is one of the current “hot” treatments in the world of cancer therapy. The goal of the drug is to alter the workings of so-called “checkpoint inhibitors.”  Said in a positive way, the goal is to further immune system attention to the tumor by “releasing a brake” on the immune system. Many similar PD-1 clinical trials are underway for other solid tumors. For a detailed, open access medical journal article, see Dolan, PD-1 pathway inhibitors: changing the landscape of cancer immunotherapy, Cancer Control, 2014 Jul;21(3):231-7.

Set out below is the pertinent portion of Merck’s press release:

“KEYTRUDA Demonstrated 28 Percent Overall Response Rate and 76 Percent Disease Control Rate in Difficult-to-Treat Cancer

First Findings from KEYNOTE-028, Merck’s Innovative Basket Trial in 20 Cancers

April 19, 2015 12:45 PM Eastern Daylight Time

PHILADELPHIA–(BUSINESS WIRE)–Merck (NYSE:MRK), known as MSD outside the United States and Canada, today announced the first presentation of data investigating the use of KEYTRUDA® (pembrolizumab), the company’s anti-PD-1 therapy, in 25 patients with advanced pleural mesothelioma, a difficult-to-treat cancer of the lining of the lungs, abdomen and other organs. The early findings presented showed an overall response rate (confirmed and unconfirmed) of 28 percent with KEYTRUDA in patients with tumors that expressed PD-L1. Additionally, 48 percent of patients had stable disease, resulting in a disease control rate of 76 percent. These data, from KEYNOTE-028, will be presented today at the American Association for Cancer Research (AACR) Annual Meeting by Dr. Evan Alley, Abramson Cancer Center, University of Pennsylvania, and were part of the AACR official press program (abstract #CT103). This is the first data to be presented from KEYNOTE-028, Merck’s innovative basket trial designed to evaluate the efficacy and safety of KEYTRUDA in patients with 20 difficult-to-treat cancers.

“This presentation at AACR marks the first time that data involving an anti-PD-1 therapy have been presented in pleural mesothelioma, which is a rare, hard-to-treat cancer with very limited treatment options”

“This presentation at AACR marks the first time that data involving an anti-PD-1 therapy have been presented in pleural mesothelioma, which is a rare, hard-to-treat cancer with very limited treatment options,” said Dr. Alley, clinical associate professor of medicine, Abramson Cancer Center. “While early, the disease control rates observed in this study are very encouraging, and indicate that further study is warranted to evaluate the potential role of KEYTRUDA in the treatment of malignant pleural mesothelioma.”

“This unique study is helping to accelerate our understanding of where KEYTRUDA may work in cancers with limited or no treatment options,” said Dr. Roger Dansey, therapeutic area head and senior vice president, oncology late stage development, Merck Research Laboratories. “These early data in advanced pleural mesothelioma reinforce the clinically meaningful results we are seeing with KEYTRUDA across multiple cancers.”

At the time of the analysis, 40 percent of patients (n=10/25) remained on treatment. Adverse events in the study were consistent with previously reported safety data for KEYTRUDA. The most common treatment-related adverse events (occurring in greater than twenty percent of patients) were fatigue (24%) and nausea (24%). Two Grade 3 treatment-related adverse events occurred: ALT increased (n=1) and thrombocytopenia (n=1). Some patients experienced adverse events of special interest, including rash (n=4), ALT/AST increased (n=1), hypersensitivity (n=1) and iridocyclitis (n=1); two required a dose interruption (one because of ALT/AST increased, one because of iridocyclitis). No patients discontinued as a result of treatment-related adverse events, and there were no treatment-related deaths.

About the KEYNOTE-028 Study

KEYNOTE-028 is an ongoing, multi-cohort, non-randomized Phase 1b basket trial evaluating the safety, tolerability, and anti-tumor activity of KEYTRUDA monotherapy (10 mg/kg dosed every two weeks) in 320 patients with PD-L1 positive advanced solid tumors that have not responded to current therapy or for which current therapy is not appropriate.

About KEYTRUDA® (pembrolizumab)

KEYTRUDA (pembrolizumab) is a humanized monoclonal antibody that blocks the interaction between PD-1 and its ligands, PD-L1 and PD-L2. By binding to the PD-1 receptor and blocking the interaction with the receptor ligands, KEYTRUDA releases the PD-1 pathway-mediated inhibition of the immune response, including the anti-tumor immune response.

KEYTRUDA is indicated in the United States at a dose of 2 mg/kg administered as an intravenous infusion over 30 minutes every three weeks for the treatment of patients with unresectable or metastatic melanoma and disease progression following ipilimumab and, if BRAF V600 mutation positive, a BRAF inhibitor. This indication is approved under accelerated approval based on tumor response rate and durability of response. An improvement in survival or disease-related symptoms has not yet been established. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Merck is advancing a broad and fast-growing clinical development program for KEYTRUDA with more than 85 clinical trials – across more than 30 tumor types and over 14,000 patients – both as a monotherapy and in combination with other therapies.”

Cancer Research and Clinical Trials Can Produce Great Results – the Wendy Harpham Example

Posted in Cancer, Cancer Research

Wendy Harpham, MD, leads Wendy’s Eagles in a 2015 fundraising walk for lymphoma research. Wendy is alive and thriving 23+  years after her first diagnosis with indolent lymphoma. Part of the reason is that she and others joined the phase I clinical trial of a then first-in-kind drug, a monoclonal antibody commonly known as Rituxan.

As a nation, we are grossly under invested in cancer research and clinical trials. Pessimists say we can never beat the various diseases we call cancer. Not so.

For some proof, consider the story of  Wendy Harpham, an internist. Wendy today is alive and thriving some 23+ years after she was first diagnosed with indolent lymphoma. In addition to promoting investment in research,  Wendy educates other doctors about interaction with persons with cancer, writes great books for patients, and writes the Healthy Survivor blog.

Wendy’s description of her history is set out below. Note especially her joinder in the phase 1 trial that paved the way for FDA approval of a then first of its kind drug. That drug today is commonly known as Rituxan, and has saved or extended tens of thousands of lives The drug – a  monoclonal antibody (Rituximab) –  is the R in a regimen commonly known as R-CHOP.  As Wikipedia explains:

“Rituximab destroys both normal and malignant B cells that have CD20 on their surfaces, and is therefore used to treat diseases which are characterized by having too many B cells, overactive B cells, or dysfunctional B cells.”


In 1990 I was diagnosed with indolent lymphoma, a type of cancer every textbook deemed incurable. My three children were all under 6 years old.

Intensive chemo put the lymphoma into remission. But it recurred a year later. After a course of radiation therapy and while still taking interferon, the lymphoma recurred again in 1993.

I discussed all my treatment options with my physicians and did some middle-of-the-night praying to make the best decision. In June 1993, I flew to the west coast to enroll in a Phase I clinical trial of the first monoclonal antibody therapy being used in humans to treat cancer. ( To watch a Stanford lecture about the trials by Dr. Ron Levy, click here. ) (emphasis added)

The investigational drug worked. Partly. For a while.

I received it again in two subsequent clinical trials and then two more times after it was FDA approved in 1997 and marketed as Rituxan.

It has been over 21 years since my diagnosis. Words fail me when I try to express my gratitude for the treatments, the researchers, my physicians and nurses, my family and friends and my good fortune. So each year I ask friends and family to support my walk in the Dallas Lymphomathon.

In addition to expressing gratitude for getting me to today, walking is also one way to help ensure that ongoing research is funded. My future still depends on research: Although my cancer is in remission right now, it may come back again. And next time, my lymphoma may be resistant to Rituxan.

Forget about me: Thousands of other lymphoma survivors today need better treatments than those that are available.

Modern textbooks still say my type of lymphoma is incurable. The textbooks are wrong:

My type of cancer is NOT incurable.

It’s one of the types for which researchers are still searching for a cure.”


You can invest in lymphoma research at Wendy’s page (here).